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Biomedical subjects

A L Mark

Publications and source records attributed to A L Mark.

At least 181 records · Page 10Linked to original sources
PubMed1974

Interaction of baroreceptor and chemoreceptor reflexes. Modulation of the chemoreceptor reflex by changes in baroreceptor activity.

The purpose of this study was to determine whether the level of arterial pressure and degree of baroreceptor activation affect responses to stimulation of chemoreceptors. Chemoreceptors were stimulated by injecting nicotine into the common carotid artery of anesthetized and paralyzed dogs. Responses were observed in the innervated gracilis muscle, perfused at constant flow while perfusion pressure was measured. Arterial pressure was lowered by bleeding the animals and raised by transient occlusion of the descending aorta. Vasoconstrictor responses to stimulation of chemoreceptors were enhanced by hypotension and inhibited by elevation of arterial pressure. Potentiation of the chemoreceptor reflex by hemorrhagic hypotension was not the result of altered vascular resistance in the gracilis muscle, sensitization of chemoreceptors by catecholamines or acidosis, or changes in cerebral perfusion pressure. Additional studies were done in which we excluded the possibility that the changes resulted from direct effects of changes in arterial pressure on chemoreceptors. Both carotid bifurcations were isolated and perfused. On one side, pressure was raised to stimulate the carotid sinus baroreceptors. On the other side, the carotid body chemoreceptors were stimulated by nicotine or by hypoxic and hypercapnic blood. Activation of baroreceptors on one side attenuated the vasoconstrictor response to chemoreceptor stimulation on the other side. This excludes a direct effect of changes in arterial pressure on the chemoreceptors and suggests a central interaction of these reflexes. We conclude that vasoconstrictor responses to stimulation of chemoreceptors are potentiated by hypotension and inhibited by transient hypertension. These effects appear to result at least in part from a central interaction of chemoreceptor and baroreceptor reflexes.

Animals↗
PubMed1973

Abnormal vascular responses to exercise in patients with aortic stenosis.

We tested the hypothesis that the normal forearm vasoconstrictor response to leg exercise is inhibited or reversed in patients with aortic stenosis, possibly because of activation of left ventricular baroreceptors. Forearm vascular responses to supine leg exercise were measured in 10 patients with aortic stenosis and in 2 control groups of 6 patients with mitral stenosis and 5 patients without valvular heart disease.Forearm vasoconstriction occurred during exercise in the control groups. In contrast, forearm blood flow increased and forearm vascular resistance did not change in patients with aortic stenosis. In six patients with aortic stenosis and a history of exertional syncope, forearm vasodilatation occurred during the second minute of leg exercise. Inhibition or reversal of forearm vasoconstrictor responses in aortic stenosis was asscociated with significant increases in left ventricular pressure. In three patients with aortic stenosis and exertional syncope, forearm vasodilator responses to exercise changed to vasoconstrictor responses after aortic valve replacement. The results indicate that forearm vasoconstrictor responses to leg exercise are inhibited or reversed in patients with aortic stenosis, possibly because of activation of left ventricular baroreceptors. The observations suggest that reflex vasodilatation resulting from activation of left ventricular baroreceptors may contribute to exertional syncope in patients with aortic stenosis.

Adult↗
PubMed1973

Reflex vascular responses to left ventricular outflow obstruction and activation of ventricular baroreceptors in dogs.

Reflex vascular responses to acute left ventricular outflow obstruction were studied in anesthetized dogs. The studies were done to compare the effects of activation of ventricular baroreceptors on vascular resistance in skeletal muscle (gracilis muscle) and skin (hindpaw); to identify afferent and efferent pathways which mediate the reflex vasodilatation; and to assess the relative contribution of ventricular baroreceptors and baroreceptors in left atrium and pulmonary vessels in responses to left ventricular outflow obstruction. The gracilis artery and the cranial tibial artery to the paw were perfused separately at constant flow. Changes in perfusion pressure to each bed reflected changes in vascular resistance. Outflow obstruction was produced by inflating a balloon in the left ventricular outflow tract for 15 s while pressures in the left ventricle and aortic arch were measured. Inflation of the balloon increased left ventricular pressure and decreased pressure in the aortic arch. Low and high levels of obstruction produced dilator responses averaging -5+/-3 (SE) and -42+/-11 mm Hg in muscle and -1+/-1 and -3+/-2 mm Hg in paw. Denervation, phentolamine, and glyceryltrinitrate caused greater dilatation in paw than did left ventricular outflow obstruction. This indicates that dilator responses in the paw were not limited by a low level of resting neurogenic constrictor tone or by a negligible dilator capacity of these vessels. Obstruction to left ventricular inflow increased left atrial pressure, but did not cause reflex vasodilatation. This suggests that low pressure baroreceptors in atria or pulmonary vessels did not contribute to vasodilator responses to left ventricular outflow obstruction. Vasodilator responses to outflow obstruction were blocked by bilateral vagotomy, sectioning the sciatic and obturator nerves, and administration of phentolamine, but were not decreased by atropine or tripelennamine. The results indicate that activation of left ventricular baroreceptors produces striking vasodilatation in skeletal muscle, but only slight vasodilatation in skin. The data suggest that the difference in dilator responses in the two beds results from greater withdrawal of adrenergic constrictor tone to skeletal muscle than to skin. Activation of sympathetic cholinergic or histaminergic dilator pathways does not contribute to the dilatation.

