bluuebunny/crossref_metadata_2025 huggingface dataset:
Glucagon-Enhanced Ventricular Automaticity in Dogs
Authors: Wilkerson R. D. , Pruett J. K. , Woods E. F. , Grover T. E.
Published: June 2012

Ventricular automaticity was studied in dogs with intact atrioventricular conduction systems and in dogs with surgically interrupted conduction systems before and after glucagon, 50 µ.g/kg. Results of these studies are in agreement with previous studies. When the influence of rate-dependent suppression of ventricular automaticity was nullified by comparing automaticity during periods of equal heart rates, highly significant increases in automaticity were observed in both preparations after glucagon administration. One index of automaticity, the number of ventricular beats occurring in a 30-second period following onset of vagal stimulation, increased from 8.7 ± 2.6 to 14.7 ± 3.1 after glucagon administration, an increase of 69%. The number of ventricular beats in a 30-second period following cessation of ventricular pacing increased from 8.6 ± 2.5 to 14.9 ± 2.1 after glucagon administration in dogs with heart block, an increase of 73%. Automaticity increases were also noted using other indexes. Beta-receptor blockade with propranolol failed to abolish automaticity changes effected by glucagon. This study demonstrated increases in ventricular automaticity produced by glucagon that heretofore had been overlooked, because a rate-dependent decrease in ventricular automaticity secondary to the positive chronotropic effect of this hormone masked the increases in automaticity.
Role of the Pressor Action of Angiotensin IIin Experimental Hypertension
Authors: Pals Donald T. , Masucci Frederick D. , Denning George S. , Sipos Frank , Fessler Dyral C.
Published: June 2012

Experiments with rabbit aortic strips and pithed rats indicated that 1-Sar-8-Ala-angiotensin II (Sar-Arg-Val-Tyr-Val-His-Pro-Ala) is a specific competitive antagonist of the vascular action of angiotensin II. Norepinephrine-induced hypertension was not affected by infusions of 1-Sar-8--Ala-angiotensin II which evoked a dose-related reduction of angiotensin II-induced hypertension in conscious rats. Infusions of 1-Sar-8-Ala-angiotensin II that caused a dose-related reduction of the blood pressure of conscious rats in the acute phase of unilateral renal hypertension were ineffective during the chronic phase of such hypertension. Infusions of 1-Sar-8-Ala-angiotensin II lasting 1 hour did not reduce the blood pressure of normotensive, spontaneously hypertensive, or metacorticoid hypertensive conscious rats. These data indicate that, under certain experimental conditions, the blood pressure of rats during the acute phase of unilateral renal hypertension is maintained hy the endogenous angiotensin II previously demonstrated to he present in the plasma in supernormal concentrations. The blood pressure of normotensive, spontaneously hypertensive, metacorticoid hypertensive, and chronic unilateral renal hypertensive rats previously shown to have normal plasma levels of renin and angiotensin II appeared to be independent of the pres.sor action of endogenous angiotensin II. This is additional direct evidence implicating the pressor action of angiotensin II in the etiology of renal hypertension.
Third Heart Sound: Possible Role of Pericardium in its Production
Authors: DUNN F. LOWELL , DICKERSON WILLIAM J.
Published: June 2012

The disappearance of a third heart sound in a case of calcific pericarditis after surgery together with a quantitative study of the time and frequency relations of the third heart sound in 70 cases suggests that the tensing of the pericardium is a factor in its production. The frequency characteristics of the third heart sound are such that it may be identified in the presence of a diastolic murmur.
Effects of Epinephrine and Calcium on the Electrogram of the Ouabainized Frog Heart
Authors: BAKER WALTER W. , BAKER JUDITH M.
Published: June 2012

The effects of bound ouabain on the electrogram of the isolated frog heart are antagonized by epinephrine and potentiated by calcium. Ouabainized hearts also develop increased ventricular automatism (paroxysmal tachycardia, flutter and fibrillation) in the presence of large concentrations of calcium but not of epinephrine. The actions of both epinephrine and calcium are readily reversed by washing the tissue with normal Ringer's solution.
Effect of Hypoadrenalism and Excessive Doses of Desoxycorticosterone Acetate upon Response of the Rat to Ouabain
Authors: UNTERMAN DAVID , DEGRAFF ARTHUR C. , KUPPERMAN HERBERT S.
Published: June 2012

The influence of alterations of adrenal function upon the responsiveness of the rat to intravenously administered ouabain was studied electrocardiographically by the string galvanometer. Conduction disturbances followed by cardiac arrest were the criteria for a definitive response. Adrenalectomized rats showed a significant increase in sensitivity to ouabain as compared with normal controls. Normal animals implanted with pellets of desoxycorticosterone acetate and continuously maintained on saline drinking water did not show a significant alteration in their responsiveness to ouabain.
Effect of l-Arterenol Infusion on "Central Blood Volume" in the Dog
Authors: SHADLE OSCAR W. , MOORE JAMES C. , BILLIG DONAL M.
Published: June 2012

Infusion of l-arterenol into anesthetized dogs increased the volume of blood in the heart and lungs, as indicated by an increase in "central blood volume," estimated lung volume and pressure changes in the heart and lungs. An analysis of pressure and flow data in the systemic venous bed during infusion of the drug suggests that important sources of the shifted blood are the peripheral veins and venules.
Measurements on the Elasticity and Damping of Isolated Aortic Strips of the Dog
Authors: LAWTON RICHARD W.
Published: June 2012

