bluuebunny/crossref_metadata_2025_split huggingface dataset:
Hemodynamic Changes in Trained Dogs During Experimental Renal Hypertension
Authors: OLMSTED FREDERICK , PAGE IRVINE H. 
Published: June 2012

The hemodynamic events, during onset of experimental renal hypertension, and during its progression to the chronic state, were recorded in 19 trained quiet dogs for 20 to 30 minutes daily for four to forty-two days. This was made possible by implanting a flow probe around the root of the aorta, and a catheter in the aortic arch for connection to an external pressure gauge. Continuous graphic recordings of blood pressure, cardiac output, stroke volume, heart rate, and peripheral resistance were made daily during a period of training to obtain control values, and after hypertension was initiated by partial occlusion of a renal artery and unilateral nephrectomy.
The average mean arterial pressure in 34 unanesthetized dogs in this study was 85 mm Hg (range, 68 to 116 mm Hg). This is about 30% below values previously reported by others in unanesthetized dogs. These low pressures were ascribed to lack of restraint, to training, and to the natural posture of the dogs.
At onset of hypertension a sharp rise in arterial pressure was accompanied by a decrease of cardiac output and heart rate, and by a large abrupt increase of peripheral resistance.
After one to four days, the continued rise of arterial pressure was associated with return of cardiac output and heart rate toward normal. Peripheral resistance eventually stabilized at a level above that of the initial large rise. A chronic state of hypertension was reached by ten to twenty days after the initial rise of pressure. At this time cardiac output and heart rate were restored to normal, while peripheral resistance remained elevated. Studies lasting for as long as forty-two days did not show further changes.
If the renal arterial constriction was severe, a third, "malignant" phase ensued with extreme elevation of diastolic pressure, reduction of cardiac output, and greatly increased peripheral resistance. This terminated in uremic death after a few days.
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.
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.
Analysis of a Recent Hypothesis of Plasma Flow in Pericapillary Spaces
Authors: HOWE JOHN T. , SHEAFFER YVONNE S. 
Published: June 2012

The hypothesis that the observed fluid annulus outside the wall of some capillaries is the reservoir of plasma responsible for ratios of organ hematocrit to large vessel hematocrit less than 1 is examined hydrodynamically. The extent to which the hematocrits can be reconciled on the basis of flow through a single capillary is examined. Results show that ratios between 0.5 and 1.0 can be accounted for even if plasma and cells travel the same distance through a common capillary without a plasma annulus. But with the annulus, ratios as low as 0.27 can be explained (ratios as low as 0.35 have been measured), and the corresponding capillary pressure gradients agree better with those cited else-where. The ratio of organ hematocrit to large vessel hematocrit for the heart, lungs, brain, gut, and carcass can be explained on a single capillary basis with or without pericapillary plasma, but that for the liver and kidney requires the plasma annulus.
The analysis predicts a linear relationship between pressure gradient and flow in the capillary with or without the annulus. The hydrodynamic result provides a plasma transit time along the annulus that agrees well with that observed between the "bulk" disappearance and subsequent reappearance of labeled plasma in the microcirculation.
Computer Simulation of the Propagation Process in Excitation of the Ventricles
Authors: OKAJIMA MITSUHARU , FUJINO TETSURO , KOBAYASHI TOSHIJI , YAMADA KAZUO 
Published: June 2012

Simulation by a digital computer of propagated excitation in the ventricular myocardium has been accomplished. Experience with the program in normal conduction and in one example of abnormal conduction, an extrasystole, is presented. Results of the simulation process were in harmony with observations in animal experiments. This justifies attempts to apply this scheme to the analysis of abnormal ventricular excitation caused by other disturbances.
A crucial role of the Purkinje network in determining the course of excitation spread was recognized in the simulated process of both normal beats and extrasystoles. New knowledge is expected from this scheme when applied to other types of abnormal excitation.
The possibility of combining the scheme with a method of reconstruction of QRS complexes by means of "transfer impedance" values was pointed out.
Reflex Regulation of Arterial Pressure during Sleep in Man
Authors: SMYTH HARLEY S. , SLEIGHT PETER , PICKERING GEORGE W. 
Published: June 2012

