..

REVIEW

Autonomic regulation of splanchnic circulation

KATIILl:EN A FR:\~ER, S . .<\1-.IUEL SLEE

KA FRASER, SS LEE. Autonomic regulation of splanchnic circulation. Can J Gastroenterol 1991;5(4):147-153. The ro le of the autonomic nervous system in c irc ulatory regulaLion of the splanchnic organs (stomach, small intestine, colon, liver, pancreas and spleen) is reviewed. In general, the symrarhetic nervous system is primarily involved in vasoconstriction , while the parasym­pathetic contributes to vasodi lation. Vasoconstriction in the splanchnic c ircula­tion appears to be mediated by alpha-2 receptors anJ vasod ilation by activation of primary afferent nerves with subsequent release of vasod i larory peptides, or by stimulation of beta-ad rcne rgic receptors. As well, an important function o f t he autonomic nervous system is to provitlc a mechanism by which splanchnic vascular reserve can be mobilized during stress to maintain overa ll cardiovascular homeostasis.

Key Words: Autonomic nervous system, Parasympathetic nerves, Splanchnic circula­tion , Sym/)athetic nerves

Regulation autonomique de la circulation splanchnique

RESUME: Les auteurs examinent le ro le Ju sysLeme n erveux autonome dans In regulation du systcme circularoire des o rganes splan chniques (esto mac, imcsrin grele, colo n, foic, pancreas Ct rate). En general, le systcme nervcux sympathique intervient principalement Jans la vasoconstriction tanJis que le parasympathi­que contribuc a la vasod ilatation. La vasoconstriction scmblc J eclench ee par les reccptcurs alpha 2 c t la vaso<li latation par !'activation des nerfs afferents primai res provoquant la liberatio n de peptides vasodilatateurs o u par In stimula­tion des reccpteurs beta aJrenergiques. Une des fonctions importantes Ju systeme ncrvcux autono mc est egalemc nt de fourni r un mecanisme permewmt de mo bilise r la reserve vasculaire splanc hnique durant le stress afin de maintenir l'homeoscasc cardiovascula ire g lobale.

GasiroenteroloJri Re~earch Grnu/J, Univerrny of Calgary. Calgary , Alberta Correspondence and ~e/>rinis: Dr SS Lee, 3330 Hos/1iwl Dri,l'e NW!, Calgary. Alberra

TlN 4N I. Tele/>hcme (403) 220-4500 Receiwd jr,r publirntion May 13, l 99 l . Accepted July H, l 99 /

CAN J GA!:>"TRL)J:NTrnrn V,11 5 No 4 JuLY/AuuusT 1991

Tl II:. SPLANCI INIC ORl;ANS ARE

capable of controlli ng their mo­

ment-to-moment blood/low and oxy­genation ro a cenain extent, even when neural and/or humora l input b d1m111ated (J ). The ability to self-regu­late hloodflow 111 the splanchnic organs has been attribureJ to myogenic , mcra­holic nnd neuroc rinc influences on

resistance and exchange vessels ( l ). Despite the auwnomy ofbloo<lflow reg­

ulation in the splanchnic orga ns, the

au tonom ic nervous system is thought to provide a more sophbticarcJ level of

control. In add ition, auronomic ne rves provide a mechanism tn mainta in over­

all cnrdiova&cular homeostasis by tive r­riding local influences, such that splanchnic blood can be quickly redi r­ected to vita l organs during emergency sta tes in the organi~m (2).

The autonomic nervous ~ystem is comprised ,)f sympathetic (thoracolum­bar) and parasympathetic (cranima­

cral) nerves. Sympathetic nerves arc primari ly involved in vasocommction

a nJ parasympathetic 111 vastKlilauon.

Preganglionic cell bodies of the sym­pathetic ne rves are located in the intcr­

meJio latcral cell column in rhe grey substance of the spinal cord. Axons from these cell hodies ex it the spinal

147

FRASER AND LEF

corJ via the ventral roots, pass ing through the white communicat ing rarnus (myelinateJ) to enter the first of two sympathetic ganglia, the paraver­tcbral or sympathet ic ganglia. The axon will do one of two things: it will synapse in the chain , either crania lly or cauJally to the point at which it entered ; or it will pass directly through the sympathe tic chain without synaps­ing, to become pan of the splanchnic nerves targeteJ to enter one of three prevertebral ganglia: celiac, superior mesenteric or inferior mesenteric ganglia. After synapsing in the prever­tebral ganglia, post ganglionic fibres travel to the organ to be innervated. In the first option, after synapsing in the chain the post ganglionic fibres exit the chain co re-enter the spinal nerve trunk via the grey communicating ramus (un­myelinated) and project co visceral structures in the periphery (3).

