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Department of Reviews and Abstracts
Selected Abs,tracts
Gottdenker, F., and Rothberger, C. J.: Lactic Acid Meltabolism of the Spon-
taneously Failing Heart and in the Heart Poisoned With NaF, Monoiodoacetic
Acid and With Euphylin. Pfliiger’s Arch. f. d. ges. Physiol. 237: 59, 1936.
Experiments were made on the heart-lung preparation alf the dog. In failure
the lactic acid corisumption decreased, and the heart even gave up lactic acid.
NaF, monoiodoacetie acid, and euphylin inhibited l&tic acid metabolism; the
latter two at first, however, increased its metabolism.
L. N. K.
Strauss, L. H.: Inhibition of Experimental Atherosclerosis by Potassium Iodide and Colloidal Silicic Acid. Ztschr. f. exper. Med. 98: 603, 1936.
Inorganic iodine alone had no effect, but when combined with silieie acid, it inhibited experimental epinephrine sclerosis in 60 per cent of all instances and
cholesterin atherosclerosis in 70 per cent of all instances.
L. N. K.
Schneyer, K.: Clinical Observations Upon the Queslkon of Hypertension Follow- ing Extirpation of the Cardiac Pressor-Receptive Nerves,, Klin. Wchnschr. 16:
192, 1937.
After reviewing the development of the experimental production of hyper-
tension by excising or severing the nerves of the carotid sinus and aortic arch, the author proceeds to draw clear distinctions between hypertension produced in
animals in this way and that seen to occur naturally in Iman. He studied 224 individuals with systolic arterial pressures above 150 mm. Hg (only 50 were over
200; and diastolic pressure is not mentioned) and 90 with pressures below 150 mm.
Hg. Observations of (1) pulse rate, (2) effect of carotid pressure, and (3)
closure of both earotid arteries by pressure were made. The findings and eon-
elusions follow.
1. Cardiac rate is essentially normal and falls, in 80 per cent of cases, between 60 and 80 beats per minute. Departure of rate from normal along with blood pressure does not then occur as in hypertension induced lby extirpation of the
cardiac pressor-receptor nerves. 2. Carotid pressure tests are positive in 75 per cent of cases of hypertension. 3. Closure of the carotid arteries gives rise to increase, reopening to decrease, in pulse rate. The author is, however, quick to point out that the value of these methods of study is doubtful because anatomical
and pathological situations may be unwittingly encountered which either prevent
or enhance stimulation of the carotid sinus and because pain due to manual pressure may alter the reaction. In general he favors the use of closure of the carotid arteries. 4. Bradycardia was not observed in cases of eoarctation of the
aorta. Since he believes hypertension in this condition to be purely mechanical,
627
628 THE AMFtRICAN HEART JOURNAL
he concludes that, whatever the immediate reaction to acute carotid sinus stimu-
lation, prolonged stimulation is in some way compensated for. 5. Clinical ob-
servation does not adduce any evidence of forms of neurogenic hypertension
which corresponds to that seen after extirpation of the cardiac pressor-receptor
nerves. J. M. S.
Hermann, H., Jourdain, F., Morin, G., and Vial, J.: Intensification by Eserine of
the Action of Acetylcholine Upon the Secretion of Adrenalin. Compt. rend.
Sot. de biol. 124: 317, 1937.
Although the action of eserine in increasing and prolonging the action of
acetylcholine is well known, the demonstration that the drug also calls forth a
greater secretion of adrenalin following the injection of acetylcholine has not
been demonstrated. By the ingenious device of connecting the adrenal vein of a
dog whose adrenal gland has been denervated to the jugular vein of a dog sensi-
tized to the effect of adrenalin by destruction of the thoracic, lumbar, and sacral
spinal cord, it was easy to demonstrate this fact. When acetylcholine is injected
into the dog with denervated adrenals (donor) arterial pressure falls promptly,
but no change occurs in the second (transfused) dog due to liberation of adrenalin
which counteracts the fall in pressure. If eserine is now given to the donor dog
before acetylcholine, not only is the fall of the arterial pressure in donor (dog
with denervated adrenals) sharper and longer, but the transfused dog (sensitized
to adrenalin) shows a marked rise of pressure. Evidently, then, the secretion
of adrenalin as well as that of acetylcholine has been markedly increased.
J. M. 8.
Battro, A., Braun-Menendez, E., and Orias, 0.: Asynchronism of Ventricular Con- traction in Bundle-Branch Block. Rev. argent. de eardiol. 3: 325, 1936.
By optically recording in the same person the apex beat, the venous pulse,
the central arterial pulse, and the heart sounds, two records at a time, it is pos-
sible to recognize whether or not both ventricles beat synchronously. Applying
these procedures in twenty patients showing electrocardiograms considered as
characteristic of the so-called bundle-branch block, the following conclusions were
drawn:
Of seventeen patients with electrocardiograms belonging to the so-ealled “common
type ” (right bundle-branch block, according to the old nomenclature), in fifteen
there were obvious signs showing that the right ventricle contracted first, thereby
indicating really a left bundle-branch block. In the other two cases no signs of
asynchronism could be detected.
From three cases with electrocardiograms characteristic, according to Wilson
and his associates, of a right bundle branch, in one, a clear precedence of the left ventricle was actually found, but in the remaining two cases all signs of
asynchronism were lacking.
The electrocardiogram by itself, therefore, is not a reliable means for estab-
lishing a diagnosis of complete bundle-branch block with its mechanical conse-
quences. It is the adequate recording of the mechanical events due to the heart action which affords the only means to determine the existence of a ventricular
asynchronism, thereby allowing the recognition of a delayed excitation through
one of the bundle branches, with possibility of ascertaining the location and the degree of the functional disturbance.
AUTKOR;