1987; 67:526-533.PHYS THER. Thomas Mohr, Thomas K Akers and Henry C Wessmanthe Rat Hind LimbEffect of High Voltage Stimulation on Blood Flow in

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Effect of High Voltage Stimulation on Blood Flow in the Rat Hind Limb

THOMAS MOHR, THOMAS K. AKERS, and HENRY C. WESSMAN

The purpose of this study was to test the effect of high voltage stimulation (HVS) on blood flow velocity (BFV) in the rat hind limb. A 20-MHz pulsed Doppler device was used to measure BFV changes in the femoral artery of 20 anesthetized rats after electrical stimulation. The animals were stimulated under the following conditions: 1) four different pulse rates, 2) changes in stimulus voltage, and 3) changes in polarity. Blood flow velocity also was measured in the unstimulated hind limb. Although each of the four pulse rates caused significant increases in BFV, the 20-pulse-per-second rate produced BFV increases significantly greater than the other three pulse rates. The BFV changes, on the average, occurred less than 1 minute from the onset of stimulation and lasted up to 14 minutes after the cessation of the stimulation. The BFV increased with increases in voltage intensity. Both the positive and negative poles elicited significant increases in BFV, but the negative pole produced the greatest increases. Blood flow in the unstimulated hind limb was unchanged after stimulation. This study indicates that HVS of muscle does cause significant increases in blood flow to the stimu­lated rat hind limb. Key Words: Blood flow velocity, Electric stimulation, Muscles, Rats.

In 1877, Gaskell noted changes in venous blood flow after tetanic stimu­lation of the crural nerve of the dog. At the onset of stimulation, he noted a sudden increase, or spurt, of blood flow and, after a few seconds, he noted a decrease in blood flow. Finally, after stimulation, he noted another increase in blood flow with a gradual return to normal.1 Gaskell thought that the initial spurt of blood might be caused by squeezing of the vessels by the contract­ing muscles and that the decreased blood flow during contraction was caused by stimulation of vasoconstrictor muscle fibers. In 1901, Bayliss found

that electrical stimulation of certain pos­terior nerve roots of the lumbosacral cord caused vasodilation, not vasocon­striction, of hind limb vasculature in the dog.2

Since those early investigations, many other researchers have studied the effect of electrical stimulation on blood flow and blood pressure responses. Johans­son found that in cats, direct peripheral nerve stimulation with a frequency of 10 pulses per second (pps) at 3 V caused an increase in muscle blood flow, whereas stimulation with 50 pps at 20 V caused a decrease in muscle blood flow.3 Other investigators also have found that stimulation of motor nerves caused an increase in muscle blood flow.4,5 Direct stimulation of the sym­pathetic chain fibers, however, has been shown to decrease muscle blood flow, apparently through sympathetic vaso­constriction.6,7 Clement and Pannier found that direct stimulation of muscles in dogs with a frequency of 40 Hz pro­duced mean blood flow increases of 101%.8 In another study, Clement and Shepherd found that direct muscle stim­ulation with a frequency of 5 Hz caused vasodilation, whereas a stimulation fre­quency of 40 Hz caused vasoconstric­tion.9 Donald and Ferguson found that stimulation of the anterior nerve roots

of T10 through L4 caused vasoconstric­tion, and stimulation of the L5 to L7 roots caused vasodilation.10 Gray and Staub found a decrease in blood flow through isometrically contracting mus­cles.11 Wakim, using an unspecified type of stimulator, applied both percuta­neous and direct motor nerve stimula­tion to test the effect of stimulation on blood flow in dogs.12 Although he used stimulation rates of 4, 8, 16, 32, 64, 128, and 256 pps, the 16-pps rate produced the greatest increase in blood flow.

Similar studies on human subjects are limited. Currier, using a 2,500-Hz stim­ulator, found significant increases in blood flow in the popliteal artery after stimulation of the gastrocnemius mus­cle.13 Dooley and Kasprak, using pa­tients with either implanted or transcu­taneously applied electrodes, found that peripheral vasodilation occurred after stimulation of either the spinal cord or specific nerve roots, but not with stim­ulation of peripheral nerves.14 Clini­cally, electrical stimulation has been found to help prevent postoperative ve­nous thrombosis, reduce ischemic pain, and facilitate healing resulting from in­creased circulation and decreased ve­nous pooling.15-17

Alon suggested that high voltage stim­ulation (HVS) may be effective in re-

Dr. Mohr is Associate Professor, Department of Physical Therapy, University of North Dakota, School of Medicine, Grand Forks, ND 58201 (USA). University of North Dakota, School of Medicine.

Mr. Wessman is Professor, Department of Phys­ical Therapy, University of North Dakota, School of Medicine.

This study was completed in partial fulfillment of the requirements for Dr. Mohr's doctoral degree in physiology, University of North Dakota, Grand Forks, ND.

This study was sponsored in part by a traineeship from the Foundation for Physical Therapy, and the results were presented at the Combined Sections Meeting of the American Physical Therapy Asso­ciation, Anaheim, CA, February 6-9, 1986.