Alternatively, cell bodies of pregan­glionic fibres in the parasympathet ic nervous system originate in either nerve nuclei of the brainstcm (iii, vii , ix or x), or sacra l levels of the spinal corJ (Sl co S3). Preganglionic fibres char­acteristically terminate in pa rasym­pathetic ganglia in or near the organ innervated, typically in the walls of the organ innervated. As such, the post ganglionic fibres are relatively short and located in che wall of the organ to be innervated as well. Parasympathetic innervation co che abdominal viscera is provided by the vagus, whereas the pel­vic nerve innervates the pelvic viscera. Typically, boch pre- and post gang I io­nic parasympathetic fibres and pregan­glionic sympathetic fibres release cholinergic agents, while post ganglio­nic sympathetic fibres release .:iJrener­gic transmitters (3).

Finally, certain spec ific visceral af­ferent fibres provide sensory feedback co higher centres. These primary af­fe rents project to the brain and spinal cord via the auronomic nerves (3).

BLOODFLOW REGULATION IN SPLANCHNIC CIRCULATION

Bloodflow co the colon and stomach is significantly le s than co the intes­tine, while in the colon and intestine,

148

proximal segments receive a greater proportion of bloodflow than Jisca l ( l ). Generally speaking, the suhmucosal­mucosal region:, receive a greater share of hlooJflow than do the muscularis layers ( l ). The microci rculatory ar­chitecture of che stomach and colon is relatively similar, while the circula tion in the small intestine is quite unique by comparison. Like the liver, the pan­c reas is perfused with both venous and arccria l blood (I) . Typically, within the microcirculation of the splanchnic o r­gans, blooJflow is modified by precapil­lary resistance vessels ( 4 ).

In the following sections the micro­vascular c irculation of the splanchnic organs (stomach , small intestin e, colon, liver, pancreas anJ spleen) and their moJification by the autonomic nervous system are J escribed.

THE GASTRIC CIRCULATION Large arteries pierce the muscle lay­

ers of the stomach to become progre:,­sive ly smaller as they supply the muscularis and submucosal regions. Ar­terial plexuses located in the submu­cosa send mucosa! arteriole:, to supply capillaries at the base of the mucosa, a fter passing perpendicularly through the muscularis mucosa. Collecting ven­ules locateJ in the mucosa carry blood from the mucosa to che submucosa, where it enters the venular plexus. Blood exiting the venular plexuses e n­ters la rger veins that drain the stomach . Within the muscle layers (superfic ial and J eep) there is free communication berween capilla ries on the same or dif­ferent planes. The muscle capillary net­works drain into venules to join veins from the venular plexus. These veins combine with larger veim ultimately to

drain che stomach (5). Because the muscle vascular beJ is parallel to the suhmucosal-muc~)sal beds, mucosa! hloodflow can be controlled by con­striction or dilation of the subrnucosal a rterio le plexus (6).

CONTROL OF GASTRIC BLOOD FLOW

Sympathetic regulation: Sympathetic input to the stomach arises from T6 to

LJ O of the spinal cord and terminates as preganglionic fibres in the celiac gang-

lion . Post ganglionic fibres exit the celiac ganglion to innerv,He the stom­ach ( 5). Arteries anJ arterioles arc more heav ily adrenergica lly supplied than veins or venules, while in capillaries aJrenergic innervation is relative ly un­common (7). However, more recent work has demonstrated some adrener­gic innervation of the capillary enJo­the lium at th e ba~a l ;,ml miJ dlc portions of the mucosa.

