bluuebunny/crossref_metadata_2025 huggingface dataset:
Sarcolemmal and Sarcoplasmic Reticular ATPase Activities in the Falling Canine Heart
Authors: Mead Richard J. , Peterson Myron B. , Welty Joseph D.
Published: June 2012

The specific activity of both the sarcoleminal Na
+
-K
+
-activated and the sarcoplasmic reticular ATPase systems was studied in dogs with right ventricular hypertrophy and congestive heart failure induced by progressive pulmonary artery stenosis. In these enzyme preparations, mitochondrial or cross contamination of either of the cellular fractions studied did not appear to be a factor. In the sarcoplasmic reticular fraction, ouabain was without effect and succinic dehydrogenase assay showed less that 10% of the activity observed in pure mitochondrial preparations. In the sarcolemmal fraction, sodium azide did not significantly inhibit the ATPase activity, but ouabain inhibited 91% of it. The activity of the sarcolemmal ATPase system of the faihng heart did not differ from that of the control; however, the activity of failing heart sarcolemmal preparations was found to be only 61% inhibited by 10
-4
M
ouabain, and the activity of control preparations was 91% inhibited. The sarcoplasinic reticular ATPase activity from right ventricles of dogs with congestive heart failure was significantly less (
P
<0.001) than the respective control activity (average 15.9 compared to 28.1 µmole hr
-1
mg
-1
), whereas the activity from left ventricles of failing hearts did not differ significantly from the respective control value. These findings suggest that a possible explanation for the diminished contractility of the chronically failing heart lies within the subcellular enzymatic ion-regulating systems.
Experimental Studies on the Facilitation of AV Conduction by Ectopic Beats in Dogs and Rabbits
Authors: Moore E. Neil , Spear Joseph F.
Published: June 2012

Experiments were performed on the hearts of open-chest anesthetized dogs and on isolated rabbit hearts. Intracellular microelectrodes and bipolar surface electrodes were used for recording from and for stimulating the atria, AV node, bundle of His, bundle branches and ventricles. Atrial or ventricular premature beats which were usually blocked or delayed within the AV node were facilitated when ectopic activity caused preexcitation and early recovery of the site of block or delay. Ectopic atrial, ventricular, nodal, and bundle of His responses allowed previously blocked or delayed antegrade and retrograde beats to be conducted only when the ectopic activity arrived at an appropriate time at the site of block within the AV node. Therefore, apparent supernormal AV conduction may occur in the human heart by this mechanism, and some reported cases of supernormal conduction may be due to the preexcitation and early recovery of a refractory barrier by ectopic activity.
Experimental Renal Hypertension in Dogs FORELIMB HEMODYNAMICS
Authors: Overbeck Henry W. , Swindall Booker T. , Cowan Daniel F. , Fleck Michael C.
Published: June 2012

Blood flow arid segmental intravascular pressures were measured in the pump-perfused forelimb vascular beds of 25 dogs with chronic perinephritic hypertension and 26 normotensive control dogs (either unilaterally nephrectomized or sham-operated) under pentobarbital anesthesia. Measurements were made under resting conditions (pump-perfusion pressure set equal to aortic pressure) and during response to: (1) stepwise changes in pump blood flow over the range 21-330 ml/min; (2) intrabrachial arterial injection of supramaximal doses of methacholine chloride; and (3) limb denervation. Total limb vascular resistance and segmental pressure gradients were calculated. In hypertensive dogs, as compared to normotensive dogs, resting blood flow was equal (
P
>0.3) and resting limb total vascular resistance was increased (
P
<0.005). Small vessel pressure gradient was increased (
P
<.005) and venous pressure gradient was decreased (
P
<0.005). Limb vascular resistance following methacholine injections and residual resistance following neurectomy were lower (
P
<0.05) in normotensive than in hypertensive dogs. The development of hypertension was accompanied by the upward displacement of limb flow-resistance curves without discernible change in shape of the curves. These data suggest that in chronic renal hypertension in dogs: (1) the limb vascular bed participates in the increased peripheral vascular resistance; (2) the increase in limb vascular resistance is confined to the small vessel segment with no evidence found for limb venoconstriction; (3) a portion of the elevated limb vascular resistance is not attributable to neural stimuli; and (4) structural changes in vessels may account for part of the increase in limb resistance.
Monoexponential Extrapolation of Tracer Clearance Curves in Kinetic Analysis
Authors: Lassen Niels A. , Sejrsen Per
Published: June 2012

Kinetic analysis of inert tracers shows that some of the most important parameters such as the average turnover rate and the total volume of distribution can he calculated only if the entire time course of the tracer clearance is known. This means that extrapolation beyond the observation period (to infinity) must necessarily be accomplished. This paper presents arguments to support the monoexponential extrapolating function which often is used without justification. The arguments show that one cannot in the general case assign any clearcut physical value to the intercept or exponential coefficient of the extrapolating function. Theoretically, a monoexponential tail of a tracer clearance curve obtained from a system in a steady state is reached when the slope of the curve is proportional to the curve. Under certain conditions this slope can be measured as an independent observation, and hence the monoexponentiality can be put to a fairly rigorous experimental test. This concept is illustrated by clearance studies of
51
Cr-EDTA and
181
I-thalamate from the isolated cat gastrocnemius muscle. Furthermore, it is demonstrated that monoexponential extrapolation as made before the appearance of the final exponential part of the outflow curve can cause considerable error in determination of the mean transit time and hence of the volume of distribution for the tracer. Even with an apparent recovery of the tracer of about 99.7%, the mean transit time was underestimated by 20%.
Kinetics of Rubidium Uptake in the Working Dog Heart
Authors: Ziegler Wilfred H. , Goresky Carl A.
Published: June 2012

