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Biomedical subjects

J E Zehr

Publications and source records attributed to J E Zehr.

At least 37 records · Page 2Linked to original sources
PubMed1981

A simple method to determine the ratio of cardiac to vascular beta-receptor blockade in the rat in vivo.

We have devised a simple method to determine the ratios of cardiac to vascular beta-receptor blockage (C:V ratios) in normotensive rats anesthetized with pentobarbital, and applied it to six beta-adrenergic blocking drugs (beta-blockers). Mean blood pressure (BP) and heart rate (HR) were recorded. Isoproterenol (3 ng-100 microgram/kg, i.v.) was cumulatively injected before and after the intravenous administration of beta-blockers at two dose-levels. Thus shifts of the dose-response curves in BP and HR were observed. "In vivo pA2" values were calculated in molar doses per kg by Schild plots. The C:V ratio was calculated as antilogarithm of the difference of the mean in vivo pA2 value in HR from that in BP. Those of atenolol, bometolol, bunitrolol, pindolol, propranolol, and sotalol were 9.77, 8.13, 2.95, 1.38, 1.20, and 0.71, respectively.

Adrenergic beta-Antagonists↗
PubMed1981

Alteration of the baroreceptor reflex by an effect of propranolol on the isolated carotid sinus.

The present experiments were designed to measure and characterize direct hemodynamic effects of propranolol on vascularly isolated carotid sinuses. dl-Propranolol, when restricted to the isolated carotid sinuses, inhibited in a dose-dependent manner the reflex increases in heart rate and mean arterial pressure during carotid sinus hypotension. When perfused through isolated sinuses at a concentration of 10 micrograms/ml, the drug totally abolished reflex changes to carotid sinus hypotension. Perfusion of the sinuses with d-propranolol or procaine at the same doses also totally inhibited the response. On the other hand, perfusion of the sinuses with sotalol, an adrenergic blocker without membrane stabilizing effects, did not alter resting levels of arterial pressure or heart rate and did not affect reflex changes during sinus hypotension. These results suggest that propranolol at high doses may affect baroreceptor afferents and inhibit the baroreceptor reflex through membrane-stabilizing and local anesthetic properties rather than through hypothesized beta receptors. It seems unlikely that these pathways contribute to the antihypertensive actions of the drug.

Animals↗
PubMed1980

Elimination of noise in telemetry systems by pulse-width discriminator.

A pulse-width-discriminator circuit (PWD) was developed and applied for noise reduction in an FM pulse-interval-ratio modulation telemetry system. The PWD was incorporated as an intermediary between the tuner and the demodulator. The application of the circuit as a noise filter is a result of its ability to distinguish between pulses of different durations and its ability to eliminate pulses whose durations are less than some predetermined value. Since spikes of radio-frequency interference (RFI) occurring at the tuner output were of significantly shorter duration than the encoding pulses, they were virtually eliminated by the PWD. This prevented false triggering of the demodulator and resulted in a noise-free final demodulated output signal. This system was tested during telemetered blood pressure measurements in an unrestrained dog and proved to be extremely effective in eliminating spurious noise caused by electromagnetic interference in the radio-frequency range.

Blood Pressure Determination↗
PubMed1978

The effect of beta adrenergic receptor blockade on the renin response to respiratory acidosis.

The effect of beta adrenergic blockade on the increase in plasma renin activity produced by acute respiratory acidosis was studied in chloralose anesthetized dogs. Sixteen mongrel dogs were given 4%, 8% and 12% CO2 in room air, successively. Propranolol (2 mg/Kg) was given to 8 dogs prior to CO2 inhalation. The other 8 dogs served as the control group. The response of elevated plasma renin activity during 4% and 8% CO2 inhalation was not different between the control and propranolol groups. However, the increase of plasma renin activity in the control group was greater than that of the propranolol treated group during 12% CO2 inhalation. It is suggested that activation of beta adrenergic receptors is not the sole factor in renin control during acute respiratory acidosis, although these receptors do mediate a significant fraction of the renin response to CO2 inhalation.

Acidosis, Respiratory↗
PubMed1976

Reflex suppression of renin secretion during distention of cardiopulmonary receptors in dogs.

We studied the effect of brief periods of left atrial-pulmonary vein distention on the rate of renin secretion in sodium-restricted dogs anesthetized with chloralose and breathing spontaneously. Series 1 consisted of 32 trials in seven dogs with intact renal nerves and intact vagi. Renin secretion, calculated as the product of renal venous minus arterial renin activity (radioimmunoassay) times renal plasma flow (electromagnetic flowmeter), was depressed to 56% of control during atrial distention despite no change in arterial pressure, central venous pressure, or renal blood flow. Series 2 consisted of 58 trials in 12 dogs which had undergone unilateral renal denervation several days prior to the studies. Simultaneous, bilateral determinations indicated that renin secretion from the innervated kidney was depressed to 58% of control during atrial distention; secretion from the denervated kidney was unchanged. Series 3 consisted of 30 trials in six dogs with bilateral cervical vagotomy. Atrial distention evoked no changes in renin secretion. We conclude that left atrial distention reflexly reduces the rates of renin secretion via vagal afferent and renal sympathetic efferent pathways.

Animals↗
PubMed1975

Partition of PGE between renal venous plasma and urine during renal ischemia.

Radioimmunoassay was used to study the effects of renal ischemia on the distribution of PGE-like material between renal venous plasma and urine in anesthetized dogs. Renal venous and urinary concentrations of these substances were equal during control, ischemia and recovery periods. This relationship obtained despite significant increases in the concentration of PGE of both compartments during the ischemic insult. The renal secretion rates of PGE, calculated as the product of renal plasma flow and renal venous concentrations, was reduced during ischemia while urinary excretion, was unchanged. The evidence suggests that the increased PGE concentrations observed in both compartments during renal ischemia are primarily due to a dilutional factor rather than an increased synthesis. Furthermore, the data suggest that the net secretion of renal PG's per unit time may, in fact, be reduced during renal ischemia.

Animals↗
PubMed1975

The effects of respiratory acidosis on plasma renin activity in the dog.

The effects of arterial PCO2 on plasma activity was studied in chloralose anesthetized dogs undergoing carefully controlled respiratory acidosis. Plasma renin activity, measured by radioimmunoassay, was enhanced (P less than 0.001) during inhalation of CO2 despite insignificant changes in renal blood flow and arterial pressure. Although underlying mechanism remained to be investigated, activation of sympathetic nervous system and intrarenal effects of CO2 seemed to be involved in this enchancement.

Acidosis, Respiratory↗