This article was submitted September 9, 1985; was with the authors for revision 12 weeks; and was accepted May 21, 1986. Potential Conflict of Inter­est; 4.

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RESEARCH ducing pain, increasing joint mobility, reducing muscle spasm, enhancing heal­ing, reducing edema, and improving pe­ripheral circulation.18 No published re­ports, however, appear to exist of the effectiveness of HVS in treating any of those conditions. Alon further proposed that increased circulation may play a role in the physiological basis for treat­ment of all of those conditions.18

Because of the proposed importance of increased blood flow in treating many clinical conditions, physical therapists should know whether HVS does have any effect on blood flow. No established guidelines, however, exist regarding op­timal pulse rates, intensity, or polarities when using HVS.

The purposes of this study were 1) to test the effect, if any, of HVS on blood flow velocity (BFV) and 2) to investigate the optimal limits for the use of HVS.

METHOD

Two series of experiments formed the basis of our study. The first series of experiments was designed to test the effect of HVS on BFV and to determine the most effective pulse rate. The second series of experiments, building on the results of the first series, investigated: 1) whether HVS of one hind limb would cause an increase in BFV in the unstim­ulated hind limb, 2) the effect of polarity changes on BFV and, 3) the effect of increasing voltage intensity on BFV. The method used in this study was ap­proved by the animal resource facility director at the University of North Da­kota before the experiment.

Instrumentation

The ultrasonic pulsed Doppler flow­meter* used in this study has a 20-MHz carrier frequency with an adjustable range control to allow depth penetration of from 1 to 10 mm.19 The output of the flowmeter is a pulsatile voltage that represents the Doppler shift frequency (0.5 V/l kHz shift) and the instanta­neous BFV. Assuming the cross-sec­tional area of the vessel monitored re­mains constant, an increased Doppler shift is indicative of increased blood flow in the vessel monitored.20 In addition to the voltage output, the flowmeter also has an audible output through the use of a built-in speaker.

The voltage output of the flowmeter was connected to a chart recorder.† The amplifier on the chart recorder was cal­ibrated before each test session using an internally generated 100-mV signal. The output voltage of the flowmeter was re­corded on the chart recorder during the entire course of the experiment.

Before use, the flowmeter range con­trol was adjusted to achieve a peak volt­age displacement on the chart recorder and the loudest audible sound from the speaker. This procedure corresponds to focusing the ultrasound on the mid­stream of the vessel where the highest flow rate occurs.20 Zero or baseline blood flow is determined by turning the ultrasound off by means of a switch on the flowmeter. This electronic zero cor­responds to zero blood flow.20

Because the Doppler flowmeter is pulsed rather than continuous wave, it requires the use of only a single crystal transducer to both transmit and receive the ultrasound signal. The requirement for only one transducer greatly enhances its use on small animals. The pulsed Doppler probe consists of a 1-mm di­ameter, 20-MHz piezoelectric crystal‡

embedded in a Silastic®§ adhesive cuff. The crystal is embedded in the cuff so as to maintain a 45-degree angle be­tween the crystal and the lumen of the blood vessel. The complete details of the probe construction have been reported elsewhere.20

The stimulator used for the study was an EGS 100-2|| stimulator. The EGS 100-2 delivers a twin peak pulse of short duration of about 65 to 75 µsec with a variable intensity of 0 to 500 V. The pulse rate can be varied from 1 to 120 pps. To accommodate the stimulator for use on small animals, we used a bipolar stimulation technique involving two 5-× 5-cm carbon electrodes.#

Procedure

Fifteen male Sprague-Dawley rats weighing 325 to 500 g were used for the first series of experiments, and 5 other rats weighing 395 to 465 g were used in the second series. To record the BFV for both series, we anesthetized the rats with

an intraperitoneal injection of sodium pentobarbitol (50 mg/kg). A 2-cm inci­sion was made just distal to the inguinal area of the left hind limb to expose the femoral nerve, artery, and vein. A sec­tion of the femoral artery, about 1 cm in length, was separated carefully from the accompanying nerve and vein. The lumen of the Doppler probe was filled with conducting gel,** and the probe was placed around the section of the artery and sutured in place with 6/0 silk through the Silastic® cuff. For the sec­ond series of experiments, we similarly placed Doppler probes around both the left and right femoral arteries. We then connected the wire leads from the probe to the input of the flowmeter.

To prepare each animal for electrical stimulation, we shaved the hair from the back and left hind limb area. For all the experiments, the dispersive electrode was coated with conducting gel and taped in place just lateral to the vertebral column and directly superior to the hip joint. The active electrode was con­structed by folding and taping the car­bon electrode to form a rounded cuff that subsequently was filled with con­ducting gel, placed over the left hind paw of the rat, and then taped in place (Fig. 1).

In preliminary studies involving three animals, we found that at voltage levels greater than 90 V, the strong muscle contraction induced by pulse rates of 80 and 120 pps caused a slight displace­ment of the Doppler probe resulting in partial vessel occlusion. To avoid the vessel occlusion, we used a stimulus level of 90 V for all pulse rates during the actual research, except for a part of the second series of experiments, in which we used a varying voltage inten­sity.