More than 50% of tracer rubidium entering the coronary circulation is actively taken up by the heart muscle cells during a single passage. Rubidium ions must traverse the capillary wall, the interstitial space, and the muscle cell membrane to enter the very large potential rubidium pool within the cells. The aim of this investigation was to determine which, if any, of these steps are rate limiting. The anterior descending branch of the left common coronary artery was perfused at its origin. Pulse injections containing
86
Rb
+
,
22
Na
+
or
14
C-sucrose, and
125
I-albumin were made into the perfusion line and timed serial samples of coronary sinus blood were collected and analyzed. A model was designed which incorporates rate constants describing both the exchange of
80
Rb
+
at the capillary wall and its entry at the muscle cell membrane. Labeled sucrose or
22
Na
+
was used to determine flow per interstitial fluid volume, a parameter necessary for the application of the model. It was assumed that the interstitial fluid volume available for labeled sucrose or
22
Na
+
was identical to that available for
86
Rb
+
. The rate constant describing exchange at the capillary wall (the permeability surface product per unit accessible interstitial fluid volume) increased with perfusion, whereas that for uptake by the myocardial cells was relatively constant and independent of flow.
Dynamic Changes in Splanchnic Blood Flow and Blood Volume in Dogs during Activation of Sympathetic Nerves
Authors: Brooksby Gerald A. , Donald David E.
Published: June 2012

Arterial inflow to and venous outflow from the vascularly isolated splanchnic region were measured simultaneously by using cannulating electromagnetic square-wave flow transducers in 25 anesthetized dogs with intact abdomens. Change in splanchnic blood volume (SBV) was calculated as the instantaneous difference between inflow and outflow. Addition of the respective increases and decreases in SBV induced by changing carotid sinus pressure from the control value (mean, 136 mm Hg) to 200 or to 40 mm Hg gave an average total volume of 93 ml of blood (
SD
, ±21.7) that could be mobilized reflexly from the splanchnic circulation, Electrical stimulation (15 v, 2 cps, 3 msec duration) of the left thoracic splanchnic nerve for 2 to 10 minutes decreased SBV by 159 ml of blood (
SD
, ±84). These mean values represent 32 and 48%, respectively, of the calculated total SBV. In both situations the translocation of blood was rapid, 50% of the total change in splanchnic blood flow and SBV occurring within 30 seconds. During a 2-minute hemorrhage (7.2 ml/kg), a mean volume of 56 ml of blood (
SD
, ±16) was mobilized from the splanchnic region. This represented 54% of the total volume bled. Under these circumstances, blood moved out of the splanchnic circulation at a fairly constant rate.
Criteria for the Onset of Vascular Murmurs
Authors: Sacks Alvin H. , Tickner E. Glenn , Macdonald lan B.
Published: June 2012

A general "sound boundary" curve was developed which establishes the combinations of minimum flow Reynolds numbers and percent stenosis required for the onset of vascular murmurs. The curve was derived by a combination of engineering analysis and animal experiments in which thin circular orifice plates were implanted in the descending aortas of anesthetized dogs. The results indicate that the sounds are prndnced by jet instability and the associated "free turbulence" in the flow. Such turbulence may occur at Reynolds numbers far below that for transition in a straight pipe, depending upon the degree of stenosis. However, below thir critical Reynolds number for any given degree of stenosis, a murmur would not be detected even with perfect hearing or an ideal microphone, since the flow remains steady and the jet (if any) is laminar and silent. In pulsating flow, sounds can be produced only when this critical Reynolds number is exceeded.
Development of Complement-Fixing 19S, Anti-Heart Mitochondria Autoantibody, Following Myocardial Infarction in Dogs
Authors: Pinckard R. Neol , Olson Merle S. , O'Rourke Robert A. , Palmer John D. , Kelley Robert E. , Goldfein Samuel
Published: June 2012

The development of anti-heart autoantibody following experimental myocardial infarction in dogs was studied with respect to (1) the subcellular localization of the heart autoantigen(s), (2) the incidence of autoantibody following myocardial infarction, and (3) the temporal development of the autoantibody and its relation to serum enzyme elevations and electrocardiographic changes. Complement-fixing anti-heart autoantibody developed following myocardial infarction induced by either two-stage coronary artery ligation or by the injection of microspheres directly into the coronary circulation. The autoantibody was directed toward an autoantigen residing in the mitochondrial fraction of myocardial tissue and was found to be associated with the 19S class of immunoglobulin. Eighteen of 20 dogs with infarction produced anti-heart mitochondria autoantibody 10 days following induction of myocardial damage; the autoantibody persisted 4 to 6 weeks thereafter. In these dogs the presence of anti-heart mitochondria autoantibody was diagnostic of myocardial infarction at times when the serum enzymes and electrocardiograms were within normal limits. Our studies indicate that a serologic test, based on the detection of complement-fixing anti-heart mitochondria autoantibody, may be a valuable adjunct to tests currently available for diagnosing recent myocardial infarction.
Observations on Factors Affecting Local Forces in the Left Ventricular Wall during Acute Myocardial Ischemia
Authors: Schelbert Heinrich R. , Covell James W. , Burns John W. , Maroko Peter R. , Ross John
Published: June 2012

