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Biomedical subjects

A M Scher

Publications and source records attributed to A M Scher.

At least 37 records · Page 2Linked to original sources
PubMed1984

Long-term responses of atrial rate and peripheral resistance to changes in ventricular pacing rate in awake dogs with atrioventricular block.

We wished to see if a maintained change in pressure at the baroreceptors leads to a maintained or a transient change in heart rate and total peripheral resistance, and if long-term changes in rate and resistance paralleled one another. In awake dogs with intact baroreceptors and complete atrioventricular block, ventricular rate was held alternately at high (90 beats/min) and low (50 beats/min) levels, each for 2 days. This cycle was repeated several times. Data were recorded for 1.5 hours each day. With this change in ventricular rate, there was a maintained change over 2 days in arterial (14.4 +/- 1.0 mm Hg) and central venous (3.0 +/- 1.2 mm Hg) pressures. These changes in pressure were accompanied by a maintained change in atrial rate of 41.1 +/- 9.4 beats/min; peripheral resistance, however, changed only transiently. In three animals, the half-cycle length was 1 week. Changes in heart rate also persisted for this period. It appears from these studies that there is long-term control of heart rate, but not of peripheral resistance. Hypotheses to explain these results are presented.

Animals↗
PubMed1984

Changes in vascular capacity in awake dogs in response to carotid sinus occlusion and administration of catecholamines.

Changes in cardiac filling pressure (central venous pressure) were measured following carotid occlusion and infusions of catecholamines in awake dogs while cardiac output was held constant. After carotid occlusion in dogs with vagi blocked, central venous pressure increased about 0.8 mm Hg (an estimated decrease in vascular capacity of 2.4 ml/kg). Carotid occlusion before vagal block or following vagal block and beta-adrenergic block with propranolol caused no significant changes in central venous pressure. Phenylephrine (0.1-2.0 micrograms/min per kg) caused dose-dependent increases in arterial pressure, but changed central venous pressure (ca. 2.5 mm Hg) only at the highest doses. Epinephrine in doses (0.03-0.51 micrograms/min per kg) that caused little change in arterial pressure increased central venous pressure up to 5.3 mm Hg (an estimated decrease in vascular capacity of 12.0 ml/kg); this response was attenuated about 50% by propranolol. Isoproterenol (0.01-0.40 micrograms/min per kg) decreased arterial pressure and caused changes in central venous pressure similar to those seen with epinephrine. These responses were abolished by propranolol. Vascular compliance, determined from the change in central venous pressure following known changes in vascular blood volume, averaged 3.0 +/- 0.6 ml/mm Hg per kg. In the conscious, resting dog, both alpha- and beta-adrenergic receptors are involved in the reflex control of cardiac filling pressure. The beta-adrenergic responses predominate.

Animals↗
PubMed1983

Cardiovascular responses to graded reductions in hindlimb perfusion in exercising dogs.

In six dogs trained to run at 2, 4, and 6 mph, we caused graded reductions in hindlimb perfusion by compressing the terminal aorta. Our goal was to examine the relationship between hindlimb perfusion [terminal aortic flow (TAQ) and femoral arterial pressure (FP)] and cardiovascular responses [aortic pressure (AP), heart rate, and ascending aortic flow (CO)]. Small reductions in TAQ and FP produced bradycardia, small decreases in CO, and small increases in AP. Further reductions in TAQ and FP produced tachycardia, increased CO, and large increases in AP. AP rose by about 1 mmHg for each 1-mmHg fall in FP. The response was similar at all speeds, but as work load increased it required smaller reductions in FP and TAQ to cause a pressor response (e.g., at 6 mph we could not demonstrate a nonlinear relationship between TAQ and AP). At low work loads the cardiovascular responses to exercise were most likely set by signals other than feedback from exercising muscle because substantial reductions in hindlimb perfusion caused no significant cardiovascular responses. At moderate-to-high work loads or where muscle perfusion is restricted, metabolic feedback from muscle may play a role in cardiovascular responses to exercise.

Animals↗
PubMed1983

Angiotensin causes vasoconstriction during hemorrhage in baroreceptor-denervated dogs.

The participation of angiotensin II (ANG II) in the maintenance of arterial blood pressure during hypotensive hemorrhage was examined in unanesthetized, baroreceptor-denervated dogs. When mean aortic blood pressure was reduced to 69.0 +/- 2.2 mmHg, plasma renin activity increased from 0.6 +/- 0.3 ng ANG I X ml-1 X h-1 during the prehemorrhage control period to 4.5 +/- 1.6. Twenty minutes after the hemorrhage, mean aortic blood pressure rose to 78.9 +/- 3.1 mmHg. Subsequent infusion of the angiotensin II antagonist saralasin (5.2-14.0 micrograms X kg-1 X min-1) decreased mean aortic pressure to 59.6 +/- 3.3 mmHg. When 5% dextrose was infused in place of saralasin, mean aortic pressure was 79.3 +/- 4.3 mmHg. The lower aortic blood pressure caused by saralasin infusion was the result of a significant decrease in total peripheral resistance. Resistance was 10.3 +/- 3.2 mmHg X l-1 X min lower during saralasin infusion than during dextrose infusion. We conclude that baroreceptor reflexes are not essential for the elevation of plasma renin activity during hemorrhage. In baroreceptor-denervated dogs subjected to hypotensive hemorrhage, the increased formation of ANG II has a vasoconstrictor action that contributes to the maintenance of arterial blood pressure.