The experimental data obtained on the viscoelastic behavior of isolated aortic strips of the dog consist of: (1) the resonant or natural frequency of forced or free longitudinal vibration; (2) the logarithmic decrement. From these data, static and dynamic moduli and the time constants for the specimens are computed. Variations of these values with frequency, temperature and elongation are presented. The experimental observations are not adequately explained by a simple mechanical analogue. An alternative explanation is offered based on studies of dynamic elasticity in high polymers.
Magnitude and Time of Development of the Collateral Circulation to the Lung after Occlusion of the Left Pulmonary Artery
Authors: WILLIAMS M. HENRY , TOWBIN EUGENE J.
Published: June 2012

Direct measurements were made of the collateral flow to the left lower lobe of the lung after occlusion of the left pulmonary artery in anesthetized, open-chest dogs. Immediately after ligation of the pulmonary artery flow ranged from 4.4 to 9 cc. per minute and varied with the height of the systemic blood pressure. The flow at a given blood pressure did not increase during 2 to 4 hours of observation. After chronic ligation of the left pulmonary artery, the flow increased, ranging from 68 to 376 cc. per minute at the end of approximately one year.
The Effects of Work Load and Heart Rate on Filling of The Isolated Right Ventricle of The Dog Heart
Authors: BUCKLEY N. M. , OGDEN ERIC , LINTON DONALD S.
Published: June 2012

Ventricular filling in the isolated right ventricle was studied. Mechanical impedance of the ventricle was estimated from simultaneous ventricular pressure and inflow measurements. Changes in work load or heart rate were accompanied by reproducible and characteristic changes in impedance and intraventricular pressure-curve contour. These were discussed in relation to changes in ventricular relaxation, elasticity, and viscosity. The right ventricle fills according to a pattern fixed by hemodynamic factors which affect the mechanical properties of the ventricle. The physical state of the ventricle early in diastole appears to be a determinant of stroke output.
Blood Volume of Representative Portions of the Musculoskeletal System in Man
Authors: KARPELES LEO M. , HUFF REX L.
Published: June 2012

A method is described for estimating the quantity of blood in the leg. Experiments evaluating the accuracy and validity of the method using I
131
labeled human serum albumin and in vivo analysis are presented. The data suggest that in the recumbent position the leg is about 5.6 volumes per cent blood. Speculation in regard to the similarity and amount of other portions of the body to the leg lead to the possibility that about six-tenths of the blood is present in the carcass and four-tenths in the viscera.
The Effect of ACTH on Experimental Myocardial Infarcts
Authors: WARTMAN WILLIAM B. , CAMPBELL LINN A. , CRAIG ROBERT L. , Jennings Robert B.
Published: June 2012

Measurable myocardial infarcts of predictable size and location were produced in dogs by low ligation of the left descending coronary artery just proximal to the origin of the apical branch. Two groups of dogs with such infarcts were studied, one group being treated intramuscularly with two daily closes of 20 units of Acthar Gel for 9 to 11 days and the other group being untreated. At the end of the experimental period there was no demonstrable difference between the two groups with respect to the size, site or histologic appearance of the infarcts.
Cardiac Output in Pregnancy: Correlation Between Evans Blue Dye and Blood Pressure Methods
Authors: HENDRICKS CHARLES H. , QUILLIGAN EDWARD J.
Published: June 2012

Cardiac output estimations done by the pulse pressure method were compared to those done simultaneously by the dye method in pregnancy, labor, and in the early puerperium. The subjects selected were young, healthy and without edema or clinical evidence of heart disease. A total of 30 determinations was carried out on 23 subjects. Agreement within 25 per cent of the dye method was attained in 90 per cent of the blood pressure method tests.
Lipoproteins in Choline Deficiency
Authors: WILGRAM GEORGE F. , LEWIS LENA A. , BLUMENSTEIN J.
Published: June 2012

Choline deficiency leads to lipomatous infiltration of the coronary arteries and to aortic sclerosis of the Moenckeberg type in young rats. In this form of experimental cardiovascular disease the total serum cholesterol and the triglyceride-bearing lipoproteins are decreased. The beta-lipoprotein classes are essentially within normal limits. The significance of these findings in particular and of serum lipid values in general as relating to different types of experimental cardiovascular disease is discussed.
Mechanism of Prolongation of the R-R Interval with Electrical Stimulation of the Carotid Sinus Nerves in Man
Authors: ECKBERG DWAIN L. , FLETCHER GERALD F. , BRAUNWALD EUGENE
Published: June 2012

To elucidate the mechanism by which stimulation of the carotid sinus nerves prolongs the R-R interval, the effects of activating an implanted carotid sinus nerve stimulator were studied in eight patients at varying levels of background autonomic activity and with varying types of efferent autonomic blockade. Beta-receptor blockade was induced with intravenous propranolol, 0.20 mg/kg, and parasympathetic blockade with intravenous atropine, 0.04 mg/kg. In the supine position, average prolongation of the R-R interval due to stimulation of the carotid sinus nerves was 269 ± 56 msec prior to autonomic blocking drugs, 442 ± 214 msec after propranolol (NS), and 44 ± 13 msec after propranolol and atropine (
P
< 0.025). Comparable changes were produced in the standing position. With moderate treadmill exercise, stimulation of the carotid sinus nerves prolonged the R-R interval by only 40 ± 30 msec prior to blocking drugs, 62 ± 19 msec after propranolol, and 40 ± 30 msec after propranolol and atropine. It is concluded that the prolongation of the R-R interval produced by stimulation of the carotid sinus nerves is secondary to augmented parasympathetic activity, and the attenuation of this response during erect exercise appears to be due to a centrally mediated reduction in the responsiveness of the parasympathetic nervous system to baroreceptor stimuli.
Physiology of Canine Intraventricular Conduction and Endocardial Excitation
Authors: MYERBURG ROBERT J. , NILSSON KRISTINA , GELBAND HENRY
Published: June 2012