The control of arterial pressure during sleep was studied in 13 untreated, unsedated subjects aged 20 to 46, including 7 with hypertension. Arterial pressure was measured directly. A transient rise of arterial pressure up to 30 mm Hg was produced by the sudden intravenous injection of 0.25 to 2 µg of angiotensin. Linear plots were obtained in 10 of 13 subjects when the systolic pressures of successive pulses during the pressure rise were plotted against the pulse intervals which began the next beat. The relationship was disturbed by movement or arousal, and was better when pulse intervals falling in inspiration were discarded.
The slope of the line (milliseconds of cardiac slowing per millimeter rise in systolic pressure) in the awake subject ranged from 2 to 15.5 msec/mm Hg, and from 4.5 to 28.9 during sleep. Reflex sensitivity was highest in dreaming sleep. In 7 of 10 subjects, baroreflex sensitivity increased significantly during sleep; in 6, the prevailing arterial pressure was inversely correlated with the baroreflex sensitivity. The pressure appeared to be the dependent variable. It is concluded that the baroreceptor reflex are can be rapidly reset, particularly during sleep. The lower arterial pressures during sleep may be actively maintained in some subjects by increased baroreflex sensitivity.
Dopamine-Induced Alterations in Coronary Hemodynamics in Dogs
Authors: BROOKS HAROLD L. , STEIN PAUL D. , MATSON JAMES L. , HYLAND JOHN W. 
Published: June 2012

The effect of intravenous infusions of dopamine on left circumflex coronary blood flow and myocardial oxygen consumption in doses ranging from 5 to 100 µg/kg/min was studied in 17 open-chest dogs anesthetized with chloralose. Flow was measured with an electromagnetic flowmeter. Dopamine caused a progressive and linear increase of coronary flow that was proportional to increases in myocardial oxygen consumption up to a dose of 80 µg/kg/min; at this dose, the increase over control was 365% (28 to 129 ml/min). These changes accompanied marked increases in stroke volume, left ventricular dP/dt, and mean systolic ejection rate. Mean aortic pressure and heart rate changed little at doses below 10 µg/kg/min, but increased steadily with doses over the range of 15 to 40 µg/kg/min.
Dopamine is a potent stimulator of coronary blood flow and myocardial contractility. The fact that the increased coronary flow was proportional to increases in myocardial oxygen consumption indicates that the induced coronary vasodilation is secondary to increased myocardial oxygen demands, rather than the result of primary coronary vasodilation.
Canine Right and Left Ventricular Cell and Sarcomere Lengths after Banding the Pulmonary Artery
Authors: LAKS MICHAEL M. , MORADY FRED , SWAN H.J.C. 
Published: June 2012

Canine hearts were fixed with glutaraldehyde at zero transmural pressure 17 to 48 weeks after main pulmonary arterial banding. Tissues were taken from the trabeculae carneae at the ventricular right base, right apex, left base, and left apex. They were placed in osmium tetroxide, embedded in Epon 812, stained with Azure II methylene blue, and sectioned at ½ µ. The mean cell lengths of the hearts with main pulmonary arterial banding were greatest at the right base, 105±5 µ and left base, 103±5.7 µ. (The means ± SE are given.) The mean cell length at the left apex was 95±4 µ and that at the right apex was 92±5 µ. All were greater (P <0.001) than the cell lengths of normal hearts, 71±1.5 µ. The mean sarcomere lengths of the right ventricle with main pulmonary arterial banding (right base, 2.04±0.006 µ right apex, 2.18±0.004 µ) were less than those of normal hearts (right base, 2.41±0.006 µ right apex, 2.46±0.003 µ). The mean sarcomere length of the left base with main pulmonary arterial banding (2.10±0.01 µ) was less than the normal (2.16±0.002 µ); however, the mean sarcomere length of the left apex with main pulmonary arterial banding (2.28±0.005 µ) was the same as the normal.
With main pulmonary arterial banding, both the right and left ventricular cell lengths increased more at the bases than at the apexes, and the sarcomere lengths decreased in the right base, right apex, and left base.
Paradoxical Effect of Vagus Nerve Stimulation on Heart Rate in Dogs
Authors: Levy Matthew N. , Martin Paul J. , Iano Thelma , Zieske Harrison 
Published: June 2012

In the anesthetized, open-chest dog, electrical stimulation of the cardiac ends of the transected cervical vagus nerves produced effects on heart rate and A-V transmission that were dependent upon the P-St interval, i.e., the-time from the beginning of the P wave to the beginning of the stimulus. When one vagal stimulus was delivered per cardiac cycle, the pacemaker response curve (curve of the P-P interval as a function of the P-St interval) was sinusoidal in configuration, with a maximum at a P-St interval of 135 msec and a minimum at 349 msec. The mean P-P interval was 568 msec, and the mean amplitude of the pacemaker response curve was 58 msec.
In any given experiment, the range of P-P intervals encompassed by the pacemaker response curve defined a range of frequencies over which S-A nodal rhythm became synchronized with the activity in the vagus nerves. Over such a range, increases in the frequency of vagal stimulation evoked paradoxical increases in heart rate. On either side of this range of synchronization, vagal stimulation elicited pronounced rhythmic oscillations of P-P and P-R intervals. The frequency of such oscillations was equal to the difference between the vagal stimulation frequency and the mean heart rate. The oscillations in P-R interval were approximately 180° out of phase with the oscillations in P-P interval.