The factors affecting local myocardial function in the presence of ischemic myocardial damage may considerably influence cardiac function and the extent of tissue damage resulting from the initial ischemic injury. However, previous attempts to study local wall forces in the ischemic myocardium have produced variable results. In the present study, a technique was developed for recording isometric left ventricular wall tension that minimized artifacts due to external forces acting on the ischemic area. Miniature isometric force gauges were implanted in 23 dogs in the left ventricular wall within a zone buffered by two rows of transmural prongs attached to a ring. During a test occlusion of a branch of the left anterior descending coronary artery, the ischemic area was defined by the presence of epicardial ST segment elevation, and force gauges were implanted in marginal or ischemic areas of the myocardium. During a subsequent coronary occlusion wall force in the ischemic area fell immediately by an average of 31 ± 8%. When the occlusion was repeated during isoproterenol infusion, wall tension decreased in previously unaffected areas of the myocardium, although in ischemic areas it remained above previous control ischemic levels. Arterial counterpulsation improved the development of wall tension in the ischemic area by 27% and decreased the extent and amount of ST segment elevation. Thus the present study clearly indicates a significant reduction but not elimination of active myocardial wall force in ischemic zones following experimental coronary occlusion. Moreover, force could be augmented by either isoproterenol or counterpulsation, and counterpulsation can produce a significant improvement in function of the ischemic myocardium while reducing the area of ischemic injury.
Activation of Phosphorylase by Cyclic AMP without Augmentation of Contractility in the Perfused Guinea Pig Heart
Authors: Kjekshus John K. , Henry Philip D. , Sobel Burton E.
Published: June 2012

This study was designed to determine whether intracellular cyclic AMP augments myocardial contractility directly. Isolated guinea pig hearts were perfused with media containing cyclic AMP and other adcninc nucleotides with or without 3% dimethylsulfoxide (DMSO) to facilitate myocardial uptake. Phosphorylase
b
to
a
transformation, detennined fluorometrically, was used as an index of increased intracellular cyclic AMP. Heart rate, left ventricular pressure and dP/dt were assessed in isovolumic preparations. DMSO, 3%, did not significantly affect myocardial performance or mask increased contractility produced by epinephrine. Cyclic AMP, 10
-4
M
, with or without DMSO depressed left ventricular pressure and dP/dt modestly, even when heart rate was maintained constant by pacing. Phosphorylase activation increased from a control value of 16.5±1.44% (mean±
SE
,
N
=12) to 40.0±3.1% (
N
=19) following perfusion with 10
-4
M
cyclic AMP with 3% DMSO; DMSO alone increased phosphorylase much less. 5'-AMP with DMSO compared to DMSO alone did not activate phosphorylase. The results indicate that increased intracellular cyclic AMP, achieved in the absence of adrenergic stimulation, does not increase myocardial contractility. Thus, they support the view that the positive inotropic effect produced by catecholamines is not mediated by a direct action of cyclic AMP on the contractile apparatus.
Factors Involved in the Antinatriuretic Effects of Acute Constriction of the Thoracic and Abdominal Inferior Vena Cava
Authors: Schrier Robert W. , Humphreys Michael H.
Published: June 2012

Studies were performed on anesthetized saline-loaded dogs to delineate the factors involved in the antinatriuretic effect of acute constriction of the thoracic (TIVC) and abdominal (AIVC) inferior vena cava. Acute TIVC constriction lowered cardiac output and arterial blood pressure and reduced urinary sodium excretion 48%; the same degree of reduction in renal perfusion pressure by suprarenal aortic constriction diminished sodium excretion only 27%. This finding suggested that factors other than a reduction in renal perfusion pressure are involved in the antinatriuretic effect of acute TIVC constriction. This conclusion was confirmed by studies in which a significant antinatriuretic effect (23%) was observed during acute TIVC constriction while renal perfusion pressure and renal venous pressure were held constant. A similar degree of constriction of the AIVC, as judged by the increase in vena cava pressure, did not cause a decrease in arterial pressure or cardiac output, and the modest antinatriuretic effect of this maneuver was not observed when renal venous pressure was held constant. The antinatriuretic effect of TIVC constriction which occurred in the absence of changes in renal perfusion pressure and renal venous pressure did not correlate with alterations in renal vascular resistance, glomerular filtration rate, and calculated initial postglomerular protein concentration and was not abolished by renal denervation or adrenalectomy. The afferent stimulus for the antinatriuretic effect may be related to the alterations in systemic hemodynamics which occur during acute TIVC, but not AIVC, constriction.
Suprapontlne Contributions to the Carotld Sinus Reflex in the Cat
Authors: Kent Barbara B. , Drane J. Wanzer , Manning John W.
Published: June 2012

Carotid sinus reflex response was measured before and after decerebration in 27 cats with and without the vagus nerves intact. Body temperature, central venous pressure, arterial oxygen saturation, P
CO
2
and pH were kept within normal limits. The anesthetized animals were uniformiy subjected to a wide range of controlied sirius pressure changes in each condition. A mathematical analog with four parameters was empioyed to relate carotid sinus pressure to systemic arterial pressure. The expression takes the form of a logistic curve, describes the reflex response with an accuracy of 98%, and provides a design in which errors are normally distributed for statistical testing of differences in parameters occurring with experimental intervention. The major effect on the sinus reflex of brainstem transection at the collicular level was a decrease in the effective range over which arterial pressure could be varied by changes in sinus pressure. Although a given change in sinus pressure in the median range of 70 to 100 mm Hg produced a proportional change in arterial pressure, transection markedly decreased reflex responses to lower sinus pressures. It was concluded that a transection at the coflicular level may not significantly change mean systemic pressure, but it does decrease the animal's ability to adjust to variations in arterial pressure. The data lend credence to the hypothesis that supramedullary areas can and do function in directing autonomic activity during the carotid sinus reflex.
Measurement of the Early Disappearance of Iodinated (I
131
) Serum Albumin from Circulating Blood by a Continuous Recording Method
Authors: PRITCHARD WALTER H. , MOIR THOMAS W. , MAcINTYRE WILLIAM J. , INKLEY SCOTT R.
Published: June 2012

