bluuebunny/crossref_metadata_2025 huggingface dataset:
Relationship Between Potassium and Vagal Action on Atrioventricular Transmission
Authors: GREENSPAN KALMAN , WUNSCH CHARLES M. , FISCH CHARLES
Published: June 2012

The relationship between the effects of potassium and vagal stimulation on transmission through the atrioventricular transmission system was investigated. It was observed that infusion of isotonic potassium chloride alleviated atrioventricular block induced by vagal activity. This occurred at plasma potassium levels ranging from 4.8 to 6.9 mEq/liter. This antagonism does not appear to be mediated by catecholamine release since infusion of epinephrine (0.23 µg/min) did not relieve the block. At plasma levels higher than those capable of inhibiting vagal action, potassium enhances parasympathomimetic actions on A-V transmission and, at still higher levels, potassium is capable of inducing A-V block which is independent of the vagus.
Calcium Exchange in Dog Ventricular Muscle: Relation to Frequency of Contraction and Maintenance of Contractility
Authors: LANGER G. A. , Serena S. D.
Published: June 2012

Calcium exchange was studied in the arterially-perfused papillary muscle of the dog under the conditions of varying frequency of contraction as well as calcium-free perfusion. The following conclusions are drawn from these studies: (1) The maximum increment in rate of Ca
++
uptake associated with increased rate of contraction occurs in the first 10 to 12 minutes following rate increase. The mean increment over this period of time is 2.5 µmoles/liter tissue water/beat. (2) The increased Ca
++
exchange which occurs in association with the increases in rate of contraction occurs within that portion of the myocardium represented kinetically by phase 2. (3) The Ca
++
associated with phase 2 remains reversibly bound. The maximum capacity of the "phase 2 system" under the present experimental conditions, is approximately 3.2 mmoles Ca
++
/liter tissue water. (4) Exceeding the capacity of the "phase 2 system" for Ca
++
is associated with the onset of contracture in the muscle. This occurs at rates of contraction which produce progressive fall in contractile tension and is associated, presumably, with myocardial hypoxia. That fraction of Ca
++
taken up in excess of the capacity of the "phase 2 system" is released very slowly. (5) The initial increment of Ca
++
uptake, following an increase in rate, is reversed if the rate increment is not associated with progressive fall in systolic tension and contracture. (6) The maintenance of the ability to develop contractile tension depends significantly upon the presence of Ca
++
in the "phase 2 system.". The rate of loss of contractile tension is very nearly the same as the rate of loss of Ca
++
from this system. (7) Ca
++
exchange between vascular and interstitial regions depends upon concentration gradient. In contrast, Ca
++
exchange of phases 2 and 3 ( ? sarcotubular system and intracellular region respectively) is unaffected by change of concentration gradient.
Electrophysiologic Effects of Isoproterenol and Beta Blocking Agents in Awake Dogs
Authors: Wallace Andrew G. , Troyer William G. , Lesage M. Alan , Zotti Enzo F.
Published: June 2012

In awake, unrestrained animals beta adrenergic stimulation by isoproterenol increased heart rate and enhanced A-V conduction with no change of conduction in Purkinje tissue or ventricular activation time. The chronotropic and dromotropic responses to isoproterenol were abolished completely by the adrenergic antagonists, propranolol (0.2 mg/ kg) and pronethalol (2 mg/kg). Beta adrenergic blockade with propranolol produced no significant change of heart rate, A-V conduction, conduction velocity in Purkinje tissue, or ventricular activation time. In contrast to the above, pronethalol produced tachycardia, enhanced A-V conduction and prolonged ventricular activation slightly. The tachycardia which followed pronethalol was largely a consequence of vagal inhibition since it could be nearly abolished by prior administration of atropine. Propranolol produced no changes in the refractory period or excitability of atrial muscle. Pronethalol did not alter the excitability of atrial muscle but did prolong the atrial refractory period. Barbiturate anesthesia was found to prolong ventricular activation time, and in anesthetized animals both propranolol and pronethalol caused further depression of conduction.

These data support the view that cardiac adrenergic activity has little or no influence on conduction in the ventricle, and suggest that the intensity of sympathetic activity in awake, unrestrained dogs is minimal. The differences in the responses of unanesthetized animals to propranolol and to pronethalol indicate that the latter agent has significant anticholinergic properties as well as certain extra-adrenergic actions on conduction. Failure of blocking doses of both the above agents to alter diastolic thresholds indicates that their anti-arrhythmic properties are not related to an effect on excitability. Beta adrenergic blocking agents appear to exert qualitatively as well as quantitatively different effects in awake and anesthetized preparations, an observation which should be taken into consideration when evaluating the pharmacologic properties of these compounds.
Comparative Changes in Segmental Vascular Resistance in Response to Nerve Stimulation and to Norepinephrine
Authors: Abboud Francois M. , Eckstein John W.
Published: June 2012

The effects of stimulating sympathetic nerve fibers and of intra-arterial norepinephrine on vascular pressures and resistances in muscle and paw of perfused forelegs of dogs were compared by means of small vessel cannulations and during constant blood flow. The following conclusions may be drawn:

1. Sympathetic nerve stimulation causes constriction of the large artery segment predominantly. The constriction appears to be most intense at the level of the carpus.