Vasoconstriction produced hy elec­trical stimulation of :.ymparheric effer­ents decreases blooJflow to the stomach and mucosa (8), incluJing celiac (9) and gastroepiploic arterial flow (10). However, with pro longed stimulation of gastric ~ympathctic fibres, escape from vasoconstriccion re­sults, and bloodflow reaches a higher but stable level. This phenomenon, tcrmeJ 'autoregulatory escape' ( 11 ), occurs in most splanchnic organs. In,­tial vasoconstriccion appear!> co he mediated by a lpha-ad renergic recep­tors, and escape from vasoconstricrion (vasoJilarion) hy bcca-adrcnergic (5) or primary afferent inne rvation.

C atecholamine effec ts on gastriL circulation arc divergent. Adrenaline typically elicits va:,oJilation, whereas noradrenaline administration results in vasoconstriction when infused intra­venously ( 12). Intra-arterial infusion of adrenaline and noradre na line into the left and right gastric arteries proJuces immediate vasoconstriccion succeeJ cd by autorcgulatory escape and subse­quent vasodila cion . The conscrictnr re­sponse is abolished hy alpha-aJrenergic blockade, and the dilatory effect b block­eJ by beca-adrenergic blockade ( 13 ). More specifically, others have shown markeJ vasoconstriccion ac the level of the gastric suhmucosal arteriolar vas­c ular bed immediately following adren­aline or noradrenaline administration (14). The literature therefore supports the conclusion that both catccholaminc.1 initially constrict gastric vessels.

Parasympathetic regulation: The areJ postrema appears co be the o rigin of che nerve fibres inne rvating the funJus and corpus o( the stomach in the rat (15). Parasympathetic fibres chat innervate rhe stomach arise from the vagus, which

CAN J GASTRl)~NTEROL VOL 5 No 4 Jut Y/ALKil/ST 1991

Autonomic regulation of splanchnic circulation

consists of both high and low threshold fibres. Stimulation of the low threshold vagal fibres results in a nonadrenergic­noncholinergic relaxarion of the stom­ach and a concomitant increase in bloodflow ( 16). Following vagal stimu­lation, the gastric arteriolar diameter increases (7), producing a sharp in­crease in bloo<lflow. Given the resis­tance of arteriolar diameter w cholinergic antagonists (arropine-mus­carinic blocker), a noncholincrgic dila­tory effect is suggested ( 7.17).

Studies of canine gastric arteries have shown that vagal stimulation can depress the vasoconstrictive response to adrcnergic stimu lation ( 18), thus suggesting cholincrgic inhibition of adrenergic neurocransm1ss1on. The study provided evidence of muscarinic receptors on sympathetic nerve en­dings inhibiting or dulling adrcnergic neu rotransm iss ion.

INTESTINAL CIRCULATION Microcirculation: The microcircula­tionof the intestine is different from rhe vascular arrangement in the stomach. Tht submucos<1, mucosa an<l muscul<1ris layers of che small intestine all maintain fairly distinct vascular beds. The arterial plexus, located in rhe sub­mucosa, supplies all three layers direct­ly, as well as sending a single arteriole to the vi llus rip. A consecutive arrange­ment between the arterioles, precapil­lary sphincters, capillaries and venules exists in each layer of the intestine. The first o rder arterioles supplying the wall of the intestine originate from mesemeric arteries. These arterioles then pierce the muscle walls (longi­tudinal and circular) and continue through rhe submucosa, where second an<l third order arterioles arise anJ supply rhe submucnsa and mucosa to

the tip of the villus. A branch of t he second and third order anerinles, the fourth order, passes back to supply the muscle layers. Small venules dram each layer independently and eventually all blcxx.lflow drains into larger veins, ulti­mately to draining the intestine ( l 9).

The arterial and venous poruons supplying the vi llus are believed to autoregulate more successfully than the

deeper vessels. The villus is supplied by a main arteriole, the smaller supplying brnnched arterioles of which extend to the capillary bed at the rip of the villus. The capi llaries drain into severa l small venules, to drain eventually into a lar­ger venule located at the base of the vil lus. A discriminating feature of villus c irculation in cats (20) , dogs (21) and humans (22) is the presence of a coun­tercurrenr exchange mechanism. The venule and arterioles supplying the vil­lus lie in close proximiry to each other ( 10 to 20 µm) (23), and as a result blocx.l in rhe venule and capillaries flows in a direction opposite ro arterial flow . It mteresting Ill note that a countercurrent mech::ini~m has nm been established 1n rat or rabbit intes­tine (24).