Angiotensin II↗
PubMed1982

Beat-by-beat control of cardiac output in awake dogs with atrioventricular block.

In dogs with atrioventricular block and implanted ascending aortic flow probes, cardiac output can be controlled on each beta. The procedure is implemented through on-line use of a digital computer. The algorithm has three steps: 1) aortic flow is measured and integrated to give stroke volume; 2) at the end of ejection, the program computes how long the current beat must be to keep cardiac output at a target level; and 3) the ventricle is stimulated at the proper time. Cardiac output can be controlled over a range of 60-110% of normal in a resting dog. This range can be expanded by combining hemorrhage or volume infusion with the control procedure.

Animals↗
PubMed1982

Effect of tissue anisotropy on extracellular potential fields in canine myocardium in situ.

The extracellular epicardial potential fields produced by simple depolarization waves in the in situ canine left ventricular myocardium were analyzed. A mathematical model that included tissue anisotrophy was developed to explain the observed fields. Values of intracellular (i), extracellular (o), longitudinal (l), and transverse (t) resistivity which gave the best fit between the model and experimental data were (in ohm-cm, mean +/- SD): rol = 852 +/- 232, rot = 1247 +/- 210, ril = 291 +/- 38, rit = 1677 +/- 331. The potential fields around simple stimulated waves on the epicardium can best be explained if the extracellular wavefront voltage is (mean +/- SD) 74 +/- 7 mV for a wave propagating parallel to the local muscle fibers, and 43 +/- 6 mV for a wave propagating perpendicular to these fibers. We conclude that the anisotrophy of the electrical conductivity of cardiac muscle has important effects on he propagation of waves of depolarization and on the potential fields produced by depolarization in the intact heart.

Action Potentials↗
PubMed1981

Hypertension following arterial baroreceptor denervation in the unanesthetized dog.

Studies were conducted on unanesthetized dogs (1) in the control state, (2) after carotid sinus denervation plus section of the cervical aortic nerves (SCAD), and (3) after carotid sinus denervation plus section of intrathoracic vegal branches which innervate arterial and cardiopulmonary baroreceptors, the heart, lungs, and other structures (STD). Mean values and standard deviations of blood pressure and heart rate were measured during many 75-minute recording sessions. The control mean arterial pressure was 94.8 +/- 8.9 mm Hg. The mean pressure after SCAD was 105.5 +/- 9.5 mm Hg, 10.0 mm Hg higher (P less than 0.05) than in the control state, whereas after STD, the mean pressure was 119.5 +/- 16.8 mm Hg, 25.3 mm Hg higher (P less than 0.001) than in the control state. The standard deviation of pressure was increased (P less than 0.01) by either denervation procedure. The mean pressure after STD was higher than after SCAD (P less than 0.05). Ten of 12 animals with SCAD showed residual baroreceptor reflexes (seven from intrathoracic receptors) whereas, after STD, six of 11 animals showed reflexes (one from intrathoracic receptors). SCAD only occasionally produces denervation as complete as that produced by STD. A larger increase in arterial pressure follows a more complete denervation of vagally innervated baroreceptors. We believe that our procedures do not denervate all arterial baroreceptors. Chronic denervation of arterial baroreceptors leads to a widely varying, elevated arterial pressure. The increase in pressure has persisted more than 1 1/2 years.

Animals↗
PubMed1979

Influence of cardiac fiber orientation on wavefront voltage, conduction velocity, and tissue resistivity in the dog.

When the canine epicardium is stimulated, the spread of epicardial excitation is 2.4 times faster parallel to the long axes of the cardiac fibers than perpendicular to them. Likewise, gross tissue resistivity is lower parallel to fibers by a factor of 3.2, and the voltage across the depolarization wave is approximately three times as great in the longitudinal direction. Equations are presented which relate these variables. Theoretical considerations confirm the experimental finding that the potentials around a wave of depolarization cannot be accounted for by the conventional hypothesis that the wavefront is a uniform double-layer current source.

Animals↗
PubMed1979

Hypertension following denervation of aortic baroreceptors in unanesthetized dogs.