The flowmeter output was recorded continuously by the chart recorder be­fore, during, and after each stimulation period. Throughout both series of ex­periments, we determined a control level of BFV before each of the stimu­lation periods by observing the baseline-to-peak voltage output of the flowmeter on the chart recorder. The stimulator was turned off during the determination of the control BFV.

First experimental series. For the first series of experiments, we set the HVS stimulator on continuous mode, the po-

* 545C-3 Directional Pulsed Doppler, Bioengi-neering Resource Facility, University of Iowa, Iowa City, IA 52240.

† Model 79 Polygraph, Grass Instrument Co, 101 Old Colony Ave, Quincy, MA 02169.

‡ DBF 120A-XS, Valpey-Fisher Corp, 75 South St, Hopkinton, MA 01748.

§ Dow Corning Corp, PO Box 1767, Midland, MI 48640.

|| Electro-Med Health Industries, Inc, 6240 NE 4th Ct, Miami, FL 33138.

# Codman & Shurtleff, Inc, Randolf Industrial Park, Randolf, MA 02368.

** Aquasonic 100, Parker Laboratories, Inc, 307 Washington St, Orange, NJ 07050.

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larity switch on negative, and the pulse rate on 2, 20, 80, or 120 pps. During each test session, the animal was stim­ulated with all four of the pulse rates. The order in which the four pulse rates were administered was determined by a random number table before the exper­iment. After obtaining a control level of BFV, we stimulated the animal for three minutes with one of the four pulse rates. After three minutes, we turned off the stimulator and allowed the BFV to re­turn to the control level. The stimula­tion procedure then was repeated using each of the other three pulse rates.

Second experimental series. Because we found the 20-pps stimulus to elicit the greatest increases in BFV in the first series of experiments, we designated it as the standard pulse rate for the second set of experiments. To test the effect of HVS on BFV in the contralateral, un­stimulated limb, we stimulated the ani­mal's left hind limb with the 20-pps stimulation rate for three minutes at 90 V while recording the BFV from both the left and right limbs.

To test the effect of changing polarity, we stimulated the animal's left hind limb for three minutes with the negative electrode. The animal's blood flow then was allowed to return to the control level, and the stimulation was repeated with the previously negative electrode changed to positive polarity.

Although we used a 90-V stimulus for all of the other sessions, we wanted to determine whether a "threshold" of blood flow response existed. We were interested in determining whether we could alter the magnitude of BFV by changing the voltage intensity. We, therefore, had to change the stimulation protocol for this portion of the experi­ment to incorporate a wide range of voltage levels available from the HVS stimulator. We arbitrarily selected a voltage range of 20 to 200 V. In prelim­inary studies, we determined that volt­ages above 200 V caused such a strong intermittent contraction that we expe­rienced movement artifact problems with the flowmeter probe wires.

To test the effect of changing voltage intensity, the animal was stimulated with increasing voltage levels in 20-V increments, ranging from 20 to 200 V with negative polarity. For this particu­lar test, the experimental protocol again was altered to accommodate the large number of successive stimulations. Be­cause the results of the first experimental series indicated that the time to reach peak flow was less than one minute, the

Fig. 1. Illustration of Doppler probe and high voltage galvanic stimulation electrode placement (anterior view). The Doppler probe was placed over the femoral artery. The dispersive electrode was placed on the animal's back (dashed lines), and the active electrode was placed over the paw (shaded area).

animal was stimulated for only one min­ute at each of the voltage levels. During this stimulation session, the stimulator was on continuously, the voltage was increased by 20 V at the end of each minute, and the animal's BFV was not allowed to return to the control level between voltage changes.

Data Analysis

At the completion of each series of experiments, we analyzed the polygraph records to determine both the prestim-ulus and poststimulus flowmeter volt­ages. The flowmeter voltages then were converted to BFV using the following equation supplied in the flowmeter tech­nical manual:

V = 78.25E/CosA

where V is the BFV in millimeters per second, 78.25 is a constant for this flow­meter, E is the baseline-to-peak voltage output from the flowmeter, and A is the angle between the sound beam and the BFV vector. The voltage used for deter­mining BFV was calculated by averag­ing the baseline-to-peak voltages of all pulses occurring during a one-second period of time, usually five or six pulses. For the prestimulus and poststimulus values of BFV, the voltage values for the calculation were taken immediately be­fore and after the stimulation. For the first set of experiments, in addition to the BFVs, our analysis included: 1) the time necessary to reach maximal BFV after the onset of stimulation and 2) the

recovery time from the cessation of the stimulation until the control level of BFV was reestablished.

For the second set of experiments, we analyzed BFV changes in both the stim­ulated and unstimulated limbs. In ad­dition, we compared BFV changes elic­ited by the negative and positive voltages and the changes in BFV at increasing voltage levels.