A method for continuous recording of flowing arterial blood in humans has demonstrated that injected iodinated (I
131
) human serum albumin disappears at variable rates from the circulation when losses are calculated from a two hour extrapolation to zero time. Losses from the circulation during the ten minute interval following injection were minimal. The recorded disappearance curve inscribed during the two hour period subsequent to mixing apparently declines as a single exponential function. In the absence of disturbed circulatory states, blood volume calculated from a single ten minute sample agreed with values obtained by extrapolation within the limits of error of counting methods.
The Interrelations of the Pulmonary Arterial and Venous Wedge Pressures
Authors: WILSON RUSSELL H. , HOSETH WAYNE , DEMPSEY MARY
Published: June 2012

Pulmonary venous wedge pressure closely reflects the pulmonary arterial mean pressure. Pulmonary arterial wedge pressure is not significantly different from the left atrial mean pressure. Neither the former nor the latter is an approximation of the pulmonary capillary pressure.
Action of Dinitrophenol and Lanatoside C on the Canine Heart-Lung Preparation
Authors: ROTHLIN E. , TAESCHLER M. , CERLETTI A.
Published: June 2012

Dinitrophenol (DNP) induces failure of the canine heart-lung-preparation and increases specifically its O
2
-consumption. Lanatoside C compensates this failure as long as the degree of dinitrophenol poisoning is moderate and the O
2
-supply sufficiently ample. This cardiac glycoside does not influence the metabolic action of dinitrophenol, i.e. the increased O
2
-consumption, nor does it counteract the failure due to a large degree of dinitrophenol poisoning. From these findings the mechanism of action of Lanatoside C is discussed.
Activation of the Interventricular Septum
Authors: SCHER ALLEN M. , YOUNG ALLAN C. , MALMGREN ARTHUR L. , ERICKSON ROBERT V.
Published: June 2012

Multipolar recording techniques have been used to study excitation of the canine interventricular septum. Activity commences in the mid left septal endocardium and slightly later near the right anterior papillary muscle. From these sites depolarization spreads over the endocardial surfaces, probably via the Purkinje tissue, at 1 m./sec. and through the septal thickness at one-third this speed. Near the upper septum, bilaterally and on the posterior right there is a lack of the rapid endocardial conduction. Septal contribution to the QRS is considered.
Studies on Distribution of Cerebral Blood Flow with Thorium B-Labeled Erythrocytes
Authors: NYLIN GUSTAV , BLÖMER HANS
Published: June 2012

This paper is a preliminary report describing adaptation of the technic used for determination of blood volume and cardiac output by thorium B-labeled red cells to estimation of cerebral blood flow and its distribution.
Nature of the Vasodilator and Vasoconstrictor Receptors in Skeletal Muscle of the Dog
Authors: YOUMANS PAUL L. , GREEN HAROLD D. , DENISON ADAM B. , BOWLING RICHARD F.
Published: June 2012

Femoral blood flow and arterial pressure responses to stimulation of the lumbar sympathetic chain at L3, L4 and L5 were compared with responses to intra-arterial injections of l-epinephrine and l-norepinephrine before and after progressively increasing levels of adrenergic blockade, and after atropine. The vasoconstrictor responses to nerve stimulation resembled most closely those caused by l-norepinephrine injections at all levels of blockade. Atropine blocked the dilator responses to sympathetic nerve stimulation and reduced reversal responses to l-norepinephrine injections but had no effect on the dilator responses to l-epinephrine. It is concluded that, in skeletal muscle, there are three types of vasoreceptors under autonomic control. Two of these, one constrictor and one dilator, are innervated; the third, a dilator receptor, is only under hormonal control.
Effects of Ovariectomy on Experimental Atherosclerosis in Rabbits
Authors: MININNI GIUSEPPE , CONTRO STEPHEN , CHECCHIA CARLO
Published: June 2012

The effect of previous ovariectomy on the development of cholesterol-induced atherogenesis in the rabbit was investigated. It was found that an ovariectomized group of animals had a significantly greater degree of hypercholesterolemia, but that the control group with intact ovaries developed slightly more aortic and coronary atheromatosis. The implications of these findings are discussed.
Protein-Lipid Relationships in Experimental Canine Atherosclerosis
Authors: BARR DAVID P. , RUSS ELLA M. , EDER HOWARD A. , KENDALL FORREST E. , ABELL LIESE L.
Published: June 2012

The applicability of Cohn's method number 10 to the study of dog plasma has made possible this investigation of experimental canine atherosclerosis. Administration of thiouracil which causes hypercholesterolemia but no atherosclerosis in dogs produces no considerable alteration in the distribution of plasma lipoproteins. High cholesterol feeding and administration of thiouracil causes both atherosclerosis and significant alterations in the distribution of lipoproteins.
Relative Efficiency of Depolarization and Repolarization of the Myocardium Determined from the Spatial Vectorcardiogram
Authors: KOSSMANN CHARLES E. , BRILLER STANLEY A. , MARCHAND NATHAN
Published: June 2012