The sequence of conduction through the intraventricular conducting system and endocardial muscle was studied by microelectrode mapping of large areas of isolated canine ventricular tissue. We found that most of the endocardium of the right ventricular free wall is activated simultaneously whereas the left endocardial muscle is activated in an apex-to-base sequence. Right septal activation is from apex to base, and the left septum is activated first at the junction of the middle and lower thirds of the septum and then as a bidirectional wave front toward the apex and the base. These right-left differences occur because the sites of impulse input into muscle on the right encompass the entire free wall, base of the papillary muscle, and the lowermost septum, and on the left are primarily limited to the lower ventricular cavity, lower septum, and bases of the papillary muscles. These patterns of left ventricular excitation relate to the presence of a functionally continuous ring of conducting tissue formed by a merger of the major divisions of the left bundle branch on the upper left ventricular free wall. The "ring" itself is electrophysiologically isolated from muscle, but connects to a network of subendocardial conducting tissue extending to the apex and having input to muscle only in its lower portions.
Influence of Caffeine and other Methylxanthines on Mechanical Properties of Isolated Mammalian Heart Muscle: EVIDENCE FOR A DUAL MECHANISM OF ACTION
Authors: BLINKS JOHN R. , OLSON CAMILLE B. , JEWELL BRIAN R. , BRAVENý PAVEL
Published: June 2012

Caffeine, theophylline, and theobromine have similar effects on the contractions of kitten atrial and papillary muscle preparations in vitro. In concentrations between 2 and 20 mM they both intensify and prolong the active state, as indicated by isometric and delayed-release isotonic contractions; contracture is not normally produced. Instantaneous force-velocity curves are shifted approximately symmetrically by caffeine; force-velocity curves derived from simple afterloaded contractions are misleading because of the great prolongation of activity. After the addition of caffeine the onset of the increased degree of activation is more rapid than that of the prolongation of activity; procaine antagonizes the prolongation of activity but not the intensification. In the presence of the methylxanthines, the duration of contraction is no longer abbreviated by isoproterenol, though it is still readily influenced by changes in frequency. The prolongation of activity by Sr
2^plus;
differs in significant respects from that induced by methylxanthines. The results suggest that the methylxanthines exert two effects on excitation-contraction coupling. One of these is presumed to be the inhibition of calcium sequestration by the sarcoplasmic reticulum; the other may be an effect on the cell membrane that leads to increased calcium entry. Most of the features of the altered mechanical response can be explained on this basis if it is assumed that intracellular calcium stores available for release are depleted as a result of the process that impairs calcium sequestration.
Synchronization of the Cardiac Pacemaker with Repetitive Stimulation of the Carotid Sinus Nerve in the Dog
Authors: LEVY MATTHEW N. , ZIESKE HARRISON
Published: June 2012

In anesthetized open-chest dogs, the right carotid sinus nerve was stimulated with brief bursts of electrical impulses. When a single burst was given with each heart beat, the reflexly induced change in heart rate depended on the time within the cardiac cycle that the stimulus was applied. The maximum response was obtained when the P-St interval (i.e., the time from the beginning of the P wave to the beginning of the stimulus burst) was approximately zero. At this P-St interval the cardiac cycle (P-P interval) was prolonged to a mean value of 583 ± 145 (SD) msec from a prestimulation control value of 408 ± 80 msec. The minimum response, a mean P-P interval 45 ± 20 msec less than the maximum, was obtained at a mean P-St interval of 322 ± 48 msec. As a consequence of this phase dependency, over a definite but small range of stimulation frequencies, the discharge of the cardiac pacemaker became synchronized with the neural activity in the baroreceptor reflex arc. Within this critical range of stimulation frequencies, the cardiac pacemaker responded paradoxically to carotid sinus nerve stimulation: a change in the frequency of stimulation evoked a parallel, rather than the well-known inverse, change in heart rate.
Alteration of the Course of Hypertension in the Spontaneously Hypertensive Rat
Authors: Freis Edward D. , Ragan Dennis , Pillsbury Harold , Mathews Mary
Published: June 2012

The blood pressure of spontaneously hypertensive rats was controlled at low normotensive levels, using antihypertensive drugs for a 6-month period beginning when the rats were 3 months of age. Treatment was then withdrawn and the rats observed for an additional 4 months, until they were 13 months of age. Treatment with antihypertensive drugs arrested the progression of the hypertension and the secondary pathology for the duration of the treatment period. Following withdrawal of drugs the blood pressure did not rise to the level of the controls of a similar age, but rather it returned to the level that existed before treatment began and then progressed at the same rate that the controls exhibited when they were 3-7 months of age. Pathological changes were found only in controls. These results indicate that, although the tendency toward hypertension is inherited, its rate of development depends on environmental factors. The hypertension can be arrested by chemotherapeutic interventions and can be aggravated by excessive salt. The hypertension appears to be a progressive time-dependent process but is independent of biological processes associated with aging per se. Finally, control of blood pressure prevents end-organ damage.
Inferior Interatrial Pathway in the Dog
Authors: Scherlag Benjamin J. , Yeh Billy K. , Robinson Morton J.
Published: June 2012

