Search PubMed⌕ Search

Biomedical subjects

G Glick

Publications and source records attributed to G Glick.

At least 55 records · Page 3Linked to original sources
PubMed1971

Importance of the carotid sinus baroreceptors in the regulation of myocardial performance.

The question of whether the carotid sinus baroreceptors modulate myocardial performance remains controversial. Several studies that have stressed their importance have been criticized because the possible role of cerebral ischemia and of other important variables was not eliminated. To reinvestigate this problem, we studied 21 dogs placed on total cardiopulmonary bypass. In each of these animals the carotid sinus regions were isolated and perfused with fully oxygenated blood at a constant flow rate; perfusion pressure was changed by varying the resistance to outflow from the isolated segments. Several indices of myocardial performance were assessed: right and left ventricular contractile force with Walton-Brodie strain gauge arches; the maximal rate of change in contractile force, dF/dt; the pressure developed within an isovolumic balloon inserted into the left ventricle; and the maximal rate of change of this pressure, dP/dt. When the pressure distending the carotid sinuses was raised from an average value of 34.1 +/-2.8 (SEM) mm Hg to 190.1 +/-4.7 mm Hg, right ventricular contractile force fell 14.9 +/-2.3% (P < 0.001); right ventricular dF/dt decreased 16.7 +/-3.0% (P < 0.01); left ventricular contractile force declined 14.9 +/-3.3% (P < 0.01); left ventricular dF/dt fell 19.3 +/-4.0% (P < 0.01); peak systolic pressure in the isovolumic balloon declined 18.2 +/-3.7% (P < 0.001); and dP/dt decreased 34.1 +/-4.0% (P < 0.01). Prior adrenalectomy and vagotomy and maintenance of heart rate at a constant level did not influence these results. The inverse relation between carotid sinus perfusion pressure and the indices of contractility that was observed in this investigation strongly suggests that the carotid sinus baroreceptors are an important regulatory mechanism in the control of myocardial performance.

Animals↗
PubMed1969

Reflex cardiovascular depression produced by stimulation of pulmonary stretch receptors in the dog.

To study the possible reflex effects of stimulation of pulmonary stretch receptors on the cardiovascular system, experiments were designed that would allow separate assessment of the responses of the heart, the total peripheral vascular resistance, and the resistance of the innervated hindlimb that was perfused at a constant flow rate. In every experiment, inflation of the lungs to a positive pressure of 20 mm Hg produced significant negative inotropic and chronotropic effects. Heart rate fell an average of 22.3+/-3.8% (SEM) (P < 0.01), pressure recorded from within an isovolumic balloon in animals on total cardiopulmonary bypass fell an average of 14.3+/-4.6% (P < 0.05), dp/dt recorded from within the balloon declined an average of 31.4 +/- 6.0% (P < 0.01), and contractile force measured with a Walton-Brodie strain gauge arch fell an average of 18.6 +/-2.2% (P < 0.01). Similarly, a depressor response to inflation of the lungs was noted in the periphery as manifested by an average decrease in total peripheral vascular resistance of 21.9+/-2.5% in the animals on total cardiopulmonary bypass (P < 0.01), and by an average decrease in perfusion pressure in the isolated hindlimb of 26.0 +/-3.8% (P < 0.01). After bilateral cervical vagotomy, the cardiovascular responses to inflation of the lungs were either abolished or markedly lessened. Thus, sudden expansion of the lungs activates the afferent arm of a depressor reflex, which produces negative inotropic and chronotropic responses, in addition to arterial vasodilation. The receptors are sensitive to stretch and the afferent pathway runs predominantly in the vagus nerves.

Animals↗
PubMed1968

Mechanisms of reflex vasodilation: assessment of the role of neural reuptake of norepinephrine and release of histamine.

The mechanisms of reflex vasodilation were studied in an innervated canine hindlimb preparation which was perfused at a constant rate. Reflex vasodilation was produced by suddenly increasing the pressure in the trunk by the intravenous injection of norepinephrine, with consequent stimulation of the baroreceptors. When the basal vasoconstrictor tone exerted by the sympathetic nervous system on the systemic arterial bed was minimized, either by pretreatment with the alpha adrenergic blocking agent phenoxybenzamine or with reserpine, which depletes endogenous catecholamine stores, reflex vasodilation was virtually abolished. Administration of cocaine, a drug which blocks reuptake of norepinephrine by the nerve terminals, significantly reduced reflex vasodilation, the response after cocaine averaging 47% of the vasodilator response in the control period. Cocaine also potentiated the vasoconstriction caused by intra-arterially administered norepinephrine but attenuated the vasoconstriction induced by tyramine. The antihistamine, tripelennamine, had effects similar to those of cocaine. It is suggested, therefore, that reflex vasodilation results from a sudden decrease in the level of norepinephrine at the neuroeffector junction, which is a consequence of the cessation of norepinephrine secretion, together with continued and possibly augmented uptake. When the uptake mechanism is impaired, either by the administration of cocaine or tripelennamine, the magnitude of reflex vasodilation is diminished. It does not appear necessary to postulate active secretion of a vasodilator substance to account for reflex vasodilation.

Animals↗