After the experiment, we analyzed the mean pretest and posttest BFVs using the Student's t test for BFV changes within each group before and after HVS. To determine differences between the means of the two experimental groups, we used either a one-way analysis of variance (ANOVA) or an analysis of covariance (ANCOVA) with the pretest as covariate. A probability level of .05 was used for all the tests.

RESULTS

First Experimental Series Table 1 gives the descriptive statistics

for changes in BFV before and after HVS for the first set of experiments. We found significant increases in BFV with all four pulse rates after three minutes of stimulation as compared with the control BFV. The overall range of in­creases in BFV across the four pulse rates was between 0% and 250%. Al­though the ranges of BFV increases were quite variable within each pulse rate group, the 20-pps stimulus consistently yielded the largest percentage increase

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TABLE 1 Mean Blood Flow Velocity Changes Before and After High Voltage Stimulation (mm/sec) in First Experimental Series Group (n = 15)

Group Pulse Rates (pps)

2 20 80

120

Before Stimulation

58.23 52.48 56.70 52.62

s

17.95 17.75 20.47 16.11

After Stimulation

97.16 145.31 91.70 91.94

s

35.64 52.49 37.22 34.16

X Change (%)

69.71 180.76 61.07 80.49

Range (%)

0-150 80-250

0-108 0-226

t

5.56a

8.60a

6.15a

5.35a

TABLE 2 Analysis of Covariance of Adjusted Posttest Blood Flow Velocity Changes Using Pretest Blood Flow Velocity as the Covariate in First Experimental Series

Source

Covariate (pretest) Group Error TOTAL

df 1 3

55 59

SS

38779.25 36559.37 47115.69

122454.31

MS

38779.25 12186.46

856.65 2075.50

F 45.27 14.23a

Posttest Blood Flow Velocity

Group Pulse Rates (pps)

2 20 80

120

Adjusted (mm/sec)

93.13b

149.27c

89.06* 95.66b

TABLE 3 Summary of Times Required to Reach Peak Blood Flow Velocity After Onset of High Voltage Stimulation and Recovery Times After Cessation of High Voltage Stimulation in First Experimental Series

Time to Peak (sec)

s Range

Recovery Time (min)

s Range

2 pps (n = 14) 49.57 30.27 20-110 (n = 14) 7.07 4.03 2-15

Pulse Rate Group

20 pps

(n = 15) 45.60 24.25 16-87 (n = 14) 14.21a

5.26 5-20

80 pps

(n = 13) 34.54 25.67 15-91 (n = 14) 4.93 2.40 2-10

120 pps

(n = 12) 24.08 15.85 12-70 (n = 14)

5.86 2.57 3-10

in BFV for any given animal. Only one of the animals did not show an increase in BFV after stimulation at 2, 80, and 120 pps, which accounts for the 0% increases in those groups, but that ani­mal did show an 80% increase in BFV with the 20-pps stimulation.

Analysis of covariance results are pre­sented in Table 2 for the first set of experiments. The analysis on the ad­justed means indicated a significant dif­ference among the pulse rate groups.

Scheffé's method of post hoc analysis showed that the increase in BFV after stimulation at 20 pps was significantly greater than the increases in each of the other three pulse rate groups. Differ­ences in BFV increases between the 2-, 80-, and 120-pps pulse rate groups, how­ever, were not significant.

The instantaneous BFV profiles ob­tained using the pulsed Doppler system were excellent, with a typical flowmeter output shown in Figure 2. The time

Fig. 2. Pulsatile flow tracings from one an­imal showing changes in Doppler shift after high voltage galvanic stimulation with differ­ent pulse rates. Scale indicates a baseline-to-peak shift of 0 to 1 kHz. Increased fre­quency shift indicates an increased blood flow velocity. The 20-pps rate shows the greatest baseline-to-peak frequency shift.

required for the BFV to reach peak ve­locity after the onset of stimulation was quite variable (Tab. 3). The mean time to reach peak BFV, however, was less than one minute for any of the four pulse rates. Although a trend appears to exist toward an inverse relationship be­tween time to reach peak BFV and pulse rate in Figure 3, an ANCOVA revealed no significant differences between the four pulse rates and the time necessary to reach peak BFV. Because of equip­ment problems, we could not calculate the time to reach peak BFV or the re­covery times for some of the animals; therefore, the size of the groups shown in Table 3 varied.

The recovery time, or the time the BFV took to return to the control level after stimulation, was also quite variable (Tab. 3). For any given animal, recovery time was consistently the longest with the 20-pps stimulation ranging from 5 to 20 minutes after 3 minutes of stimu­lation (Fig. 4). Animals in the 2-, 80-, and 120-pps groups had mean recovery times of about 5 to 7 minutes.

An ANOVA indicated significant dif­ferences among the four pulse rate groups in recovery time, and Scheffé's method of post hoc analysis showed that the recovery time for the 20-pps group was significantly greater (p < .01) than that, for any of the other groups. We found no significant differences in re-

a Significant change, p < .001.

a Significant change, p < .001. b No significant change, p > .05. c Significant change, p < .01.

a Significant change, p < .001.