Sympathetic regulation: Low freque n­cy ( 4 rn 8 Hz) sympathetic stimulation of nerves in the intestinal vascular bed results in marked vasoconstriction fo l­lowed by a decrease in bloodflow w the whole mtestine mucosa, submucosa and muscle layers. As well, catecholamine re lease from either sympathetic post synaptic receptors or the adrenal cortex produces intense vasnconstriction with subsequent dilation and increased flow - an autorcgulatory respome (25). The mechanism responsible for autoregula­rory escape m the intestine had been unclear until a recent stu<lydemonstrat ­ed that post gang I ionic sympathetic nervous stimulation activates bmh vasoconstricror sympathetic fibres and vasodilator afferent capsaicin-scnsirive C-fibres (26) . It is generally accepted 1 hat the miual vasoconstriction is mediated by alpha-2 adrenergic recep­tors (27), whereas st imulntion of af­ferent nerves releases vasodilattH peptides such as substance P or c.11-c itonin gene- rclarcJ peptide.

Adrcnergic agents have been heavi ­ly mvestigated as to their effects on intestinal bloodflnw. LeNoble cc al (28) compared the effects of sympa­thetic stimulation with exogenously applied adrcnergic agents \ll1 both macmvascular and microvnscular dynamics. Intra-arterial (superior mes­enrcnc ;mery) application of both phcnylephrinc (an alpha-adrcnergic

CAN J CA~TROENTEROL Vt)l 5 Nt) 4 )Lil Y/Alft,LJ~T 1991

agonist) and noradrenaline prnduced sharp decreases in superior mesentenc bloodflow, (ollowed by a decrease in Jiameter at the level of the A2 arterioles in the small intestine, as measured hy intravital microscopy.

ln summary, the bulk of evidence demonstrates functionally different roles for alpha- and heta-adrenerg1e receptors in the intestine. A lpha-2 receptor activation with phenylephrine results in vasoconstricrion, while vaso­dilation is prtx.luced by either bera­adrenergic activation (29) or sumula­tion of primary afferent fibres and the subsequent release of vasodilator pep­

tides (28). As well, agents such as digitalis (30) and nicotine (31) appear to act through noradrenaline.

Parasympathetic regulation: Evidence for parasympathetic regulaLion of intes­tinal bloodflow is ar best unclear. Ar present, evidence for parasympathetic regulation of the mesencery is lacking (5); acwrdingly, direct vagal stimula­tion hc1s no vasoactive effect (32).

However, stu<lies examining the mechanisms of postprandial hyperemia have demonstrated both sympathetic and parasympathetic involvement. The splanchnic vascular response LO

feeding can be <livided into two phases: that developing during the anticipc1Lory phase prior ro food ingestion; and that produced following digestion and ab­sorption.

During the first phase, the resistance of the mesenteric vascular bed in­creases (33), while overall cardiac ~,ut­put increases. This is thought co be due to a higher cortical ant1c1parory response mediated by increased sym­pathetic activity. After feeding, in the second phase, mesenteric vascular resistance decreases and cardiovascular variables return to normal 04,35) . Decrease<l resistance is marked by an increase in blcxx.lfl0w from 28 to l '2% in the superior mesenteric artery en). This vasodilat ion can be inhibited by atropine, implying cholinergic inner­vation of the superior mesenreric artery ( 33). Microsphcrc experiments have localized the hyperemic response to the mucosa-submucosa and muscularis regions of the intestinal wall.

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FRA~ER A!'lD LEE

COLON AND RECTUM The microvascular design of the

colon is very similar to that of the stomach. BlooJ vesseb supplying the submucosa and mucosa parallel those supplying the muscle layers. Evidently, the muco. a-suhmucosa receives the greatest blooJflow (36).

Sympathetic regulation: Sympathet ic nervous innerva1 ton of the colon 1s pro­vided hy hoth splanchn1c and lumhar nerves. The proximal colon is inner­vated by planchnic vasoconsmcror fibres, whereas the distal colon is inner­vated hy the lumhar ne rves (37). Sym­pathettc \t1mula1t(m produc~ immediate

hut brief vasncomtricuon followed by autoregulatory escape. There appears to be no escape at the level of t he precapil­lary \phmcters. Response~ mediated hy resistance o r exch ange vesse ls in the colon arc less dramatic than those tn

the small intesti ne (37). There is scam informatio n ahout sympathetic influ­ence on circul;i11on in the rectum ( 36).