2. The large artery constriction at the level of the carpus diverts blood flow away from the paw and into more proximal muscular parts of the foreleg.

3. Changes in segmental vascular resistances during nerve stimulation differ in paw and muscle. In the paw, venous segments constrict markedly whereas small vessel segments usually dilate and may constrict minimally; but in the muscle, arterial and small vessel segments constrict more than venous segments.

4. The effects of norepinephrine differ from those of nerve stimulation. Norepinephrine causes constriction of small vessels in paw predominantly. Constriction of both small vessel and venous segments in paw exceeds constriction of corresponding segments in muscle.
Relationship of Heart Sounds to Acceleration of Blood Flow
Authors: Piemme Thomos E. , Barnett G. Octo , Dexter Lewis
Published: June 2012

A concept has been presented that abrupt acceleration or deceleration of blood flow is associated with an energy source sufficient to displace the mass of the heart, and that, consequently, this mass will oscillate at a sum of frequencies that are a function of chamber mass and restoring forces. Induced pressure transients may be observed in all chambers, the lower frequencies appearing on conventional pressure tracings, the higher frequencies as intracardiac sound.

Using high frequency response instrumentation in dogs, intravascular sound has been compared with pressure and flow events throughout the cardiac cycle.

(1) The first component of the first heart sound occurs during early isometric ventricular contraction and is associated with lower frequency pressure transients that may berecorded from all chambers of the heart. The left atrial "c-wave" is one of these transients.

(2) The second component of the first heart sound occurs during ventricular ejection, and appears to be a function of acceleration of aortic blood flow.

(3) The second heart sound begins significantly before aortic valve closure, while forward flow is still going on, and is proportional to the magnitude of deceleration of blood flow.

(4) The third heart sound appears only in the presence of left ventricular failure at the time of rapid ventricular filling, and is associated with a low frequency wave recordable from the central aorta. The production of these transients is presumed to be deceleration of inflow as the limits of ventricular relaxation are reached.

(5) A fourth sound arises coincident with pressure transients in other chambers as atrial systole further distends the left ventricle.

It is proposed that acceleration and deceleration of blood flow is a sufficient and necessary condition for the origin of cardiovascular sound transients.
Effects of Altered Heart Rate on Chloroform-Epinephrine Cardiac Arrhythmia
Authors: Vick Robert L.
Published: June 2012

In chloroform-anesthetized dogs receiving epinephrine, slowing of the heart rate invariably accompanies conversion of arrhythmia to normal supraventricular rhythm by vagal stimulation, and restoring the faster heart rate reestablishes arrhythmia. Increasing the heart rate during epinephrine infusion can induce arrhythmia or increase the proportion of ventricular ectopic beats. These observations are taken to indicate that the vagal influence on ventricular arrhythmia in these conditions is indirect and mediated through the frequency of excitation entering the ventricle.

It is suggested that during chloroform anesthesia an increased heart rate favors the emergence of ventricular arrhythmia when activity propagated after successively shorter intervals encounters delay or local conduction block in the Purkinje system, and re-entry excitation is made possible. It is proposed that in these conditions ventricular tachycardia is a self-sustaining arrhythmia that must maintain a critical frequency, either intrinsically or from external (supraventricular) input. The arrhythmia is susceptible to termination by vagal stimulation when atrial slowing decreases the probability of an atrial impulse entering the ventricle at a critical time.
Cardiovascular Reactivity in Acute and Chronic Renal Hypertensive Dogs
Authors: Page Irvine H. , Kaneko Yoshihiro , McCubbin James W.
Published: June 2012

Both before and after pentobarbital anesthesia, cardiovascular responsiveness to norepinephrine, epinephrine and serotonin was increased and that to angiotensin was decreased when experimental renal hypertension was first elicited. Response to tyramine was strikingly enhanced.

Several weeks later, during the chronic phase of hypertension, there was a slight and scarcely significant heightened response to norepinephrine, a clearly increased response to tyramine, and no change in that to serotonin, dimethylphenylpiperazinium iodide, and 3-hydroxy-phenyl-ethanolamine HCl.

Study of the problem of variability of responsiveness showed relatively little difference in mean response to any of five pressor drugs with or without anesthesia and after sham operation.

Hypertension produced by infusion of angiotensin into normal anesthetized dogs did not change the response to norepinephrine but more than doubled that to tyramine. When acute renal hypertension was produced in the same dogs, angiotensin infusion failed to cause further change in response to either substance. Infusion of angiotensin into dogs with chronic renal hypertension caused increased response to tyramine but not to norepinephrine.

The perfused hind legs of dogs with acute renal hypertension showed clearly reduced responses to angiotensin with no concurrent change in responses to norepinephrine. The pressor response to serotonin was increased while that to tyramine was unchanged. During chronic hypertension responses were like the normal values.

Hypertension caused by infusion of angiotensin decreased greatly the vasoconstrictor response to superimposed injections of angiotensin into the perfused leg circuit while norepinephrine responses were unchanged. Response to another peptide, vasopressin, was reduced like that to angiotensin.