In 20 anesthetized dogs, close bipolar electrograms consisting of two deflections were recorded along the ligament of Marshall in the posterior left atrium. At the inferior portion of the ligament the deflections were separated by an interval of 10-15 msec and at the level of the left superior pulmonary vein by an interval of 60 msec or more. Histological and electrophysiological studies indicated that both deflections were associated with striated cardiac muscle; the first deflection was designated as a left atrial muscle potential and the second as a left atrial tract potential. Although the left atrial muscle potential was coincident with the middle portion of the P wave, the left atrial tract potential occurred during some part of the P-R segment. Conduction to the left atrial tract potential was altered, delayed, or completely blocked during retrograde conduction in the atrium, rapid pacing of the atrium (300-500/min), or local cooling at the point where the ligament of Marshall joined the inferior left atrium near the origin of the coronary sinus. Crushing Bachmann's bundle caused delay in conduction to the left atrial muscle but not to the left atrial tract. Left cardiac sympathetic nerve stimulation induced an atrial activation pattern consistent with pacemaker activity in the inferior left atrium, with inversion of the P wave in lead II. Pacing from the edge of the ligament of Marshall in the posterior left atrium produced the same change in P-wave morphology. These data indicate that the left atrial tract represents a terminal, insulated tract which is activated through an inferior interatrial pathway connecting the inferior right and left atria along the coronary sinus. The terminal end of the tract showed no reinsertion into atrial musculature.
Studies on Renin
Authors: Goldblatt Harry , Haas Erwin , Haas Robert
Published: June 2012

We have devised a method of evaluation, in terms of Goldblatt units (GU), of the data obtained in various laboratories for the excretion of renin from canine and human kidneys. An average value of 1.3 x 10
-4
GU/min g
-1
normal renal tissue resulted for both dog and man. A blood pressure increase of 18-45 mm Hg was induced in normal or nephrectomized, conscious or anesthetized dogs by the continuous infusion of homologous renin at even lower rates (0.25-0.50 x 10
-4
GU/min g
-1
renal tissue), i.e., at 20-40% of the rate excreted by the kidney. This suggests that renin, even at its normal rate of excretion from the kidney, participates in the maintenance of normal blood pressure. The increase of blood pressure and of concentration of renin in the dog's blood was measured at infusion rates (
C
) of 0.0042, 0.0083, 0.0167, 0.0333, and 0.0667 GU/min. At each rate, after a fixed period of infusion (
t
= 60 minutes), a constant fraction (54% of the infused renin) was retained in the circulation. From this and the results of infusion experiments carried out for 30, 60, and 120 minutes, the total amount of exogenous renin,
R
, present in the circulation at time
t
can be expressed as
R
=
C/K
(1 -
e
-Kt
).
K
= 0.0232 minutes
-1
and represents the fraction of exogenous and, presumably, also endogenous renin that is being eliminated from the circulation of the normal dog per minute. Thus, the time required for removal of 50% of the renin from the blood is t
½
= log
e
2/
K
= 30 minutes.
Coronary Vascular Responses to Stimulation of Chemoreceptors and Baroreceptors: EVIDENCE FOR REFLEX ACTIVATION OF VAGAL CHOLINERGIC INNERVATION
Authors: Hackett James G. , Abboud Francois M. , Mark Allyn L. , Schmid Phillip G. , Heistad Donald D. , Bollard Dennis , Brooks Leonard
Published: June 2012

Coronary vascular responses to stimulation of chemoreceptors were studied in anesthetized, artificially ventilated dogs. The circumflex coronary artery was perfused at constant flow so that changes in perfusion pressure reflected changes in coronary resistance. Practolol, a myocardioselective beta-receptor antagonist, and pacing were used to minimize indirect effects of myocardial responses on coronary resistance. Carotid and aortic injections of nicotine produced decreases in coronary perfusion pressure averaging -21 mm Hg and -22 mm Hg, respectively. Decreases with carotid and aortic injections of cyanide averaged -8 mm Hg and -17 mm Hg, respectively. These coronary dilator responses were abolished by bilateral vagotomy or atropine. Changes in perfusion pressure with carotid injections of nicotine averaged +3 mm Hg after vagotomy and +2 mm Hg after administration of atropine. The coronary dilator responses to carotid chemoreceptor stimulation were accompanied by increases in coronary sinus Po
2
in five studies and no change in two studies. Carotid sinus nerve stimulation caused abrupt and sustained coronary vasodilatation. After vagotomy or administration of atropine, the response to carotid sinus nerve stimulation was no longer abrupt but occurred gradually, suggesting that a component of the reflex response was blocked. These studies indicate that stimulation of chemoreceptors activates a vagal cholinergic vasodilator pathway to coronary vessels in the dog. Activation of this pathway appears also to contribute to reflex coronary responses to stimulation of baroreceptors.
Effect of Intracardiac Blood on the Spatial Vectorcardiogram
Authors: Nelson Clifford V. , Rand Peter W. , Angelakos Evangelakos T. , Hugenholtz Paul G.
Published: June 2012