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Pulse Rate (pps) Fig. 3. Mean time to reach peak blood flow velocity after onset of high voltage galvanic stimulation.

Pulse Rate (pps) Fig. 4. Mean recovery time for blood flow velocity to reach control level after cessation of high voltage galvanic stimulation.

covery times between the 2-, 80-, and 120-pps groups.

Second Experimental Series

The relationship between the voltage intensity and the mean BFV for the five animals used in this series of experi­ments is illustrated in Figure 5. No in­crease in BFV occurred with a stimulus of 20 V, and only two animals showed an increase BFV with the 40-V stimulus. At 60 V, the BFV increased sharply in all the animals tested. Although a visible muscle contraction was not apparent at 40 V, the 60-V level did correspond to a visible contraction of the muscles in the lower limb of the animals.

A significant mean increase in BFV occurred in the stimulated limb (152%),

although no increase in BFV (0%) oc­curred in the unstimulated limb (Tab. 4). An ANCOVA revealed a significant difference between the adjusted means of the BFV in the stimulated and un­stimulated limbs (Tab. 5).

We found a significant increase in BFV after stimulation with both the negative and positive polarity settings (Tab. 6). In all five animals, stimulation with the negative pole over the paw generated a larger increase in BFV than the same stimulation with the positive pole. An ANCOVA indicated a signifi­cant difference between the adjusted BFV means after polarity changes (Tab. 7). A significantly greater increase in BFV was found with the negative pole than with the positive pole.

DISCUSSION

The results of our experiments indi­cate that HVS can significantly increase blood flow to the stimulated rat hind limb. In this study, we used percuta­neous stimulation, but our results were in agreement with several other animal studies using either direct nerve or mus­cle stimulation.4,5,8,10,12 The results of our research are also in agreement with studies on human subjects using percu­taneous stimulation.13,14

Although numerous studies have been conducted, the mechanisms in­volved in the cardiovascular responses to electrical stimulation and muscle contraction still are not understood fully. Johansson suggested that low threshold, type III afferents were respon­sible for depressor responses (eg, vaso­dilation and decreased blood pressure), whereas high threshold type IV (C-fiber) afferents were responsible for pressor re­sponses (eg, vasoconstriction and in­creased blood pressure).3 The results of other studies also indicate that type III and IV afferents are responsible for the reflex cardiovascular changes seen dur­ing muscle contraction.21-23 These re­ceptors are thought to be activated in some way by various stimuli such as muscle pressure, stretch, contraction, pain, and various chemical stimuli and metabolites. Thus, the type III and IV afferents may act as mechanoreceptors and as nociceptors or chemoreceptors, or both. Whether those afferents were involved in the blood flow changes seen in this study is not known. Further in­vestigation would be required, but based on prior studies, stimulation of the type III and IV afferents provide the most plausible explanation for the significant results of this study.

Crayton et al found that blood flow increases to contracting muscles were not affected by alpha or beta blockade and, therefore, they concluded that the blood flow increases were not mediated by alpha or beta adrenergic receptors.4

The sympathetic cholinergic vasodilator system that may cause vasodilation in the dog and cat after stimulation has not been shown to exist in the rat. We, therefore, would exclude this system as a mechanism for the increase in BFV that we found in our study.24

The reason the 20-pps stimulus in­duced a significantly greater increase in BFV than the other pulse rates is diffi­cult to explain. Frequencies of 40 and 50 Hz have been shown to cause vaso­constriction, whereas frequencies of 5

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RESEARCH

Fig. 5. Effect of voltage changes on mean percentage of change in blood flow velocity with stimulation at 20 pps.

and 10 Hz caused vasodilation.3,9 Other investigators demonstrated maximal vasoconstriction with direct sympa­thetic nerve stimulation and impulse rates of 16 pps or more.25,26 Based on those findings, we expected the 2-pps rate to produce the greatest vasodilation and subsequent increase in BFV.

The 20-pps stimulus may have pro­duced a strong, nontetanizing, rhythmic contraction that acted as a muscle pump in the contracting muscles, thereby aid­

ing blood flow.5 Wakim suggested that stimulation rates of less than 8 pps did not produce an adequate mechanical pumping effect, whereas pulse rates greater than 32 pps caused the resulting muscle contraction to interfere with blood flow.12 If Wakim's theory is cor­rect, pulse rates between 8 and 32 pps should produce an optimal muscle pumping effect, which would help ex­plain the large increase in BFV seen with the 20-pps stimulation in our study.