These studies suggest that during acute renal hypertension increased quantities of angiotensin are present and that there is a decrease in neural tone. The finding that during the chronic phase of hypertension, the response to tyramine alone remained elevated, suggests the presence of small amounts of angiotensin, i.e., enough to increase the pressor effectiveness of endogenous norepinephrine released by tyramine. During the chronic phase of hypertension, peripheral resistance appears relatively more dependent on neural control.
Myofibrillar Adenosine Triphosphatase Activity of Human Heart Tissue in Congestive Failure: Effects of Ouabain and Calcium
Authors: Gordon Michael S. , Brown Arnold L.
Published: June 2012

Ouabain had no effect on myofibrillar adenosine triphosphatase (ATPase) activity in normal, hypertrophic, and failing hearts with concentrations of calcium chloride varying from 0 to 5.0 mM. The quantitative effects of CaCl
2
on myofibrillar ATPase were the same in all groups studied.

At necropsy it was found that myofibrillar ATPase activity of heart tissue from patients with clinical and pathologic diagnoses of failure from left ventricular volume and pressure overload was significantly lower than that of normal controls. The ATPase activity in patients with failure due to right ventricular volume and pressure overload was not significantly lower than that in normal controls. There was no difference in myofibrillar ATPase activity between normal left and normal right and between failing left and failing right ventricles.

The difference demonstrated at necropsy between normal and failing hearts was not a function of age or of hypertrophy per se.

Myofibrillar ATPase activity of hypertrophic nonfailing surgical pulmonary infundibular tissue was the same as that of normal postmortem ventricles. The ATPase activity of failing surgical papillary muscle in a small number of experiments was in the range of that found in failing postmortem ventricles.
Blood Flow in the Testis of the Conscious Ram Measured with Krypton
85
Authors: Setchell Brian P. , Waites Geoffrey M. H. , Thorburn Geoffrey D.
Published: June 2012

Krypton
85
in saline was injected through a catheter into the testicular artery or directly into the testis, and the radioactivity in the testis measured by external monitoring with a scintillation detector. The disappearance of Kr
85
from the testis followed a single exponential curve during a fiftyfold decrease in radioactivity and showed no delay before beginning to fall. The partition coefficient for Kr
85
between testis and blood was 0.85.

The mean nutrient blood flow through the testes of 11 conscious rams was 8.4 ml/100 g/min (66 observations; standard deviation between rams 2.4; standard deviation of estimates on individual rams 2.1).

Testicular blood flow was reduced by intraarterial infusions of epinephrine or norepinephrine, practically unaffected by acetylcholine, and increased by isoproterenol. Testicular blood flow was not changed by raising deep testicular temperature from the normal range (32 to 34°C) to body temperature (39 to 40°C). These results are discussed with a view to explaining, in vascular terms, the damage to spermatogenesis caused by elevation of environmental temperature.
In Vitro Phospholipid Synthesis in Normal and Atheromatous Rabbit Aortas
Authors: NEWMAN H. A. I. , DAY ALLEN J. , ZILVERSMIT D. B.
Published: June 2012

The incorporation of P
32
-phosphate and C
14
-choline into normal and atherosclerotic rabbit aortas was studied extensively
in vitro
. The same results as observed
in vivo
were found, namely an enhanced synthesis of phospholipids by the atheromatous aorta, localized primarily in the intima. Aortic intimal phospholipids incorporated more choline than phosphate. Tests with cyanide and fluoride showed that the higher incorporation of choline could not be attributed to exchange with preformed aortic phospholipid but presumably was due to differences in intermediate metabolic pools. The difference in distribution of P
32
between the two most active phospholipid classes, phosphatidyl choline and phosphatidyl inositol, of normal and atherosclerotic aortas was similar
in vivo
and
in vitro
. In the normal aorta, phosphatidyl inositol had a higher percentage of P
32
than phosphatidyl choline; in the atheromatous aorta, these percentages were reversed. The studies
in vitro
were used as evidence to show that the enhanced synthesis observed
in vivo
was probably not mediated by neural factors or stretch of the aorta, and that synthesis
in situ
could account for the higher amounts of phospholipid present in the atheromatous aorta.
Studies on Digitalis XIV: Influence of Cardiac Norepinephrine Stores on the Response of Isolated Heart Muscle to Digitalis
Authors: SPANN JAMES F. , SONNENBLICK EDMUND H. , COOPER THEODORE , CHIDSEY CHARLES A. , WILLMAN VALLEE L. , BRAUNWALD EUGENE
Published: June 2012

On the basis of studies on cardiac tissue removed from animals treated with antiadrenergic drugs, a number of investigators have suggested that the positive inotropic response to digitalis requires norepinephrine in the cardiac muscle. In the present study the action of strophanthidin was studied in isolated papillary muscles obtained from normal cat hearts, from chronic, totally cardiac-denervated, norepinephrine-depleted hearts, and from reserpine-treated, norepinephrine-depleted cats. Complete force-velocity and length-tension curves were recorded. Following the addition of strophanthidin (1.0µg/ml) to the bath, maximum isometric tension rose by averages of 2.17 ± 0.32 g/mm
2
in the normal muscles and 2.65 ± 0.50 g/mm
2
in the muscles from the denervated cats, but increased significantly less (
P
< 0.05) in the muscles from the reserpine-treated animals (1.09 ± 0.36 g/mm
2
). In addition to these changes in isometric tension, strophanthidin increased the maximum velocity of contraction (V
max
) to a comparable extent in normal and denervated muscles, with a smaller elevation of V
max
in reserpine-treated muscles. Strophanthidin reduced the absolute refractory period to an equal extent in all three groups of muscles. From a comparison of the inotropic responses of the muscles from normal and cardiac-denervated cats it is concluded that cardiac norepinephrine stores and neural integrity are not essential for the positive inotropic effect of strophanthidin or for its effects on the duration of the absolute refractory period. However, it appears that prior reserpine treatment may interfere with the inotropic response to digitalis by a mechanism other than norepinephrine depletion.
Plasma Indicator Dispersion in Arteries of the Human Leg
Authors: BASSINGTHWAIGHTE JAMES B.
Published: June 2012