Parasympathe tic regulation: Parasym­patheuc innervat ion to the colon and rectum a rises from rhe pelvic nerves. Stimulatton of the pelvic nerve inmates very different responses in the colon and rectum (38). Pelvic nerve timula­uon produces a brief hyperemia fo l­lowed by an increase in blooJflow to the colo n (37). The same stimulatton causes immediate and sustamed vaso­dilation in the rectum (38). Ganglionic blockade destroys pelvic nerve vasoJtl­ation of the colon and rec tum, , uggest­ing invo lvement of a noncholincrgic rran,m1tter.

Vasoact1ve intestina l polypcpude (VIP) has been suggested as the no n­cholinerg1c trammmer involved (39). Pelvic nerve sumulat1nn releases VIP from both rectum (38) and colon (40) . Sympathetic release of VIP correlates with vasodi latory respomcs m the ves­sels of the colon. A nalogously, exogen­ous VIP ( intra-artcrml infuMon) applicanon proJuccs vas0Jilat1on m hoth colon and rec tum (38). Further­more, other substances have been sug­gested as p0Sl>1ble mediators of the vaS<xlilation evidenced after pelvic nerve stimulation (substance P, serotonin, purinergic nerve, kmin system) ( 41 ).

150

HEPATIC CIRCULATION lntrahcpatic branches of the portal

vein become progressively smaller as they course through the liver. Con ­ducting vcms (400 µm) branch into distributing ve ins (less than 28 µm , either margina l or maximal) which fur­ther subdivide into smaller terminal vcnules to unite eventually with s inu­,mdal beJs via small inlet venules (42).

The hepatic artery runs alongside the portal vein in to the portal canals of the liver. O nce mside the liver, the hepatic artery branches into arterioles. Terminal arterioles (10 to 50 µm) e nd as precapillaries {sphincters) co penetrate the capillaries of the liver. Capillaries then drain into specialized capillaries lined with Kupffer and endo­thelial cells, termed 'liver sinusoids'.

Sphincters have been identified in numerous locanons throughout the liver. Consequently, hlooc.lflow regula­tion inside the liver can be modified at the bifurcation of t he arterioles in the portal canals, in precap1llancs, at the point where arte rio les join the ~inusoids, 111 the inlet venules, and in the branches of the porta l vem ( 43 ).

Because portal flow is the sum of blooJflow from the extrasplanchnic c 1rculat1on , res istance is largely detcr­m111cd hy arteriolar adjustment in the splanchnic organs. Portal resistance within the liver had been thought to be largely presmusoidal (2), but Lautt and colleagues (44,45) have recently dem­onstrated the existence of sphincter­like structures in the small hepatic ve ins of ca ts and J ogs, suggesting a predominantly post sinusoida l s ite of resistance.

Innervation: The liver ma111tains the abi lit y to co ntrol total hepattc hloodflow by the hepatic arteria l buffer response (as portal venous flow ri~cs o r decreases, hepatic arte rial flow com­pen arcs by dec reasing or increasing). A I though intrinsic mechanisms ex isl to

regulate hloodflow in the liver, the hepatic c irculation is also influenced hy a host of extrinsic nerves that have s1g-111ficant hcmodynamic consequences. Extrinsic nervous supply rn the liver an ses by two plexw,es, the anterior plexus and the posterior plexus. The

anterior plexus, composed of branche, originating m the left and right ccliac ganglion and the left vagus nerve, ts lncateJ along the commo n hepauc artery. The posterior plexus, derivcJ from the right ccliac ganglion and right vagus, wrap~ around the htlc ducr anJ portal vein. Both plexuses can com­municate with one arnlther. Sympa­thetic and parasympathe tic f1hre, .ire earned by the amen or plexus ( 46). Anterior p lexus dcnervation sig­nifican tl y a l ters sy mpat he tically mediated vasoconstricnon (47).