TABLE 4 Blood Flow Velocity Changes in the Stimulated and Unstimulated Limbs After High Voltage Stimulation (mm/sec) in the Second Experimental Series

Group (n = 5)

Stimulated Unstimulated

Before Stimulation

s 49.94 11.71 38.96 4.85

After Stimulation

s 125.73 36.18 38.96 4.85

Change (%)

152.31 0.0

Range (%)

112-240 0

t

6.03a

1.00b

TABLE 5 Analysis of Covariance of Adjusted Posttest Blood Flow Velocity Changes Using Pretest Blood Flow Velocity as the Covariate in the Second Experimental Series

Source

Covariate (pretest) Group Error TOTAL

df 1 1 7 9

SS

15220.26 6690.59 2243.62

24154.47

MS

15220.26 6690.59 320.52

2683.83

F

47.49 20.87a

Posttest Blood Flow Velocity

Group

Stimulated Unstimulated

Adjusted (mm/sec)

113.7a

51.0

This observation would suggest further that pulse rates of 2, 80, and 120 pps may not produce a muscle pump effect. Because we found a significant increase in BFV with all pulse rates used in this study, we suggest that in addition to the muscle pump effect, HVS may have some direct local effect on the type III and IV afferent nerves. Because of this hypothesized direct effect, therefore, all of the pulse rates caused a significant increase in BFV. We further suggest that the 20-pps rate may have had both a direct effect and a muscle pumping ef­fect, which resulted in the significantly greater increase in BFV with the 20-pps rate than with the other pulse rates.

In this study, blood flow increases occurred within less than one minute after the onset of stimulation even though most clinical applications of HVS probably would require a longer stimulation period. The clinically signif­icant finding, however, is the quick re­sponse of the circulatory system to the HVS.

The observed recovery times suggest that increased blood flow continues for several minutes after stimulation, a find­ing that also has been reported by other investigators.10 Our findings further sug­gest that the recovery time is related to the relative increase in BFV, because the 20-pps stimulus had both a significantly greater effect on BFV and recovery time than the other three pulse rates tested. Clinically, this phenomenon would im­ply that BFV remains elevated for a period of time after HVS, thereby en­hancing the physiological effects of in­creased blood flow.

In this study, the threshold for in­creased BFV was about 40 V. The large increase in BFV at 60 V in all of the animals appeared to be related to a vis­ible muscle contraction. This finding indicates a direct relationship between the strength of a muscle contraction and the blood flow through that muscle, which is consistent with the theory that type III and IV afferents are responsible for the cardiovascular responses ob­served. Kniffki et al found that a con­tractile force equal to 20% of maximal was required to fire the low threshold, type III afferents, whereas the type IV afferents required a near maximal con­traction to respond.23 This observation would suggest that for HVS to be effec­tive clinically in increasing blood flow, one should try to elicit a muscle con­traction rather than just a cutaneous sensation.

a Significant change, p < .004. b No significant change, p > .05.

a Significant change, p < .003.

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TABLE 6 Blood Flow Velocity Changes After High Voltage Stimulation with Negative and Positive Polarities (mm/sec) in the Second Experimental Series

Group (n = 5)

Negative Positive

Before Stimulation

s 49.94 11.71 56.67 13.43

After Stimulation

s 125.73 36.18 103.06 26.93

Change (%)

152.31 81.80

Range (%)

112-240 60-117

t

6.03a

6.56b

TABLE 7 Analysis of Covariance of Adjusted Posttest Blood Flow Velocity Changes Comparing Negative and Positive Polarities Using Pretest Blood Flow Velocity as the Covariate in the Second Experimental Series

Source

Covariate (pretest) Group Error TOTAL

df 1 1 7 9

SS

3639.48 3073.26 2709.56 9422.30

MS

3639.48 3073.26

387.08 1046.92

F

9.40 7.94a

Posttest Blood Flow Velocity

Group

Negative Positive

Adjusted (mm/sec)

132.7a

96.1

The BFV changes that occurred in this study apparently were confined to the stimulated extremity, a finding con­sistent with studies of dogs.4,8,12 In those studies, blood flow increased in con­tracting muscles and decreased or re­mained the same in noncontracting muscles. Clement and Pannier con­cluded that the circulatory reflexes in­volved consisted of somatic nerve fibers from the contracting muscles as the af­ferent pathway and adrenergic sympa­thetic nerves as the efferent pathway.8

This system apparently allows rather fine control over circulatory changes, causing vasodilation in contracting muscles and vasoconstriction in non-contracting muscles.

Although both the positive and nega­tive polarities caused significant in­creases in BFV, the negative pole had an even greater capacity to increase BFV in our study. The reason for this effect is not apparent, because neither of the stimulation electrodes were placed over motor points of the muscles fed by the femoral artery or its branches. Even though the instruction manual supplied with the EGS 100-2 stimulator sug­gested using negative polarity for in­creasing blood flow,27 no studies appear to exist that offer a physiological basis for this recommendation.

Clinical Implications

Although we studied small animals only, some important clinical implica­tions may be gained from this type of basic animal research. Ours is the first study that has attempted to measure and describe the effect of HVS on blood flow response. Our results are particularly significant because increased blood flow apparently is an important physiological factor in 1) reducing pain, 2) reducing muscle spasm, 3) enhancing healing, 4) reducing edema, and 5) improving pe­ripheral circulation.18, Our results indi­cate that significant blood flow increases can be induced with various pulse rates and, although the 20-pps rate may be the most effective, any of the pulse rates used in this study apparently can be used to increase blood flow.