Indicator-dilution curves were recorded from the femoral and dorsalis pedis arteries of five normal men after injections of indocyanine green into the superior vena cava or thoracic aorta. By considering the femoral curves as inputs to a mathematically linear system and the dorsalis pedis curves as outputs, transfer functions (the distribution of transit times) for the arterial segment between these sites were obtained in terms of a four-parameter model, the lagged normal density curve, over a sixfold range of flow rates. The parameters of the spread (dispersion) of 57 transfer functions were proportional to the mean transit time. The mean difference between transit time and appearance time was 0.30 t; the square root of the variances was 0.18 t. These linear relationships suggest that flow rate has no significant influence on dispersion and that, since no transition from laminar to turbulent flow was apparent, arterial flow characteristics were not significantly changed over a wide range of flow rates. The secondary implication is that the rate of spatial longitudinal spreading of indicator with distance traveled is primarily a function of the geometry of the arterial system, not of the rate of flow, and, therefore, that the spatial distribution at any instant is a function of this rate and of the distance traveled through the system.
Aimed Electrocardiography with Simple Bipolar Leads
Authors: FISCHMANN EUGENE J. , BARBER MARK R. , HEDAYATI HEDAYATOLAH
Published: June 2012

All currently employed ECG and VCG leads vectorially record added contributions from all cardiac regions. Aimed leads, if feasible, would yield information cancelled during addition.

Three artificial dipoles (µ
1
, µ
2
, µ
3
) are placed within a torso model in the approximate right ventricular free wall, posterobasal wall of left ventricle, and inferior cardiac surface, respectively. Dipoles are excited in turn and torso surface potential fields are mapped for each dipole. A bipolar lead connecting any pair of points on the same equipotential of the field produced by µ
1
does not show a deflection when µ
1
is excited, but responds to µ
2
and µ
3
. If this lead is now so placed that its two electrodes, while remaining on the µ
1
equipotential, are on the same equipotential of the µ
2
field as well, then it will respond to µ
3
alone; it is aimed at the latter.

Superimposing the three field maps and searching for those equipotential lines of one map which cross the same equipotential line of another map twice, provides a large number of suitable leads, each aimed at one of the three dipoles. Five leads are described and tested in detail.
Ventricular Echoes
Authors: MIGNONE ROBERT J. , WALLACE ANDREW G.
Published: June 2012

These experiments were designed to examine further the concept of a dual pathway for AV transmission in the heart, and to determine whether or not the atrium is a necessary link in the reentry pathway used for a ventricular echo. Studies were performed on anesthetized and awake dogs with recording electrodes implanted on the atrium, bundle of His, and right ventricle. When paired stimuli (V
1
V
2
) were applied to the ventricle with an appropriate delay, the second stimulated beat was followed by a nonstimulated ventricular echo. The echo response was of supraventricular origin. During paired stimulation with echoes, stimulation of the atrium prior to arrival of the retrograde response to V
2
produced a propagated ventricular beat in advance of the expected echo. Stimulation of the atrium immediately after an echo was associated with apparent supernormal AV conduction. These observations support the conclusion that the AV node can be dissociated functionally into at least two pathways. It was possible to render the atrium refractory without abolishing the echo. This finding indicates that the atrium per se does not participate in the reentry path used for ventricular echo.
Failure of Beta-Adrenergic Blockade to Alter Ventricular Fibrillation Threshold in the Dog
Authors: ROSATI ROBERT A. , ALEXANDER JAMES A. , WALLACE ANDREW G. , SEALY WILL C. , YOUNG W. GLENN
Published: June 2012

The effects of two beta-adrenergic blocking agents, pronethalol and propranolol, on ventricular fibrillation thresholds were tested in dogs. Pronethalol (4.0 mg/kg, 5 dogs) produced a mean increase of 45% in the fibrillation threshold. Propranolol (0.4 mg/kg, 7 dogs) failed to produce a significant change of the fibrillation threshold. To examine the possibility that the difference between the responses to pronethalol and propranolol might be related to the difference in dose of the beta-blocking agents, 4.0 mg/kg of propranolol was given to 3 dogs; this dose also failed to produce a consistent change of ventricular fibrillation threshold. These data indicate that under the conditions of our experiments it was possible to block the beta-adrenergic receptors with propranolol without producing a change of the ventricular fibrillation threshold. The increase of the fibrillation threshold produced by pronethalol was probably a consequence of its quinidine-like properties rather than of its beta-receptor blockade.
Studies on Components of RNA in Cardiac Muscle with Emphasis on the Rapidly Labeled 4 to 18 S Fraction
Authors: POSNER B. I. , FANBURG B. L.
Published: June 2012