Sympathetic regulation: The l Iver

receives neural 111ncrvation from sym­pathetic fibres (T 7 ro TIO) vin thc celiac plexus (46). Rat liver hcpato­cytes appear to have very l1ttlc adrencr­gic inne rvation . However, nerve fibres urrounding the prcterminal hcpattC

artery and portal vein are innervated hy both adrenerg1c and cho line rgic fihrcs. Gen erally speaking, the re seems to he a minimal role for hepauc nerves in thr control of hepatic arterial bloodflow, given that hepatic dencrvation produces no effect on hepatic bloodflow (48).

The hepatic artery is abundantly supplied by adrenergic nerves. St 1mula­tion of ne rves surroundmg the celtac artery in rats produces intense vaso­constriction of po rtal venules, hepatic arterio les and sinu~ot<.b ( 49). The vaso­constriction is presumably mediated hy alpha-adrenerg1c receptors (50), as tt can be blocked by phentolamme (;i lpha-adrenergic antagonist) ( 51 ). Following cessation of srimulauon, a pemxl of hyperemia b produced 111 the hepatic artery. The mechanism of vas­cular escape is poorly unde rstood, but 1s thought to involve bcta-adrcnoceptor acuvation (51 ).

I lcpatic venous sph incters appear w be under sympathetic control , s111er noradrenaline and angtotemm admm­istnnion produce marked comtriction (50).

There appears to be no neura l con­trol of the porta l ve in itsel(, w pressure changes arc mainly due to changes m resistance vessels in the splanchnic vis­cera ( 4). Branches of t he portal vem 1mide the liver may he influenced hy a lpha-adrenc rg1c mechanisms (46).

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Autonomic regulation of splanchnic c irculation

Parasympathetic regulation : Vaga I ,timulat inn is thought to result in Jila­tton of smustltJs with a decreasl' tn the veloci ty of hloodOow and mcre,1ses in the numher of smusoids hcing perfused at any one time (52,53). 1 lnwc\'l'r, this is sti ll controversial ,h nthcrs have found no effect nf vagal stimularton nn hepatic h loodflow regulation (54). Reilly et ,11 (55) found that cholmcrgiL agents produced vasoconstricuon 111 hoth sinusoids and pc,na l and terminal hepatic vcnules, ,1 response that could he hlocked hy alpha-adrcncrgic hlnck­crs hut not atropine.

PANCREAS Microvascula r ana tomy: Little mfor­mation 1s ava tlahle on the pancrcatlL microci rculation (4). The mrn;t accept­ed view of pancreauc c1rculatinn hnlds that the pancreas, like thl.' liver, 1s char­acteri:ed hy a pnnal Lirculm,on, with exocrine ussuc being perfused hy both venous and arterial hlood (56). The .irtcries supply mg the pancrem, advance along the ducts to diverge imn intra­lohular arteries, which then div ide inw arteriolar branches w supply the captl­hiry net\vmk of islets, the capi llary plexus oft he ac1111, and the pemluLtular capi llary plexus. Efferents nf tlw islet capillary network either pass through the msuloacmar portal vesseb to thl' acmar capi llary plexus, or dra in through the intrnlohu lar veins. Vesseb L'Xtting the acinar capillary net work either pass through the capillary plexus or empty mw the mtralnbular vcms w ex 1t the gland ( I ).

The u ,rrent view holds that arterial flow wpplies the islets anJ exocrine tissue separately, whi le blood flnws to the exocrine pancreas , 1a rnptllanes from the islets (57).

A Jetermmmion of arterial blood­flow supplytng the islets ,tnd acini in­Jividually was founJ to he 11 lo 23% ~nd 77 to 89%, respectively (58).

Sympath e tic and pa rasym pa the tic regulation: Very lmlc work has l:,cen Jone on autonomic cnmrol of the pan­creat ic urcula t inn, because mo,t ~tudies have concentrated primarily on its secretory role (insulin and gluca­gon). Autonomic regu lat 10n of the pan-

creas ;ippcars ln he s imilar to that ot the rest of thL· gast niintest mal system. Su mu lat1on of sympatheuc efferents el iL its p rompt V,lsoconstriction, ,dwreas vagal ,umulation produLe, va,od i lr111on.