Studies were done on dogs in vivo to determine the effect of intracardiac blood on the electrocardiogram. By exchange transfusions of packed cells or of Rheomacrodex, hematocrit was raised to over 70% or lowered to 16%. The electrical resistivity of the blood changed accordingly from control values of 150 ohm-cm to over 500 ohm-cm or to as low as 67 ohm-cm. The x-, y-, and z- vector leads were processed by analog computer. Computer output signals were: spatial dipole moment, M, vertical angle, V°, and horizontal angle, H°. Three peaks of M (M
1
; M
2
, and M
3
) were found at mean times of 29%, 42%, and 64% of QRS duration. Increases in blood resistivity to values near that of the myocardium caused M
1
to decrease to 33% and M
2
to 40% of control values, but M
3
rose to 125% of control values. These results are in accord with radial excitation for M
1
and M
2
and tangential excitation for M
3
. Decreases in hematocrit below control values caused opposite changes. Normal intracardiac blood causes an apparent increase of M
1
by a factor of 3 and of M
2
by 2.5 and a decrease in M
3
of about 25%.
Coronary Circulation in the Conscious Dog with Cardiac Neural Ablation
Authors: Gregg Donald E. , Khouri Edward M. , Donald David E. , Lowensohn Howard S. , Pasyk Stanislaw
Published: June 2012

The left coronary circulation at rest and during its response to natural stresses was studied in five conscious dogs whose hearts had been externally denervated (stripping technique). The values were compared to those obtained under similar conditions in normal dogs of comparable weight and training. A high degree of hyperemia after temporary circumflex occlusion and a coronary flow pattern with a dominant diastolic component under the different conditions were similar to that of the normal dog. At rest, circumflex flow and myocardial oxygen use were only about half the values obtained in the normal dog. In moderate exercise, the rise of circumflex flow was delayed 10-30 seconds, being always preceded by an elevation of stroke volume. In excitement, the increase in circumflex flow was delayed 7-12 seconds, and this was also generally preceded by a rise in stroke volume. The large rise of coronary flow in exercise was associated with a marked increase in myocardial blood oxygen extraction; in excitement, coronary flow also rose greatly but oxygen extraction decreased markedly. Although these trends during natural stress states were similar to those found in the normal dog, the maximum coronary flow and myocardial oxygen use were no more than half those found in the normal dog for an equivalent stress. The addition of beta-receptor blockade still further reduced the coronary responses to these natural stresses. Thus the denervated heart appears to function at a lower metabolic level than the heart with intact cardiac nerves.
Electrophysiological Studies on Preexcitation in the Dog Using an Electronically Simulated Atrioventricular Bypass Pathway
Authors: Moore E. Neil , Spear Joseph F. , Boineau John P.
Published: June 2012

Experiments were performed on open-chest dogs. In the in situ heart, electronic circuits were used to simulate atrioventricular (AV) bypass pathways as they are found in the preexcitation syndrome. Bipolar electrograms were recorded from the atria, His bundle, Purkinje system, and ventricles. A Systron-Donner SD-80 computer was used to simulate conduction over the Kent or the James bundle and over Mahaim fibers. The electronic bypass circuits had the properties of an excitation threshold, conduction delay, and refractoriness and the ability to conduct in the antegrade or retrograde directions. Simulated lateral accessory AV pathways at various regions of the base of the left and right AV margin produced electrocardiogram (ECG) patterns corresponding to type A, type B, and intermediate types of the Wolff-Parkinson-White syndrome. Stimulation of the ventricular septum along that region of the His bundle corresponding to Mahaim fibers did not produce prominent delta waves or obvious fusion of ECG complexes when the timing of ventricular septal stimulation was coincident with His bundle activation or preceded it by 18 msec. The characteristics of the fusion beats during introduction of premature atrial beats and during phasic changes in vagal tone were also investigated. Retrograde conduction through a simulated Kent bundle caused the development of a self-sustained supraventricular tachycardia. Spontaneously occurring echo beats during simulated preexcitation exhibited distorted ECG complexes and verified the possibility of a nodal reentrant atrial tachycardia with rapid antegrade conduction over the Kent bundle. The danger of atrial tachyarrhythmias in individuals with preexcitation was demonstrated by showing that, with the proper conduction parameters across a bypass tract, atrial fibrillation could lead to ventricular fibrillation.
Mechanism of Enhancement by Angiotensin II of Sympathetic Adrenergic Transmission in the Guinea Pig
Authors: Bell Christopher
Published: June 2012

An electrophysiological analysis was made of the mechanism underlying the potentiation by angiotensin II of responses to adrenergic nervous stimulation of the isolated vas deferens and the uterine artery of the guinea pig. Concentrations of angiotensin II up to 5 x 10
-7
g/ml did not affect resting muscle cell membrane potential, cause spontaneous transmitter release, or increase transmitter release induced by single nerve stimuli. The time courses of excitatory junction potentials were not increased, indicating that the neuronal mechanism for transmitter inactivation was not inhibited. Angiotensin II did, however, increase the degree of facilitation of successive excitatory junction potentials during repetitive low-frequency nerve stimulation, leading to greater depolarization of the muscle cells than under control conditions. That this enhancement of facilitation was the primary mechanism underlying potentiation of transmission by angiotensin II was supported by the finding that the potentiation of mechanical responses to nerve stimulation decreased markedly as the frequency of stimulation was raised over the range where facilitation is replaced by summation as the major factor in depolarizing the muscle cells to firing threshold (2-6 pulses/sec). This mechanism of action of angiotensin II means that its potentiating effect on transmission is relatively specific for the low frequencies of nervous activity which are thought to be important in tonic cardiovascular control.
Effects of Mineralocorticoids, Altered Sodium Intake, and Adrenalectomy on Urinary Kallikrein in Rats
Authors: GELLER RONALD G. , MARGOLIUS HARRY S. , PISANO JOHN J. , KEISER HARRY R.
Published: June 2012