Studies on RNA from cardiac muscle of rats were performed by labeling the RNA with
32
P, extracting it with phenol, and purifying it prior to fractionating and analyzing it on a sucrose density gradient. The major components of RNA found had sedimentation values of 28, 18, and 4 S. Early
32
P-labeled RNA ranged in size from 4 to > 45 S. Characterization of RNA from 4 to 18 S showed it to be more rapidly labeled and to have a higher turnover rate than 28 S RNA, to be located, at least in part, in the microsomes, and to have a base composition lower in guanine and cytosine content than 28 S RNA. Labeling of 4 to 18 S and 28 S RNA was equally inhibited by actinomycin. The possibility that 4 to 18 S RNA may represent a portion of messenger RNA in cardiac muscle is considered.
Active Stiffness of the Intact Canine Left Ventricle
Authors: FORWAND STANLEY A. , McINTYRE KEVIN M. , LIPANA JOSE G. , LEVINE HERBERT J.
Published: June 2012

Three methods were employed to measure the overall active stiffness of the intact left ventricle in anesthetized dogs. In two of these, isovolumic contractions of the ventricle were examined, and in the third the response to a minor increase in afterload was analyzed. The average modulus of active stiffness of the normal left ventricle by all three methods was found to be lower than that reported for the cat papillary muscle (57-76%).

Myocardial infarction studied 1 hour and 2 to 3 weeks following ligation of the anterior descending coronary artery did not alter active stiffness of the left ventricle. When sufficient time had elapsed, however, for complete scarring and thinning of the infarction to occur, active stiffness was significantly reduced. It is suggested that a functional defect of the overall active stiffness (series elasticity) of the ventricle may be operative in the pathogenesis of congestive failure due to ventricular aneurysm.
Longitudinal Tethering of Arteries in Dogs
Authors: PATEL DALI J. , FRY DONALD L. , Janicki Joseph S.
Published: June 2012

The magnitude and properties of longitudinal vascular tethering were studied in the thoracic aorta, abdominal aorta, and femoral artery of 23 dogs. The tethering was found to consist of a dominant viscoelastic restraining element that demonstrated a moderate degree of stress relaxation and a significant inertial component that was related to the mass of the vessel and its surrounding tissues (the "added mass"). Static and dynamic studies of these properties showed them to be surprisingly linear. The simplest linear model that could simulate these experimental data consisted of two elastic components, two frictional components and a lumped inertial component. Within the physiologic range of frequencies (1 to 20 cycles/sec), the two elastic components became dynamically coupled so that they appeared to act as a single spring, the stiffness of which could be characterized by a "dynamic spring constant." The mean value of the dynamic spring constant was 12 g/cm
3
for the thoracic aorta; it increased along the aorta toward the femoral artery to almost 70 times that value. Contrary to the simple tethering model assumed by Womersley, these data showed that the mechanical behavior of the system is strongly influenced by frictional components.
Counterpulsation Effects of Coronary Blood Flow and Cardiac Oxygen Utilization
Authors: HIRSCH L. J. , LLUCH S. , KATZ L. N. , Ellis A.
Published: June 2012

Counterpulsation in dogs with normal systemic arterial blood pressure produced a reduction in myocardial oxygen consumption without a significant concomitant change in total coronary flow. In dogs with a deteriorating heart and low systemic arterial blood pressure, myocardial oxygen consumption became dependent on coronary flow. Under these circumstances, counterpulsation produced an increase in coronary flow, and with it a secondary augmentation of cardiac oxygen consumption. Counterpulsation reduced the mean systemic arterial blood pressure during ventricular ejection to a greater degree when the control level of this pressure was normal than when it was hypotensive. This lessened effect may also occur when the heart has deteriorated. The mechanisms involved in causing the several effects of counterpulsation are discussed.
Selective Activation of Noradrenaline and Adrenaline Producing Cells in the Cat's Adrenal Gland by Hypothalamic Stimulation
Authors: FOLKOW B. , VON EULER U. S.
Published: June 2012

By stimulating different parts of the hypothalamus in the cat, it has been possible to show that adrenal medullary secretion often contains preferentially adrenaline or noradrenaline. The results indicate that the two horomones are secreted from different cells with separate innervation.
Decreased Resistance to Hemorrhage in Neurohypophysectomized Dogs
Authors: FRIEDEN JULIAN , KELLER ALLEN D. , HlCKMAN CLEVELAND P. , WATERS JOHN H.
Published: June 2012

The diabetes insipidus dog is more susceptible to hemorrhage than the normal dog as determined by a standardized hemorrhage procedure. When aqueous pitressin is administered in subpressor dosages, this susceptibility to hemorrhage is reversed to or toward normal. Aqueous pitressin does not increase the intact dog's resistance to hemorrhage. The foregoing observations are interpreted as demonstrating that the neurohypophysial pressor principle serves a physiologic role in maintaining blood pressure during hemorrhage.
The Effect of Immersion Hypothermia on Coronary Blood Flow
Authors: BERNE ROBERT M.
Published: June 2012

In severe hypothermia resistance in the coronary vascular bed is reduced and flow continues despite very low aortic pressure. Moderate artificial acceleration of the hypothermic heart at constant coronary perfusion pressures produces a decrease in coronary blood flow. This decrease in flow is roughly proportional to the increase in heart rate and is due to the longer periods of extravascular compression in each cardiac cycle. Epinephrine produces transient improvement in blood pressure and coronary blood flow but is followed in a matter of minutes by ventricular fibrillation.
Ventricular Function
Authors: CASE ROBERT B. , BERGLUND ERIK , SARNOFF STANLEY J.
Published: June 2012