Utilizing differential vectorcardiography and certain calculations, a method is presented by which the relative quantities of electrical energy expended in depolarization and repolarization of the myocardium in man can be determined.
Composition and State of Protein in Heart Muscle of Normal Dogs and Dogs with Experimental Myocardial Failure
Authors: BENSON ELLIS S.
Published: June 2012

In comparing protein composition of cardiac muscle of normal dogs and dogs with experimental valvular lesions and chronic heart failure, it was found that the concentration of actomyosin was lower in the experimental than in normal dogs. Furthermore, cardiac actomyosin in the experimental animals showed decreased viscosity, decreased viscosity response to ATP, and sedimentation patterns that differed from the normal.
Right-Sided Congestive Heart Failure in Dogs Produced by Controlled Progressive Constriction of the Pulmonary Artery
Authors: DAVIS JAMES O. , HYATT ROBERT E. , HOWELL DAVID S. , CASPER ALFRED
Published: June 2012

Right heart failure was produced in dogs by controlled progressive stenosis of the pulmonary artery. Cardiac enlargement, systemic venous engorgement, tachycardia, hepatomegaly and ascites were consistent findings. The course of cardiac failure was characterized by continual changes in cardiovascular hemodynamics; either cardiac decompensation became progressively severe or circulatory function improved and diuresis resulted. Sodium (Na) retention was always associated with high central venous pressure. Cardiac output was reduced during Na retention except during spontaneous anemia superimposed on cardiac failure. Glomerular filtration rate was frequently normal at the onset of cardiac failure.
The Effects of Diphenylhydantoin Sodium, Glucose and β-Diethylaminoethyl Diphenylpropylacetate Hydrochloride on Cyclopropane-Epinephrine Arrhythmias in the Dog
Authors: WHITE C. W. , MEGIRIAN ROBERT , SWISS EDWARD D.
Published: June 2012

Diphenylhydantoin sodium, glucose, and β-diethylaminoethyl diphenylpropylacetate hydrochloride were tested for their effects upon the cyclopropane-epinephrine arrhythmias. Diphenylhydantoin in a small dose enhanced the arrhythmias and in a larger dose controlled them when given by vein, but its action following oral administration was uncertain. Glucose increased both the duration and the severity of ventricular ectopic rhythms while β-diethylaminoethyl diphenylpropylacetate increased the dose of epinephrine which initiated them.
Studies on the Antithrombin and Heparin Co-factor Activities of a Fraction Adsorbed from Plasma by Aluminum Hydroxide
Authors: MONKHOUSE FRANK C. , FRANCE EVELYN S. , SEEGERS WALTER H.
Published: June 2012

A chemical method has been devised for the quantitative determination of plasma antithrombin. A concentrate of antithrombin has been prepared from plasma. It also contains heparin cofactor activity. The two distinct activities could not be separated and may quite possibly be the properties of a single substance. When the concentrate is combined with heparin the capacity of the concentrate to destroy thrombin is not increased but there is interference with the thrombin fibrinogen interaction. In a mixture of the concentrate and thrombin there is simultaneous destruction of antithrombin, and thrombin activities. Small amounts of the concentrate significantly prolong the clotting time of blood.
The Speed of Ventricular Activation Measured in the Spatial Vectorcardiograms
Authors: SIMONSON ERNST , SCHMITT OTTO H. , BLACKBURN HENRY W. , LEVINE RAPHAEL B.
Published: June 2012

The total QRS interval or R wave crest time in single leads is not accurate for measuring the total ventricular activation time, and is inadequate for an estimate of the ventricular activation rate, as related to the directional time rate of excitation of the total contributing muscle mass. For a more detailed and precise analysis of the ventricular activation, the angular speed in the central segment of the spatial QRS loop was determined in 103 normal men and 26 patients, and significant differences independent of the total QRS duration were obtained.
The Acute Effects of Elimination of the Moderator Reflexes Upon Cardiac Output and Total Peripheral Resistance in the Anesthetized Dog
Authors: LEVY MATTHEW N. , BRIND SHIRLEY H. , BRANDLIN FREDERICK R.
Published: June 2012

The abrupt rise in mean arterial pressure resulting from elimination of the moderator reflexes is not accompanied by a significant increase in cardiac output. The acute hypertension is therefore attributed to a severe generalized vasoconstriction. The severity of this vasomotor response progressively diminishes during the interval immediately following denervation.
The Effect of Inotropic Drugs on Filling of the Isolated Right Ventricle of the Dog Heart
Authors: BUCKLEY N. M. , OGDEN ERIC , McPHERSON R. C.
Published: June 2012

Selected inotropic drugs were studied in an isolated right ventricle preparation in which the work load and heart rate could be controlled. Records of ventricular pressure and volume were made. Rate of ventricular relaxation was estimated, and mechanical impedance to inflow was calculated as the ratio of intraventricular pressure to inflow. The negatively inotropic drugs slowed relaxation and increased impedance. Strophanthin-K reversed these effects. Adrenalin decreased impedance. It is concluded that, during the filling period, inotropic drugs alter those physical properties of ventricle wall which contribute to mechanical impedance.
The Conjugated Lipids of Connective Tissue of the Rat and Rabbit
Authors: BOUCEK ROBERT J. , NOBLE NANCY L. , KAO KUNG-YING TANG
Published: June 2012