After cervical aortic nerve section, mean arterial pressure in the unanesthetized dog increased by an average of 7.4 mm Hg. Following a more extensive denervation of aortic arch receptors by section of intrathoracic vagal branches, arterial pressure increased by 16.7 mm Hg. The above changes were seen in the stable state after the effects of surgery had disappeared. In both cases carotid baroreceptors were functional. After administration of nitroglycerin and phenylephrine subsequent to either denervation procedure, blood pressure changes were larger and heart rate responses were smaller than in the control state. The unanesthetized dog regulates mean arterial pressure at a higher-than-normal pressure after aortic baroreceptor denervation. Reflexes from the aortic baroreceptors continuously participate in the normal control of mean arterial pressure. Section of the cervical aortic nerves only partially denervates aortic baroreceptors. Our findings may be relevant to human essential hypertension.

Animals↗
PubMed1977

Zero offset in electromagnetic flowmeters.

In electromagnetic square-wave flowmeters, it should be theoretically possible to determine zero flow by turning off the magnet drive. In actuality, this is not possible. A major source of zero offset in many commercial flowmeters lies in the fact that the very large voltage transients, seen as the flowmeter drive switches polarity, are distorted by the input amplifiers. This can be corrected by improved amplifier design. A second source of zero offset when flow probes have been immersed in conducting fluids is resistive leakage between the drive voltage and the input electrodes. This can be minimized through the use of shielded coils, with shield grounded, and by the use of a magnet drive isolated from ground. If both of these sources of zero offset are corrected, offset is greatly reduced. Polarization of the flowmeter electrodes, which has previously been suggested as a cause of zero offset, was not detected.

Animals↗
PubMed1977

The canine heart as an electrocardiographic generator. Dependence on cardiac cell orientation.

Traditionally it is assumed that during cardiac depolarization the macroscopic current generators that produce electrocardiographic voltages can be represented as a uniform double-layer source, coincident with the macroscopic boundary between resting and depolarized cardiac fibers as measured with extracellular electrodes ("uniform" hypothesis). A segment of this boundary is thus considered as a current dipole oriented perpendicular to the boundary. We present evidence that, contrary to the above, the effective dipoles largely parallel the long axes of cardiac fibers ("axial" hypothesis). Calculated potentials in volume conductors differ markedly in the two cases. The magnitudes of rapid local "intrinsic" deflections also differ markedly. In our experiments, potential fields prodlced by stimulation at several cardiac sites and measured magnitudes of intrinsic deflections during normal depolarization and that caused by stimulation support the axial hypothesis and are incompatible with the uniform hypothesis. Our results suggest that axial orientation of sources is sufficiently strong so that predictions assuming the uniform hypothesis would be seriously in error, although the axial theory alone does not exactly describe all the measured potentials. Axial orientation of current generators must be considered in quantitative prediction of electrocardiographic potentials. tfurther study of the geometry of the intracellular depolarization boundary and its relation to fiber direction and to the frequency of lateral intercellular junctions is required to describe the generators exactly.

Action Potentials↗
PubMed1976

Atrial rhythm during ventricular fibrillation in the dog.

Depolarization of the atrioventricular junctional tissues and of the atrial septum was examined in the perfused dog heart before and during ventricular fibrillation by (1) recording the potentials from the junctional tissues in the regions of the interatrial and interventricular septum and examining the relationship of activity at these sites to atrial depolarization, (2) computing histograms and autocorrelograms of atrial firing intervals to study atrial rhythmicity, and (3) plotting the sequence of atrial septal depolarization. The junctional tissue was generally randomly depolarized by the fibrillating ventricles. The histograms and autocorrelograms indicate that during ventricular fibrillation the atrial depolarization intervals do not remain constant, but vary widely. This seems to be due to the retrograde excitation from the junctional tissues. Plots of the depolarization sequences of the interatrial septum also indicate that retrograde depolarization takes place. The junctional tissues decrease the number of impulses that can pass from ventricle to atrium, and they similarly decrease the number of impulses that pass in an antegrade direction during atrial fibrillation.

Animals↗
PubMed1975

Heart rate response to sympathetic stimulation before and after sodium pentobarbital.

Heart rate response to electrical stimulation of the right stellate ganglion of vagotomized cats was studied before and after the administration of sodium pentobarbital. The increase and decrease of heart rate with the initiation and cessation of sympathetic stimulation could be accurately described by separate exponential time functions. The time constants of rise and decline, the maximum steady-state heart rate, and the time between cessation of stimulation and initial decrease of heart rate (lag) were functions of the frequency and voltage of stimulation. The main effects of sodium pentobarbital were: 1) to prolong the rise of heart rate by 20-30 percent (P smaller than 0.0001),2) to prolong the decay of heart rate by 36-56 percent (P smaller than 0.005), and 3) to decrease the resting heart rate. The effects were observed 10 min after administration of the drug and lasted at least 4 h.

Animals↗