Left main coronary artery blood flow, cardiac output and pressures in the pulmonary artery, the aorta and both atria were continuously recorded in the dog. Restriction of left coronary flow increased left atrial pressure substantially, but right atrial pressure only slightly; left ventricular work, cardiac output and arterial pressure fell markedly. During restriction of left coronary flow, the left ventricular function curve (modified Starling curve), which does not normally show a descending limb even at high filling pressures, developed a pronounced descending limb. Unilateral ventricular failure was demonstrated.
Effects of Barium Chloride on Resting and Action Potentials of Ventricular Fibers of the Frog
Authors: KLEINFELD MORRIS , STEIN EDWARD , MEYERS STANLEY
Published: June 2012

By means of an intracellular capillary electrode the effects of barium chloride on the resting and action potentials of ventricular fibers of the frog were recorded in hearts with circulation intact and hearts isolated and perfused. The changes were essentially similar in both preparations. The major change observed was a statistically significant (p <0.01) increase in duration of the action potential. Changes were also observed in the magnitude of the resting and action potential, in the rate of depolarization, and in rhythm, but these did not occur invariably. By a series of exclusion experiments it was demonstrated that barium has a direct effect on the ventricular fibers of the frog's heart.
The Effect of Digitalis (Cedilanid) on the Mechanical and Electrical Activity of Extracted and Nonextracted Heart Muscle Preparations
Authors: STUTZ H. , FEIGELSON E. , EMERSON J. , BING R. J.
Published: June 2012

The purpose of this investigation was to study the effect of Cedilanid on the mechanical and electrical activity of extracted and nonextracted heart muscle strips of dogs. The glycoside did not influence the work, the speed of contraction, or the length-resting tension relationship of extracted heart muscle. It produced changes in membrane action potentials, but none in membrane resting potentials. The problem of whether digitalis is bound to the membrane or the cell protein was investigated by temporary destruction of the cell membrane by water. The effects of cardiac glycosides on contractile proteins and on membrane activity are probably inseparable; they act through changes in ionic gradient between muscle cells and the surrounding medium.
Cross-Circulation Experiments on the Mechanism of the Natriuresis during Saline Loading in the Dog
Authors: JOHNSTON C. I. , DAVIS JAMES O. , HOWARDS STUART S. , WRIGHT FRED S.
Published: June 2012

Cross-circulation through normal recipient dogs of blood from saline-loaded donor dogs that had escaped from desoxycorticosterone acetate (DCA) resulted in a sixfold rise in renal sodium excretion in the recipients. The change occurred without a detectable alteration in filtered sodium (F
Na
). To investigate the locus of secretion of a humoral factor responsible for the natriuresis, a series of ablational procedures was performed in DCA-escaped, saline-loaded donors. Nephrectomy, hepatectomy, or decapitation before saline loading and cross-circulation failed to block the increase in renal sodium excretion in the recipients. Analysis of periods during cross-circulation with a decrease in F
Na
lower than the lowest control value showed that sodium excretion was elevated significantly above control levels in experiments with normal, hepatectomized, and decapitated donors. In contrast, with nephrectomized donors the increase in sodium excretion in the recipients was negligible. This finding points to the need for further study of the kidney as a possible source of a humoral factor in the control of renal salt excretion.
Catecholamine Metabolism in Experimental Hypertension in the Rat
Authors: DE CHAMPLAIN JACQUES , KRAKOFF LAWRENCE R. , AXELROD JULIUS
Published: June 2012

The role of catecholamines was investigated in uninephrectomized Sprague-Dawley male rats made hypertensive by administration of desoxycorticosterone and a high salt diet. The accumulation of tritiated norepinephrine and the endogenous norepinephrine levels were measured in the various organs. The content of endogenous norepinephrine and the accumulation of
3
H-norepinephrine 1 hour after its injection were reduced in the heart, spleen, intestine, skeletal muscle, and kidney of hypertensive rats as compared to controls. Simultaneously, an increase in total
3
H-metabolites was also found in the hypertensive animals.

A highly significant inverse relation was established between the level of blood pressure and the accumulation of
3
H-norepinephrine or endogenous norepinephrine levels in the heart.

The abnormalities observed in the disposition of exogenously administered and endogenous norepinephrine do not appear to be secondary to a change in the distribution of cardiac output to the various organs. Since the initial uptake was normal in the hypertensive rats, the reduced capacity to accumulate norepinephrine seems to be related to a defect in the storage of norepinephrine.
Responses to Drug-Induced Myocardial Necrosis in Rats with Various Degrees of Arteriosclerosis
Authors: WEXLER BERNARD C. , KITTINGER GEORGE W. , JUDD JOSEPH T.
Published: June 2012