The conjugated lipids of connective tissue of the rat and rabbit obtained by the sponge-biopsy technic and the aortic
intima
of the rabbit were divided into two portions by differential saline solubility and the saline-soluble portion was further fractionated into the alpha and beta fractions of Cohn. No apparent relationship was observed between the protein, amino acids or lipids of the serum and the connective tissue of the rabbit. The sponge-connective tissue differed from the aortic
intima
in certain respects but appeared to be similar in the saline-insoluble fractions of amino acid and cholesterol. The effects of sex and age upon connective tissue of the rat is described.
Injury and Repair in Arterial Tissue in the Rabbit
Authors: LINDY SEPPO , TURTO HEIKKI , UITTO JOUNI , HELIN PEKKA , LORENZEN IB
Published: June 2012

The aortic wall in rabbits was injured by pulling an inflated balloon catheter through the aorta. This was followed by an increase of the RNA-DNA ratio in the aortic wall 3 days after the injury. At the same time, the cathodic lactate dehydrogenase (LDH) isoenzymes composed of M subunits increased. The changes in LDH may reflect tissue hypoxia at the early phase after the injury. At 6 days protocollagen proline hydroxylase activity was increased, suggesting increased capacity for collagen formation in the injured aorta. Two weeks after injury the total content of hydroxyproline and DNA were increased, indicating connective tissue proliferation and hyperplasia in the injured aorta. The biochemical changes were interpreted as a repair response of the arterial connective tissue to injury. Gross arteriosclerosis of the aorta developed simultaneously with the biochemical alterations.
Relationship of Heart Rate to Ventricular Automaticity in Dogs During Ouabain Administration
Authors: WITTENBERG STEPHEN M. , GANDEL PAUL , HOGAN PERRY M. , KREUZER WILLIAM , KLOCKE FRANCIS J.
Published: June 2012

Spontaneous changes in ventricular automaticity were determined from changes in idioventricular rate in eight dogs with heart block. The mediating effects of imposed rate were assessed in terms of (1) changes in post-pacing depression after ventricular pacing in 14 dogs and (2) changes in vagally induced ventricular escape time after atrial pacing in five dogs with intact AV conduction. Spontaneous ventricular automaticity decreased throughout the major portion of digitalization. The transition to a ventricular tachycardia was late and abrupt. Transient increases in rate transiently enhanced ventricular automaticity throughout digitalization. In animals with heart block, this was recognized at 38 ± 3% (SE) of the toxic dose of ouabain as blunting of postpacing depression, i.e., a significant decrease in the depression of the first post-pacing beat. Blunting was progressive and was replaced at 72 ± 3% of the toxic dose by post-pacing acceleration, i.e., the cycle length of the first post-pacing beat became shorter than the average pre-pacing cycle length. In vagal stimulation experiments ventricular escape time decreased earlier during atrial pacing at 180-190 beats/min (74 ± 3% of the toxic dose) than during atrial pacing at 140-150 beats/min (92 ± 3%). Early ventricular escape was not seen after pacing at 100 beats/min. These findings indicate that heart rate is a critical determinant of early increases in ventricular automaticity during digitalization.
Effects of Repetitive Bursts of Vagal Activity on Heart Rate
Authors: LEVY MATTHEW N. , LANO THELMA , ZIESKE HARRISON
Published: June 2012

The effect of the timing of discrete bursts of efferent vagal impulses on heart rate was determined in anesthized dogs. Two modes of stimulation were employed. In the first mode, one stimulus burst was delivered per cardiac cycle. As the time from the beginning of the P wave to the vagal stimulus (P-St interval) was progessively increased, there was first a progressive lengthening of the cardiac cycle (P-P interval), then a rapid decrease in P-P interval, and finally a gradual augmentation of the P-P interval. The amplitudes of curves of P-P interval as a function of P-St interval increased as the number of stimuli per burst was augmented, with 10 stimuli/burst yielding nearly maximal effects. Vagal stimuli applied at P-St intervals which coincided with the negative-slope (d[P-P]/d[P-St]) region of such curves tended to evoke sinus arrhythmias. With 5 stimuli/burst or more, these arrhythmias were pronounced and consisted of alternate short and long P-P intervals. In the second mode of stimulation, bursts of stimuli were delivered to the vagus nerve at a frequency independent of heart rate. The cardiac pacemaker tended to become synchronized in some fixed ratio of vagal stimuli to P waves, and this tendency became greater the larger the number of stimuli per burst of impulses. Within any range of synchronization, a paradoxical effect was manifest--increasing frequencies of vagal stimulation produced increasing rather than decreasing heart rates.
Inhibition of Converting Enzyme of the Renin-Angiotensin System in Kidneys and Hindlegs of Dogs
Authors: AIKEN JAMES W. , VANE JOHN R.
Published: June 2012

The activity of angiotensin-converting enzyme in hindlegs and kidneys was compared in anesthetized dogs. Intra-arterial injections of angiotensin I or angiotensin II to one kidney or one hindleg caused dose-dependent decreases in blood flow in that vascular bed. An inhibitor of angiotensin-converting enzyme activity did not affect the vasoconstrictor activity of angiotensin II but substantially reduced that of angiotensin I. The reduction in vasoconstrictor activity of angiotensin I during enzyme inhibition was used to calculate conversion of angiotensin I to angiotensin II. There was 40% conversion in hindleg but only 2.1% in kidney. After intra-arterial injection of angiotensin I, bioassay of angiotensin II in the renal or iliac venous blood indicated that 60-90% of freshly formed angiotensin II was inactivated before leaving the kidney or hindleg. The results show that converting enzyme activity is much greater in hindlegs than in kidneys and that the endogenously formed angiotensin II following intra-arterial injection of angiotensin I is destroyed to the same extent as intra-arterially injected angiotensin II. Intra-arterial infusion of the enzyme inhibitor increased hindleg blood flow in half of the dogs; renal blood flow increased in only one dog. The inhibitor did not affect vascular responses produced by norepinephrine, histamine, vasopressin, or prostaglandin F
2α
but the effects of bradykinin were potentiated.
Neurally Mediated and Direct Effects of Acetylstrophanthidin on Canine Skeletal Muscle Vascular Resistance
Authors: STARK JAMES J. , SANDERS CHARLES A. , POWELL W.M. John
Published: June 2012