The urinary excretion of kallikrein was examined in rats whose mineralocorticoid level was increased by the administration of deoxycorticosterone or a low-sodium diet and decreased by adrenalectomy. Administration of deoxycorticosterone by injection or by subcutaneous implantation of pellets resulted in a threefold increase in kallikrein excretion after 10-30 days (
P
<0.01). Low-sodium intake produced a twofold increase in kallikrein excretion after 2 and 4 weeks (
P
<0.01). Urine volume and blood pressure were normal and unchanged throughout the study. Sodium excretion was unaltered by deoxycorticosterone but was essentially zero during low-sodium intake. Adrenalectomized rats excreted less than half the kallikrein of shamoperated control rats (
P
<0.01). These data show a direct relationship between mineralocorticoids and kallikrein excretion and suggest that mineralocorticoids are a primary factor regulating the urinary excretion of kallikrein in rats.
Reactive Hyperemia in Arterioles and Capillaries of Frog Skeletal Muscle following Microocclusion
Authors: GENTRY ROBERT M. , JOHNSON PAUL C.
Published: June 2012

We studied the localization of blood flow control in skeletal muscle by short-term microocclusions (30-60 seconds) of capillaries and arterioles of the pectoralis muscle in anesthetized frogs (
Rana pipiens
). The muscle was surgically exposed to permit transillumination and measurement of red cell velocity in the microvessels, but innervation and blood supply were kept intact. About one-third of the arterioles showed postocclusion hyperemia. In some muscles every arteriole showed hyperemia following occlusion, but in others none responded, presumably because of preparatory trauma. The average duration of hyperemia after a 1-minute occlusion was 74 ± 45 (SD) seconds. We also compared the effectiveness of arteriolar and capillary occlusions in producing reactive hyperemia in capillaries. Peak capillary blood flow after occlusion of the supply arteriole was 233% above control, and flow debt repayment was 278%. After occlusion of several capillaries, peak capillary blood flow was 67% above control, and flow debt repayment was 74%. In an individual capillary, peak blood flow after occlusion of that capillary was 15% above control, and flow debt repayment was 13%. In a majority of instances there was no discernible reactive hyperemia with single capillary occlusion. The results do not support the concept that flow in individual capillaries is regulated in accordance with each capillary's metabolic environment. Rather, flow in a capillary appears to depend on the metabolic environment of the arteriole supplying that capillary.
Normal Myocardial Function and Energetics in Volume-Overload Hypertrophy in the Cat
Authors: COOPER GEORGE , PUGA FRANCISCO J. , ZUJKO KAREN J. , HARRISON CARLOS E. , COLEMAN HENRY NEAL
Published: June 2012

Depressed contractility with a paradoxically increased myocardial oxygen consumption has been associated with pressure-overload hypertrophy. The present experiments investigated myocardial hypertrophy induced by volume overload. Right ventricular volume overload was produced in 19 cats by surgically creating atrial septal defects (ASD); these cats were compared with 10 sham-operated control cats. The ASD cats showed an increase in the ratio of pulmonary blood flow to systemic blood flow from 1.04 ± 0.01 (
SE
) (control) to 3.30 ± 0.28 (ASD) (
P
< 0.001). Hypertrophy was evidenced by a ratio of right ventricular weight to body weight of 0.59 ± 0.03 g/kg for control cats and 0.97 ± 0.03 for ASD cats (
P
< 0.001). A polarographic muscle bath was used to study papillary muscles from 8 control and 8 ASD cats. ASD muscles demonstrated normal force-velocity curves, with maximal measured preload velocities of 1.32 ± 0.05 muscle lengths/sec: control velocities were 1.33 ± 0.05 muscle lengths/sec (
P
> 0.9). The myocardial oxygen consumption of isotonic contractions was normal for ASD muscles. The length-tension curves were comparable, with developed tensions at Lmax of 6.20 ± 0.31 g/mm
2
for ASD muscles and 6.34 ± 0.23 g/mm
2
for control muscles (
P
> 0.7). Myocardial oxygen consumption pergram of tension development at Lmax was 0.66 ± 0.06 µliters/mg beat
-1
x 10
-3
in the ASD muscles and 0.65 ± 0.05 µliters/mg beat
-1
x 10
-3
in the control muscles (
P
> 0.8). The mitochondrial oxidative indexes from control and hypertrophied right ventricles were similar, with respiratory control indexes of 14.3 ± 0.8 for ASD hearts and 12.8 ± 1.6 for control hearts (
P
> 0.1). These data demonstrate that contractility and energetics are normal in volume-overload hypertrophy, although these same factors are abnormal in pressure-overload hypertrophy. Thus, hypertrophy alone is not a common denominator for abnormal myocardial function and energetics.
Characteristics of Single Aortic and Right Subclavian Baroreceptor Fiber Activity in Rabbits with Chronic Renal Hypertension
Authors: ANGELL-JAMES JENNIFER E.
Published: June 2012