Severe myocardial necrosis was produced in virgin Sprague-Dawley rats without preexisting arteriosclerosis and in breeder Sprague-Dawley rats with various degrees of arteriosclerosis by giving two subcutaneous injections of isoproterenol; the virgin rats received 50 mg/100 g and the breeder rats 25 mg/100 g body weight. Breeder rats withstood the stress and shock of myocardial necrosis with fewer untoward effects than the virgin animals. Changes in the thymus and adrenal glands also indicated that the arteriosclerotic breeder rats responded with a different pattern of adrenocortical activity. There were marked differences between the nonarteriosclerotic and arteriosclerotic rats in the fluctuation of serum transaminases and lactic dehydrogenase levels during the stress of myocardial necrosis. During the acute stages of myocardial necrosis there was intense activation of lipid metabolism with gross and microscopic evidence of intense fatty infiltration of the liver; during myocardial repair this lipid was removed concomitantly with reduction of hypercholesteremia. The dichotomy of response has been ascribed to the possibility that the preexisting arteriosclerosis in the breeder rats led to the development of increased collateral coronary artery circulation which afforded some degree of protection to the myocardium.
Microvascular Hypersensitivity Subsequent to Chemical Denervation
Authors: BAEZ SILVIO , KOPMAN AARON F. , ORKIN LOUIS R.
Published: June 2012

Microscopic observation and micrometric measurements of microarterial vessels in the mesentery of the anesthetized rat, during chemical interference with the vasomotor nerve supply, showed (A) marked (average 25x) hypersensitization to epinephrine; (B) persistent vasoconstriction; and (C) depression or cessation of vasomotion. These and concomitant similar reactions of the precapillary sphincter resulted in relative ischemia and frequent reversal of blood flow through the endothelial capillary network. A comparable hypersensitization to epinephrine, observed in six isolated perfused microarterial vessels, upon shift in internal static pressure strongly suggests that the change in reactivity of the vascular smooth muscle cell seen in vivo might also be related to a local change in transmural pressure. The plot of the logarithm of epinephrine threshold concentration vs. the approximate circumferential wall tension (computed for selected in vivo and in vitro experiments neglecting wall thickness) showed a steep rise in vessel sensitivity occurring concomitantly with decrease in wall tension. Thus it appears that hypersensitization of microarterial muscle cells which develops during the hypotensive episode of acute chemical nerve blockade in the rat may be primarily related to a modification in wall tension.
Active Transport of Potassium Ion in Heart Mitochondria
Authors: SAFER BRIAN , SCHWARTZ ARNOLD
Published: June 2012

Several factors affecting K
+
transport by rabbit heart mitochondria were examined, using a K
+
-sensitive electrode. The histone fractions f
2
a and β-7 produced an energy-dependent efflux of K
+
. Inorganic phosphate was required for optimal activity; K
m
for phosphate was 60 µ
M
. Both rate and extent of K
+
efflux decreased as K
+
concentration in the reaction medium was increased. The direction of valinomycin-induced K
+
movements was shown to depend on the net resultant of an active transport mechanism and increased membrane permeability. The detergent triton X-100 produced a nonspecific increase in membrane permeability that led to a rapid efflux of K
+
. Evidence is presented for competition between ion transport and ATP formation for some common energy intermediate. Possible mechanisms of action of histones and other agents affecting heart mitochondrial K
+
transport are considered.
Effect of Left Ventricular Hypertension, Ischemia and Vasoactive Drugs on the Myocardial Distribution of Coronary Flow
Authors: MOIR THOMAS W. , DEBRA DON W.
Published: June 2012

Distribution of coronary flow to the inner and outer layers of the left ventricle of the anesthetized, open chest dog was estimated by the myocardial uptake of
86
Rb chloride infused into the cannulated common left coronary artery. With normal relationship of coronary perfusion pressure and left intra-ventricular pressure, there was no significant underperfusion of the endocardium. When left intraventricular pressure was raised and coronary perfusion pressure was held at levels sufficient to provide normal coronary flow, endocardial distribution remained equal to or slightly greater than that to the epicardium. However, when coronary perfusion pressure was lowered, particularly to levels causing obvious signs of myocardial hypoxia, maintenance of a normal left intraventricular pressure resulted in marked underperfusion of the endocardium. The coronary vasoactive drugs, dipyridamole, norepinephrine, vasopressin, and the β-adrenergic receptor blocking agent, propranolol, increased the flow distribution to the endocardium of both the normotensive and hypertensive left ventricle. It is concluded that the systolic tissue pressure which increases from epicardium to endocardium does not cause significant underperfusion of the endocardium in either the normotensive or hypertensive left ventricle as long as normal coronary perfusion pressure and flow are maintained.
Adrenergic Receptor Activity in the Coronary Arteries of the Unanesthetized Dog
Authors: PITT BERTRAM , ELLIOT ERIC C. , GREGG DONALD E.
Published: June 2012

Both α- (vasoconstrictor) and β- (vasodilator) receptor activity was demonstrated in the coronary arteries of the unanesthetized dog independent of adrenergic receptors in the myocardium. In the β-receptor blocked animal, α-adrenergic receptor activity was demonstrated after intravenous and intracoronary injections of epinephrine and norepinephrine by the occurrence of coronary vasoconstriction which could be eliminated by blocking α-adrenergic receptors as well. Coronary vasoconstriction was also seen prior to β-receptor blockade after intravenous phenylephrine and, on occasion, after intracoronary injections of norepinephrine. β-adrenergic receptor activity was demonstrated in several instances after intravenous or intracoronary injections of catecholamines by an initial vasodilatation which could be eliminated by β-adrenergic receptor blockade and which occurred before there was any change in myocardial or systemic hemodynamics. The role of this independent adrenergic receptor activity in the control of the coronary circulation remains to be determined.
Capacity of the Terminal Vascular Bed during Normal Growth, in Cardiomegaly, and in Cardiac Atrophy
Authors: RAKUšan KAREL , DE ROCHEMONT WOLFGANG DU MESNIL , BRAASCH WOLFGANG , TSCHOPP HANS , BING RICHARD J.
Published: June 2012