The effects of acetylstrophanthidin on the vascular resistance of the isolated canine gracilis muscle were examined in 38 anesthetized mongrel dogs. The neurally mediated effect of intravenous acetylstrophanthidin (0.5 mg) on the vascular resistance of the innervated, separately perfused (constant flow) right gracilis muscle was a transient mean fall of 4.0 ± 0.9 resistance units (RU) (
P
< 0.001) at 1 minute followed by a sustained rise to 4 RU (
P
< 0.05) above control from 8 to 18 minutes after injection. The sustained increase in resistance was blocked by intra-arterial phenoxybenzamine. The combined direct and neurally mediated effects of intravenous acetylstrophanthidin were directionally similar and greater in magnitude in the innervated, autoperfused (intact circulation) left gracilis. Following denervation of the muscle, however, the initial decrease in vascular resistance was abolished and the prolonged subsequent rise was greatly reduced. Hence the initial fall and most of the subsequent rise in vascular resistance are neurally mediated. There was no consistent change in aortic pressure to explain either of these changes in vascular resistance solely on a reflex basis. Thus, systemically administered acetylstrophanthidin produces skeletal muscle vasoconstriction through both a direct and a neurally mediated effect. The latter is mediated through alphareceptor stimulation and appears to be the predominant mechanism whereby this drug increases muscle vascular resistance.
Manifest and Concealed Reentry: A MECHANISM OF AV NODAL WENCKEBACH PHENOMENON
Authors: DAMATO ANTHONY N. , VARGHESE P. Jacob , LAU SUN H. , GALLAGHER JOHN J. , BOBB GUSTAVUS A.
Published: June 2012

The mechanism of the AV nodal Wenckebach phenomenon was studied in 25 dogs by multiple atrial and His bundle electrogram (HBE) recordings. During ventricular stimulation with 1:1 retrograde conduction, the interval from the stimulus artifact to the retrograde His deflection (S-H) interval) remained constant. Decreasing the cycle length of stimulation (CLS) resulted in retrograde AV nodal Wenckebeach cycles. When retrograde AV nodal delay reached a critical value, the Wenckebach cycles were terminated by a reciprocal beat (manifest reentry). The His bundle and ventricles were antegradely depolarized by the reentrant impulse. A further decrease in CLS produced what electrocardiographically looked like ordinary Wenckebach cycles. However, the HBE tracing revealed that reentry was occurring but was concealed by the CLS. This was confirmed by noting that the His deflection of the last ventricular paced beat of the Wenckebach cycle was antegradely depolarized and had a shorter S-H interval then all other beats of that cycle. The reentrant and retrograde impulses collided in the bundle-branch system. Further decreases in CLS masked the reentrant phenomenon on both standard ECG and HBE tracings. The S-H interval remained constant for all ventricular paced beats of the Wenckebach cycle. Under these circumstances, reentry could still be uncovered by turning off the stimulator at an appropriate time during the Wenckebach cycle. This maneuver exposed the reciprocal beat. Thus collision of the reentrant and retrograde impulses occurred within the AV node. These findings provide a satisfactory explanation for why the last beat of the Wenckebach cycle is not conducted retrogradely to the atria.
Electrophysiologic Properties of Isolated Preparations of Human Atrial Myocardium
Authors: GELBAND HENRY , BUSH HARRY L. , ROSEN MICHAEL R. , MYERBURG ROBERT J. , HOFFMAN BRIAN F.
Published: June 2012

The electrophysiologic properties of human atrium were studied with intracellular microelectrodes in 22 preparations of human right atrial tissue obtained at the time of corrective open heart surgery. Two types of fibers were identified: the first had electrical characteristics typical of atrial contractile cells and the second those of atrial specialized fibers. Automaticity developed only in the latter type of cell. In 36 impalements of specialized atrial fibers, resting membrane potential was -86 ± 5 mv (mean ±SD), transmembrane action potential amplitude was 102 ± 12 mv, transmembrane action potential overshoot was 16 ± 4 mv. Similar results were obtained in 49 impalements of contractile fibers. Conduction velocity measured 0.28-0.33 m/sec in contractile fibers and 0.41-0.45 m/sec in specialized atrial fibers. Action potential duration of specialized atrial fibers was linearly related to the basic cycle length between 200 and 1000 msec. At cycle lengths greater than 1000 msec the increase in action potential duration was no longer linear. There was a decrease of 58 mv in resting membrane potential of specialized atrial fibers when exposed to a tenfold increase in extracellular [K
+
]. This decrease occurred in a linear fashion in [K
+
] above 5 mM. These experiments provide reference values for future studies dealing with electrophysiology of human atrial tissue.
Long-Term Effects of Hypertension on the Rat Aortic Wall and Their Relation to Concurrent Aging Changes: MORPHOLOGICAL AND CHEMICAL STUDIES
Authors: WOLINSKY HARVEY
Published: June 2012