When using HVS specifically to in­crease blood flow, our results indicate that a maximal muscle contraction may aid in creating a muscle pumping effect and perhaps in stimulating maximally the type III and IV afferents in and around muscles. This finding would seem to be useful in treating patients with what Cailliet terms "ischemic pain," which is accompanied by a mus­cle spasm and a decrease in blood flow because of the contracting muscle re­stricting its own blood supply.28 With

this type of problem, HVS might be of benefit by causing an intermittent mus­cle contraction, increasing blood flow, and breaking the cycle of muscle spasm and reduced blood flow. Our findings suggest that muscle blood flow increases are related to stimulus intensity. When using HVS specifically to increase mus­cle blood flow, therefore, clinicians may find the use of a maximally tolerated muscle contraction to be beneficial. High voltage stimulation also may be useful in cases where an increase in blood flow is indicated but where a heat­ing effect, such as from hot packs, would not be desirable. Ours is the first study to show that polarity is important when using HVS to increase blood flow. Stim­ulation with the negative pole appears to give a much better blood flow re­sponse than the positive pole; therefore, polarity should be an important clinical consideration when using HVS. Because of their short-duration pulses, HVS stimulators apparently do not cause chemical or thermal changes under the positive and negative electrodes as do the traditional, low voltage, long-dura­tion galvanic stimulators nor are they effective for use in iontophoresis.18

The effect of the increased blood flow seems to be quite local in nature and may be limited to the muscles being stimulated. The correct placement of stimulating electrodes, therefore, be­comes an important clinical considera­tion when using: HVS tonncrease blood flow.

Further research certainly is needed to study both the basic physiological and clinical treatment effects of HVS. This type of research will be required if we are to justify the use of HVS current in treating the wide variety of clinical dis­orders that currently are being treated with HVS. We hope to undertake simi­lar research on human subjects to study the effects of HVS on blood flow.

CONCLUSION The results of this study indicate that

HVS has the ability to cause significant and relatively long-lasting increases in BFV and subsequent blood flow to the stimulated muscles. The blood flow in­creases appear to be related to a muscle contraction and confined to the stimu­lated limb. Even though both negative and positive polarities caused significant increases in blood flow, the negative polarity produced the greatest increases. The physiological mechanisms involved in the circulatory changes observed in this study remain unclear.

a Significant change, p < .004. b Significant change, p < .003.

a Significant change, p < .03.

532 PHYSICAL THERAPY

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RESEARCH REFERENCES

1. Gaskell WH: On the changes of the blood­stream in muscles through stimulation of their nerves. J Anat 11:360-402, 1877

2. Bayliss WM: On the origin from the spinal cord of the vasodilator fibres of the hind limb, and on the nature of these fibres. J Physiol (Lond) 26:173-209, 1901

3. Johansson B: Circulatory responses to stimu­lation of somatic afferents. Acta Physiol Scand 57:(Suppl198):1-91, 1962

4. Crayton SC, Aung-Din R, Fixler DE, et al: Dis­tribution of cardiac output during induced iso­metric exercise in dogs. Am J Physiol 236:H218-H224, 1979.

5. Folkow B, Gaskell P, Waaler BA: Blood flow through limb muscles during heavy rhythmic exercise. Acta Physiol Scand 80:61-72, 1970

6. Kjellmer I: On the competition between meta­bolic vasodilation and neurogenic vasocon­striction in skeletal muscle. Acta Physiol Scand 63:450-459, 1965

7. Donald DE, Rowlands DJ, Ferguson DA: Simi­larity of blood flow in the normal and the sym-pathectomized dog hind limb during graded exercise. Circ Res 26:185-199, 1970

8. Clement DL, Pannier JL: Cardiac output distri­bution during induced static muscular contrac­tions in the dog. Eur J Appl Physiol 45:199-207, 1980

9. Clement DL, Shepherd JT: Influence of muscle afferents on cutaneous and muscle vessels in the dog. Circ Res 35:177-183, 1974

10. Donald DE, Ferguson DA: Study of the sym­pathetic vasoconstrictor nerves to the vessels

of the dog hind limb. Circ Res 26:171-184, 1970

11. Gray SD, Staub NC: Resistance to blood flow in leg muscles of dog during tetanic isometric contraction. Am J Physiol 213:677-682, 1967

12. Wakim KG: Influence of frequency of muscle stimulation on circulation in the stimulated ex­tremity. Arch Phys Med 34:291-295, 1953

13. Currier DP: Electrical stimulation effect on lo­calized blood flow. Abstract. Phys Ther 63:761, 1983

14. Dooley DM, Kasprak M: Modification of Wood flow to the extremities by electrical stimulation of the nervous system. South Med J 69:1309-1311, 1976

15. Lindstrom B, Korsan-Bengtsen K, Jonsson O, et al: Electrically induced short-lasting tetanus of the calf muscles for prevention of deep vein thrombosis. Br J Surg 69:203-206, 1982

16. Doran FSA, White HM: A demonstration that the risk of postoperative deep venous throm­bosis is reduced by stimulating the calf muscles electrically during the operation. Br J Surg 54:686-689, 1967