Vascular capacity representing the terminal vascular bed was determined by albumin
131
I in the rabbit myocardium during normal and pathological growth of the heart. A considerable increase in the vascular capacity in the first postnatal weeks indicated growth of the terminal vascular bed during this period. Highest values were reached in animals approximately 6 weeks old. From this time, vascular capacity gradually decreased in relation to the increase in heart and body weight. The growth rate of the terminal vascular bed was very rapid during the first postnatal weeks and later became slower; no growth was detected in adult and old animals. Growth of the terminal vascular bed during pathological increase in heart weight followed the same trend. In young animals pathological growth of the heart was accompanied by an increase in the capacity of the terminal vascular bed; in adult animals the total capacity remained unchanged. A decrease in heart weight in animals kept on a protein-free diet was characterized by a relatively small vascular capacity.
Myocardial High Energy Phosphate Stores in Cardiac Hypertrophy and Heart Failure
Authors: POOL PETER E. , SPANN JAMES F. , BUCCINO ROBERT A. , SONNENBLICK EDMUND H. , BRAUNWALD EUGENE , Seogren Shirley C.
Published: June 2012

The aim of this study was to determine whether the impairment of contractility in the myocardium obtained from hypertrophied and failing hearts is due to a decreased store of energy and whether an imbalance exists between energy production and energy utilization in these hearts in vivo. Right ventricular hypertrophy and right ventricular failure were produced in cats by constriction of the main pulmonary artery. Concentrations of creatine phosphate (CP) and adenosine triphosphate (ATP) were determined in samples removed from the right ventricles of these animals during life and in papillary muscles isolated from these same hearts. The papillary muscles from the cats with hypertrophy and failure exhibited depressed intrinsic contractility. The stores of ATP were normal in both the ventricular muscles and the papillary muscles in animals with hypertrophy and failure. Although the stores of CP were significantly depressed in the right ventricles of these animals, the stores had increased toward normal in papillary muscles isolated from these same hearts in vitro. The finding of normal energy stores in the papillary muscles from animals with hypertrophy and failure indicates that their intrinsically depressed contractility cannot be due to reductions of their energy stores in vivo such as were found in the samples from the ventricular wall. The differences between high energy phosphate stores in failing heart in vivo and these stores as they are replenished in vitro also indicate that the in vivo depressions are secondary to an imbalance between energy production and energy utilization in the overloaded, hypertrophied and failing heart.
Protein Synthetic Activity of Heart Microsomes and Ribosomes during Left Ventricular Hypertrophy in Rabbits
Authors: MOROZ LEONARD A.
Published: June 2012

Certain aspects of cytoplasmic protein synthesis have been studied during the early stages (0 to 5 days) of left ventricular hypertrophy produced by supravalvular constriction of the ascending aorta in adult rabbits. At 5 days after constriction, cell-free protein synthesis by microsomal preparations from hypertrophied heart muscle was increased, both from free phenylalanine or leucine (50 to 130%), and from phenylalanyl-soluble RNA, both with (70 to 250%) or without (70 to 150%) polyuridylic acid as artificial messenger. Such increased activity was observed as early as 24 hr, and persisted to 5 days (the limit of the study). Sham preparations also displayed increased activity at 24 hr, which subsided by 5 days. The increased activity could be localized to the microsomal fraction: no differences were found when soluble fractions from normal, sham, and hypertrophied hearts, or from liver, were interchanged. Ribosomes from hypertrophied hearts were no more active than normal ribosomes. Increased yields of microsomal, ribosomal, and soluble RNA were found. It is suggested that the increased protein synthesis occurring in hypertrophy is localized in the microsomes, that soluble factors are not of major significance, and that an increased number of ribosomes (and microsomes) play a major role.
Sinus Node Impulses and Atrial Fibrillation
Authors: SANO TOYOMI , SUZUKI FUMIO , SATO SADAYUKI
Published: June 2012

In atrial muscle strips from rabbits, fibrillation occurred in a solution low in potassium, with or without a high calcium content, and the role of the sinus node in inducing atrial fibrillation was examined by microelectrodes and by direct close bipolar lead electrocardiograms. In right atrial strips that included the sinus node, the sinus node action potential often just preceded spontaneous fibrillation or premature beats. In left atrial strips in a similar condition, the incidence of spontaneous fibrillation or premature beats was very low. However, when electrical stimulation simulating sinus node impulses was applied, fibrillation or the premature beat frequently appeared immediately after the stimulating pulse waves, and its incidence was also remarkably increased, being fairly close to that of the right atrial strip. These findings suggest that the sinus node impulses occasionally caused fibrillation or premature beats during these experiments in a medium low in potassium. In addition, fibrillation was frequently induced even when the impulse fell outside the vulnerable period of the preceding beat.