Experimental renal hypertension was induced in rabbits by wrapping polyethylene around one kidney and removing the other. The impulse activity in single baroreceptor fibers of the aortic nerves to the aortic arch and the right subclavian areas was studied 7-19 weeks postoperatively during nonpulsatile perfusion of an isolated aortic arch preparation. The results were compared with those obtained in normal rabbits. Curves relating the impulse frequency to the aortic arch pressure were constructed. In rabbits with hypertension, the threshold pressure of the aortic baroreceptor fibers was increased from a normal value of 52.5 ± 5.5 to 106.5 ± 5.8 mm Hg, and the point of inflection was increased from 112.4 ± 6.2 to 163.4 ± 5.1 mm Hg. The sensitivity of the baroreceptors to changes in pressure was reduced from 1.19 ± 0.14 to 0.64 ± 0.06 impulses/sec mm Hg
-1
. Similar results were obtained for the right subclavian area. Hysteresis, as indicated by the separation of the curves produced by first increasing and then reducing the aortic pressure, was more evident in rabbits with hypertension than in normal rabbits. The changes in baroreceptor activity in rabbits with hypertension were associated with alterations in the mechanical properties of the arterial walls, which were demonstrated by the pressure-volume curves. Also, there were demonstrable histological lesions of the arterial walls and the receptors in rabbits with hypertension.
Electrophysiological Studies in the Denervated Transplanted Human Heart
Authors: CANNOM DAVID S. , GRAHAM ANTHONY F. , HARRISON DONALD C.
Published: June 2012

To date, no studies have documented the conduction characteristics of the atrioventricular conduction system in the transplanted human heart. Three patients who had undergone cardiac transplantation 1-2 years previously formed the basis of this study. All were functional class I symptomatically and had normal hemodynamics and coronary arteriograms at the time of study. Each patient was in sinus rhythm with a normal P-R interval and QRS configuration. None was taking medications known to affect the atrioventricular conduction system. Using the His bundle technique, all were shown to have normal base-line atrium-His bundle (AH) and His bundle-ventricle (HV) conduction times. Recordings were made of both the donor (A
D
) and the recipient (A
R
) electrograms. The A
D
rate was more rapid than the A
R
rate by an average of 24 beats/min. Right atrial pacing to a rate of 170 beats/min resulted in a progressive lengthening of the AH interval to an average of 205 msec, a result comparable to that in normal patients. At the cessation of rapid pacing, A
D
recovery time averaged 770 msec, which is normal. The administration of 1-2 mg of atropine increased the A
R
rate by an average of 28% but did not alter the A
D
rate; the AH intervals did not change. We conclude that (1) the normal AH intervals at rest and the increased AH intervals during pacing demonstrate the inherent conduction delay imposed by the atrioventricular node independent of autonomic influence, (2) the A
D
recovery time after overdrive is an inherent property of the A
D
sinus node, and (3) the absence of change in the A
D
rate or the AH interval after administration of atropine suggests that parasympathetic reinnervation has not occurred in these patients.
Structural Basis for the Ascending Limb of Left Ventricular Function
Authors: YORAN CHAIM , COVELL JAMES W. , ROSS JOHN
Published: June 2012

Midwall sarcomere lengths near maximal have been reported at left ventricular end-diastolic pressures at the upper limits of normal, but an ascending limb of cardiac function can exist at much higher filling pressures. Accordingly, an analysis was made of sarcomere length distributions across the left ventricular wall over a range of end-diastolic pressures between 2 and 20 mm Hg. In 11 dogs, significant ascending limbs of ventricular function were documented at filling pressures between 2 and 12 mm Hg and between 12 and 20 mm Hg. Nine hearts were arrested and rapidly fixed in diastole with intracoronary glutaraldehyde perfusion, and tissues from five sites equally distributed across the left ventricular free wall were examined by electron microscopy. At filling pressures at the lower end of the normal range (2, 6, and 12 mm Hg), an uneven distribution of sarcomere lengths across the wall was noted: mean sarcomere lengths were shortest at the subendocardial layer, longest at a site between the subendocardial and the midwall layers, and then progressively shorter toward the epicardium. All differences were highly significant. At an end-diastolic pressure of 20 mm Hg, the difference in sarcomere lengths between layers was small; sarcomere lengths decreased only slightly from endocardium to epicardium. Despite maximal sarcomere lengths just inside the midwall in hearts fixed at 12 mm Hg (2.253µ), sarcomere lengths in other layers-the subendocardial and the subepicardial regions-were increased substantially from 2.129 and 2.183µ, respectively, at 12 mm Hg to 2.283 and 2.247µ at 20 mm Hg (
P
< 0.001 and
P
< 0.002, respectively). Therefore, sarcomeres from all layers of the wall increase in length up to a filling pressure of 12 mm Hg; however, as filling pressure is increased further, only short sarcomeres from the subendocardial and the subepicardial layers are recruited. The latter mechanism forms the ultrastructural basis for the ascending limb of normal ventricular function at elevated left ventricular filling pressures.
Relationship of Stimulation Frequency to Automaticity in the Canine Purkinje Fiber during Ouabain Administration
Authors: HOGAN PERRY M. , WITTENBERG STEPHEN M. , KLOCKE FRANCIS J.
Published: June 2012