The effects of long-term (16 months) hypertension on the thoracic aorta of male rats were compared to previously reported short-term (2.5 months) changes and to concurrent aging changes. Hypertension was produced by clipping a renal artery. Although short-term hypertension was characterized by a disproportionate increase in noncollagenous alkali-soluble proteins, which have been attributed primarily to vascular smooth muscle, with long-term hypertension there was no further increase in these proteins but instead there were striking increases in mural accumulations of elastin and collagen. Chronically elevated wall tension in hypertensive vessels was associated with a progressive increase in wall thickness which resulted in a value for wall stress no different from that of control vessels. Concurrent aging changes were qualitatively similar to, but much less pronounced than, those seen with hypertension and were attributed to an increase in wall tension in controls resulting from a combination of significant increases in diameter and systolic blood pressure with age. This study of the interaction of vessel structure and function has revealed common features of what appears to be a diverse group of vascular alterations.
Effect of Acute Volume Loading on Heart Rate in the Conscious Dog
Authors: HORWITZ LAWRENCE D. , BISHOP VERNON S.
Published: June 2012

The effect on heart rate of rapid elevation of ventricular filling pressure by intravenous infusion of isotonic solution was studied in 31 conscious dogs with autonomic innervation intact and during vagal, beta-receptor, or combined vagal and beta-receptor blockade. When parasympathetic innervation was intact, heart rate always rose during infusion and there was a consistent relationship between mean left atrial pressure and heart rate described by
f
=
f
m
- (
f
m
-
f
l
) e
-kp
where
f
is the heart rate at any left atrial pressure,
p
,
f
m
the maximum heart rate,
f
l
the initial heart rate, and
k
a rate constant. Sympathetic blockade reduced the magnitude of the response and parasympathetic blockade prevented the response. It is concluded that a steady rise in filling pressure during intravenous infusion in a normally innervated, conscious dog invariably results in a tachycardia, which is due to either reflex inhibition of the parasympathetic nervous system or direct mechanical stimulation of the sinoatrial node.
Regional Hemodynamic Effects of a Digitalis Glycoside in the Conscious Dog with and without Experimental Heart Failure
Authors: HIGGINS CHARLES B. , VATNER STEPHEN F. , BRAUNWALD EUGENE
Published: June 2012

The effects of intravenous ouabain (G-strophanthin), 20 µg/kg, on the superior mesenteric, renal, and external iliac beds were studied over a 30-minute period in eight normal conscious dogs before, and in five of them after, cholinergic blockade and in six conscious dogs with heart failure produced by tricuspid avulsion and progressive pulmonary stenosis. Blood flows were measured with Doppler ultrasonic and electromagnetic flowmeters. In normal dogs, prior to cholinergic blockade, ouabain caused early increases in mesenteric, renal, and external iliac resistances but later, between 15 and 30 minutes, mesenteric resistance decreased below the control level while renal and external iliac resistances remained elevated. After cholinergic blockade, the ouabain-induced alterations in renal and iliac resistance were unaltered, but the later decline in resistance in the mesenteric bed was reversed, resulting in sustained constriction. The late decline in mesenteric resistance also was not observed in the conscious animal after the injection of ouabain, 5 µg/kg, directly into the mesenteric artery or in the majority of dogs given ouabain intravenously after having been anesthetized with pentobarbital sodium. In the conscious dogs with heart failure, ouabain resulted in increased renal and iliac resistances initially, and in vasodilatation later while mesenteric resistance fell initially and remained below control for the entire 30 minutes. Thus, in the normal conscious dog, ouabain causes vasoconstriction in the regional vascular beds, apparently by its direct vascular action, and, in addition, a cholinergically mediated vasodilatation in the mesenteric bed. In the conscious dog with heart failure, ouabain increases blood flow to all beds, reducing the compensatory vasoconstriction of the low output state.
Myofibrillar Mass in Rat and Rabbit Heart Muscle: CORRELATION OF MICROCHEMICAL AND STEREOLOGICAL MEASUREMENTS IN NORMAL AND HYPERTROPHIC HEARTS
Authors: PAGE ERNEST , POLIMENI PHILIP I. , ZAK RADOVAN , EARLEY JUDY , JOHNSON MARGARET
Published: June 2012

A sequestered fraction of myofibrillar magnesium presumably bound to thin filaments during polymerization of actin was used to determine myofibrillar mass in rat left ventricles and rabbit hearts. Myofibrillar volume was also determined by stereological measurements on electron micrographs of rat ventricles. Myofibrillar Mg (1.11 mmoles/kg dry ventricle) can be determined in glycerinated ventricle either by measuring
28
Mg-inexchangeable Mg or Mg remaining after extraction with EDTA, KCl, and a nonionic detergent. These measurements, combined with the Mg content of myofibrillar suspensions similarly extracted (3.2 mmoles/kg protein), indicated that myofibrillar mass was 347 g myofibrillar protein/kg dry ventricle. In rabbit hearts, increases in myofibrillar Mg per unit dry weight were as follows: auricular appendage < right ventricle < left ventricle ⋍ interventricular septum. After production of left ventricular hypertrophy in rats by constriction of the ascending aorta, both myofibrillar Mg and volume increased within 24 hours. After 10 or more days, myofibrillar Mg and myofibrillar volume increased proportionately more than tissue dry mass and cell volume, and the ratio of mitochondrial volume to cell volume decreased.