17. Cook AW, Oygar A, Baggenstos P, et al: Vas­cular disease of extremities. NY State J Med 76:366-368, 1976

18. Alon G: High Voltage Stimulation. Chatta­nooga, TN, Chattanooga Corp, 1984, pp 4-16

19. Marcus M, Wright C, Doty D, et al: Measure­ments of coronary velocity and reactive hyper­emia in the coronary circulation of humans. Circ Res 49:877-891, 1981

20. Haywood JR, Shaffer RA, Fastenow C, et al: Regional blood flow measurement with pulsed Doppler flowmeter in conscious rat. Am J Phys­iol 241 :H273-H278, 1981

21. Coote JH, Hilton SM, Perez-Gonzales JF: The reflex nature of pressor response to muscular exercise. J Physiol (Lond) 215:789-804, 1971

22. Kalia M, Mei SS, Kao FK: Central projections from ergoreceptors (C-fibers) in muscle in­volved in cardiopulmonary response to static exercise. Circ Res 48(Suppl 1):48-62, 1981

23. Kniffki KD, Mense S, Schmidt RF: Muscle re­ceptors with fine afferent fibers which may evoke circulatory reflexes. Circ Res 48(Suppl 1):25-31, 1981

24. Bolme P, Novotny J, Unvas B, et al: Species distribution of sympathetic cholinergic vasodi­lator nerves in skeletal muscle. Acta Physiol Scand 78:60-64, 1970

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26. Folkow B: Impulse frequency in sympathetic motor fibers correlated to the release and elim­ination of a transmitter. Acta Physiol Scand 25:49-76, 1952

27. High Voltage Electrogalvanic Stimulator In­struction Manual. Miami, FL, Electro-Med Health Industries, Inc. 1982, p 6

28. Cailliet R: Neck and Arm Pain. Philadelphia, PA, F A Davis Co, 1978, pp 40-44

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opinions and comments Goniometric Measurements at the Knee

To the Editor: I read with serious interest the article

by Gogia et al, "Reliability and Validity of Goniometric Measurements at the Knee," which appeared in the February 1987 issue of PHYSICAL THERAPY. I commend the authors' efforts to clarify the reliability and validity of goniomet­ric measurements at the knee. Reliabil­ity and validity studies of goniometry, basic evaluation procedures, are ex-

Errata

In the March 1987 issue, the article by D. M. Basso and L. Knapp, entitled "Comparison of Two Continuous Passive Motion Protocols for Patients with Total Knee Implants," should have the following corrections:

1) The sixth line of the Abstract should read (p < .001).

2) The third paragraph of the Results section, lines 10 and 12, should read df= 1,21 in each instance.

In the article "Reliability of the Attraction Method for Measuring Lumbar Spine Backward Bend­ing" by P. Beattie, J. M. Roth-stein, and R. L. Lamb, also in the March 1987 issue, Table 5 (Val­ues for Backward Bending by Age and Sex) is inaccurate. The two columns headed "n" should be reversed.

In the April 1987 issue, an au­thor's affiliation inadvertently was left out of the article entitled "Ef­fect of High Voltage Stimulation on Blood Row in the Rat Hind Limb," page 526. Please note that Thomas K. Akers is Professor, Department of Physiology, Unir versity of North Dakota, School of Medicine. We apologize for the omission.

tremely important. I was concerned after reading the article, however, be­cause the conclusions drawn by the au­thors, that "1) goniometric measure­ments obtained by different therapists to assess the position of a patient's knees can be used interchangeably and 2) measurements recorded using the spec­ified technique reflect the actual posi­tion of the knee joint," are misleading. I believe, based on my own interpreta­tion of the procedures used, that the conclusions do not reflect accurately the results of the study. I offer my observa­tions to help readers gain a more accu­rate interpretation of the results than that presented by the authors. More­over, I encourage the authors to reex­amine their results and clarify their con­clusions based on their specific findings.

I have difficulty accepting the conclu­sions of the study because the knee an­gles measured consisted of different an­gles within a wide range of motion and the angles were "pooled" for analysis. The authors reported that the joint an­gles "ranged from 0 to 120 degrees; their average mean and standard deviation

were about 59 and 15 degrees, respec­tively " Careful examination of these data reveals that the majority of the measurements (about 68%, assum­ing a normal distribution) ranged from 44 to 74 degrees (±1 s). About 96% of the measurements ranged from 29 to 89 degrees (±2 s). This means that knee-flexion angles less than 29 degrees and greater than 89 degrees either were rep­resented minimally in the results or were not represented. For me, accepting go­niometric measurements of knee-flex­ion angles less than 29 degrees as reliable and valid, based on the results of this study, is particularly difficult given the results of published studies that have reported examining the reliability and validity of measuring knee angles near terminal extension.1,2 The authors ac­knowledged that Rothstein et al re­ported poor intertester reliability for knee extension with different patients.1

In a more recent study, Enwemeka com­pared goniometric knee measurements with radiographic bone angle measure­ments in healthy adults and found that, within the first 15 degrees of knee flex-

Volume 67 / Number 6, June 1987 979