Spontaneously beating Purkinje-papillary preparations stimulated transiently at 60-180 beats/min exhibited typical overdrive suppression of spontaneous rate in normal Tyrode's solution. When superfused with ouabain (2 x 10
-7
g/ml), the same preparations showed a progressive diminution of overdrive suppression and, ultimately, an acceleration of spontaneous rate in the immediate postoverdrive period. Usual effects of stimulation frequency on electrogenic activity associated with automaticity in the Purkinje fiber were altered significantly during the administration of ouabain. With ouabain, rapid stimulation reduced the maximum diastolic potential and the threshold potential by approximately the same amount and increased the rate of diastolic depolarization. During overdrive, the minimum diastolic potential decreased as a function of maximum diastolic potential, rate of diastolic depolarization, and cycle length. The magnitude of all effects increased directly with the stimulation frequency and the exposure time. At any given time, frequency-induced changes were quickly reversible on return to a lower frequency. However, a single early depolarization during recovery transiently reevoked changes in diastolic depolarization similar to those seen during rapid drive. The increase in the rate of diastolic depolarization appears to be the major change responsible for frequency-dependent enhanced automaticity. The effects observed during transient rapid stimulation resemble the electrophysiological alterations responsible for the final toxic effects of ouabain but occur well before any glycoside-induced change in the spontaneous rate. These effects appear to explain the frequency-dependent acceleration of ventricular pacemakers and the phenomenon of repetitive ventricular response previously described in intact animals during digitalization.
Electrophysiological Properties of Cardiac Muscle in the Anterior Mitral Valve Leaflet and the Adjacent Atrium in the Dog
Authors: WIT ANDREW L. , FENOGLIO JOHN J. , WAGNER BERNARD M. , BASSETT ARTHUR L.
Published: June 2012

Transmembrane action potentials were recorded from multiple sites in isolated canine anteromedial left atrial wall preparations with the anterior mitral valve leaflet attached. The preparations were superfused with Tyrode's solution. When the left atrial wall was electrically stimulated, activity propagated into the mitral valve leaflet. Typical atrial action potentials occurred in atrial wall fibers. However, maximum diastolic potential, total action potential amplitude, and rate of depolarization decreased markedly in the atrium overlying the fibrous annulus (junctional region), and repolarization characteristics were altered in this region. Mitral valve muscle fibers demonstrated still lower maximum diastolic potential, action potential amplitude, and rate of depolarization. Electrical excitation of single discrete regions in the mitral valve leaflet did not result in conduction to the atrium; conduction block occurred in the junctional region. However, simultaneous excitation of several mitral valve sites did cause an impulse to propagate to the atrium, but transmembrane action potentials of junctional fibers were characteristically different from those recorded from the same junctional fibers during activation from the atrium. Muscle fibers in the mitral valve leaflet were capable of developing spontaneous diastolic depolarization, which resulted in automatic impulse initiation, when they were exposed to epinephrine or norepinephrine (1 x 10
-7
to 1 x 10
-5
M) or when they were stretched. Spontaneous diastolic depolarization and automaticity also occurred occasionally without pharmacological or other experimental interventions; moreover, spontaneous activity originating in the mitral valve leaflet could propagate into and activate the atrial wall. Acetylcholine abolished spontaneous activity. These data suggest that the mitral valve could act as a site of ectopic impulse initiation in the left atrium.
Cellophane Perinephritis Hypertension and Its Reversal in Rabbits
Authors: CAMPBELL DUNCAN J. , SKINNER SANDFORD L. , DAY ALLAN J.
Published: June 2012

Plasma renin activity and renin substrate levels were measured during the development of cellophane perinephritis hypertension induced by either a bilateral renal wrap procedure or a wrap-nephrectomy procedure in 28 rabbits. Unoperated and unilaterally nephrectomized controls were also studied. Plasma renin concentration was derived from plasma renin activity and plasma renin substrate levels using a measured K
m
of 2.3 x 10
-6
M. All surgical operations were followed by a transient increase in plasma renin substrate levels and a fall in plasma renin concentration. Unilateral nephrectomy in normotensive controls suppressed plasma renin activity and concentration for a 20-day period. Similar suppression occurred during the onset of hypertension in rabbits subjected to the wrap-nephrectomy procedure. Decapsulation accompanied by a fall in blood pressure again suppressed plasma renin activity and concentration. With bilateral wrapping, hypertension developed gradually without a change in renin levels. Decreased renin secretion during the evolution of perinephritis hypertension probably reflects a decreased renal excretory capacity for salt and water that overrides the renin-releasing effect of renal compression.
Control of Total Systemic Vascular Capacity by the Carotid Sinus Baroreceptor Reflex
Authors: SHOUKAS ARTIN A. , SAGAWA KIICHI
Published: June 2012

To attain a quantitative understanding of carotid sinus baroreceptor reflex control of cardiac output, we studied the reflex control of total systemic vascular capacity in vagotomized dogs. In experiments measuring blood volume shifts caused by the carotid sinus reflex (series 1), venous return was diverted into a reservoir while cardiac output and central venous pressure were maintained at constant levels. The pressure in the isolated carotid sinuses (ISP) was lowered or raised in 25-mm Hg steps between 75 and 200 mm Hg. This procedure mobilized blood into or out of the reservoir, indicating a decrease or an increase in total vascular capacity, respectively. The mean maximum volume shift, 3.6 ml/kg body weight, occurred in the same ISP region, 135 ± 12.5 mm Hg, where reflex control of total peripheral resistance was strongest. The total volume shift was approximately 7.5 ml/kg for ISP changes from 75 to 200 mm Hg. When mean arterial blood pressure was maintained constant during the ISP step changes, the volume shift almost doubled. In experiments measuring the reflex effect on total systemic vascular compliance (series 2) and in experiments determining the reflex control of arterial compliance (series 3), total systemic vascular and lumped arterial compliances were measured in the same dogs that were used in series 1 experiments. The total systemic vascular and arterial compliances were approximately 2.0 ml/mm Hg kg
-1
and 0.0677 ml/mm Hg kg
-1
, respectively. The reflex did not affect these compliances. We concluded that the reflex controls the total systemic venous capacity to a degree that changes cardiac output potentially by 30-10% per 25-mm Hg change in ISP.