SPLEEN Sympa thetic regulation : Symp,nhct ic 111nervat1on of the spleen arise!> from the splcnK nerve , rn the celtac gnngl 1-on. According ln Baron and Janig ( 59), of the appn1ximatcly 13,200 neunms that project lll tl1l' splen1c nerve, 1255 a rl' ,ympa t hct tl po.-.r ga ngl Hlll 1c ncun1ns arismg from either I he prc,·L·r­tebrnl (98%) or parnvenehral (2'\,) sympathcrn: ganglia. As well, 650 ,tf­fcrent neurons project to the splen,c nerve. Sympathetic stimulat 1011 of the splenlC nerve 111 dogs and cats results 111 Jecreased hlooJ/low (60), presumably a result of activation of the sympathetic nomJrenerg1c neurons thnt innervate the arterioles, ve in, and trahecuh1c of th\.' spleen (61 ) .

Autoregulatory abil ity of the splenic circulat ion is thought to he weak, presumably due to tts lcs1>cr funct tonal imp()rtance tn r11ne, of stress (62). Vas()ddauon of vcsscb in the spleen ts presumed Lo result from ,tctivartnn of primary afferents earned in the ,picnic nerve, triggermg hrndyl..111111 ( vasodator pepttdc) receptor release (6' ).

VISCER AL AFFERENT S AND REFLEX ARCS

The central ne rvous system receives considerable 111nervaticm from visceral afk'rents 111 the splanchniL organs. The majority (54'X, ) of th,1se afferents travel with the sympathet ic nerves. The centrnl nervous system also receives vag,11 afferL·nts, the mainrny of which travel rhrough the thoracic vagus. The primary afkrents 1:,111 he activa ted hy any one of the followmg ,umul1: v1hra­Lion , smooth muscle contraction, nox ious ,umuli or chemnreccpwrs (64). Therefore, stimulation of the primary vbceral affcrems can invoke a reflex response 111volv111g spinal or supraspmal neural pathways. As men ­t1oneJ prev iously, some primary af­ferents may he mvolved in the

(.AN] Gt\~Til11:l\TIRl1l Vl1l 5 No4 JL'LY/AL'l~LST 1991

\'asoddmmy responsL· of au tnregula­non. Howe\'cr, other physt()logtL,11 rnlcs 111 the splanc hnic urLLtlat tllll rema111 yet unclear ( l ).

THE ROLE OF THE SPLANCHNIC CIRCULAT ION

IN OVERALL CARDIO­VASCULAR HOMEOSTASIS The capacnance vessels of the

splanchnic hed contain approximately 20 ro 30% of the total blooJ volume of the body (65). The liver, spleen and mte:,tine together form t he splanchn,c blood reservoir a reservoir that can he mobilized hy the sympathetic nervous sy,tem w mamtam card1nvascular homeostasis. Approximately 30 to 40% of this volume can he expelleJ hy sym­pathetic stimulation m response to an emergency (2). For instance, when blood is removed or inf used at a fairly slow pace, compensawry mec.hanisms can all either w remove hlood from the reservrnr and redi rect it to the ap­propriate region or, m the case of ex­<.:es:., direct 1t to the splanchnic reserve (66).

Mohtl1znt1nn of t he ~planchnic hlood appears to be t he result of sym­path etic vasoconstrict io n of arterioles ( B). More specifically, the mohi liza­t t(lll of ,planchn1c blood during hemor­rhage can heM he characterize<l hy three ,cages. In the m1tial stage, low and high pressun: barorcceptors in the carotid arteries an<l aortic arch lessen venous return hy responJ ing to decreasing pressure. Suhscquently, chcmorecep­wrs located m the intrathorac. tc ves~els and heart are activated by decreased arterial pH. The consequence of both of these actions is to in itiate vasocon­strict ion of the resistance vessels a rcspomc accomplisheJ primarily hy symp.uhetic nerves. The vasoconstrtc­uon evoked hy hemorrhage accounts for roughly one-chm! of the mcreascd overall peripheral res1w1nce.

To conclude, the autonomic nerv­ous sy~tcm plays an essential role in the regulat ion of blood/low to mdividual splanchnic organs. In aJJiuon, tt helps to mobilize the splanchnic vascular reserve to help main min overall cardio­vascular homeostasis 111 an emergency.

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FRASl'R ANP LH:

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