Animals↗
PubMed1972

Differences in direct effects of adrenergic stimuli on coronary, cutaneous, and muscular vessels.

Direct effects of adrenergic stimuli on coronary vessels in dogs were compared with effects on vessels to skin (hind paw) and skeletal muscle (gracilis muscle) after intravenous administration of practolol (2 mg/kg), a selective myocardial beta receptor blocker which minimized indirect effects of myocardial stimulation on coronary vascular resistance. The left circumflex coronary, cranial tibial, and gracilis arteries were perfused separately but simultaneously at constant flow. Perfusion pressures, left ventricular pressure and dP/dt. and heart rate were recorded. Changes in perfusion pressure to each bed reflected changes in vascular resistance. The direct constrictor effects of sympathetic nerve stimulation, norepinephrine and phenylephrine on coronary vessels were minimal compared with effects on cutaneous and muscular vessels. Subsequent blockade of vascular beta receptors did not augment the constrictor responses. Angiotensin, a nonadrenergic stimulus, produced striking coronary vasoconstriction which exceeded that in skin and approximated that in muscle. These results suggests that there is a paucity of alpha adrenergic receptors in coronary vessels compared to cutaneous and muscular vessels. Direct dilator responses to isoproterenol were similar in coronary and cutaneous vessels, but were greater in muscular vessels. Responses to glyceryl trinitrate, a nonadrenergic dilator, also were greater in skeletal muscle. Therefore, differences in effects of isoproterenol on the three beds may reflect differences in reactivity to dilator stimuli rather than differences in the density of beta receptors. In contrast to norepinephrine, the predominant direct effect of epinephrine on coronary vessels was dilatation mediated through activation of vascular beta receptors. A constrictor effect caused by stimulation of alpha receptors was unmasked by propranolol.Finally, the order of potency of agonists in stimulating coronary vascular beta receptors and the demonstration of selective beta receptor blockade with practolol suggest that beta receptors in coronary vessels resemble those in peripheral vessels more than those in myocardium.

Adrenergic beta-Antagonists↗
PubMed1972

Impaired reflex vasoconstriction in chronically hypoxemic patients.

Acute hypoxia impairs vasoconstrictor responses in normal men. The present study was done to determine whether reflex vasoconstriction is impaired in chronically hypoxemic patients and whether correction of hypoxemia in these patients improves their cardiovascular reflexes. In eight chronically hypoxemic patients, arterial P(O2) was increased from an average of 45 mm Hg while breathing room air to 161 mm Hg while breathing 40-100% oxygen, with minimal changes in arterial P(CO2) or pH. Correction of hypoxemia did not cause changes in resting arterial pressure or in forearm vascular resistance, but it caused a small increase in resting heart rate. Reflex responses to lower body negative pressure, which causes pooling of blood in the lower part of the body, were observed. When the patients were hypoxemic, lower body negative pressure caused a fall in arterial pressure, slight constriction of forearm vessels, and a small increase in heart rate. When hypoxemia was corrected, the same intervention caused marked vasoconstriction and a greater increase in heart rate, and there was no decrease in arterial pressure. The results indicate that reflex vasoconstrictor responses are depressed in chronic hypoxemia, indicating that adaptive mechanisms which occur in chronic hypoxemia do not include preservation of sympathetic reflexes.

Adult↗
PubMed1972

Effects of adrenergic stimulation on ventilation in man.

The mechanism by which catecholamines affect ventilation in man is not known. Ventilatory responses to catecholamines were observed in normal subjects before and after adrenergic receptor blockade. Intravenous infusions of norepinephrine and isoproterenol caused significant increases in minute volume and decreases in end-tidal P(Co2) which were blocked by the administration of propranolol, a beta adrenergic receptor blocker. The hyperventilatory response to hypoxia was not altered by propranolol. Intravenous infusion of phenylephrine caused a small but significant decrease in minute volume which was antagonized by phentolamine, an alpha adrenergic receptor blocker. Angiotensin, a nonadrenergic pressor agent, also decreased minute volume significantly.100% oxygen was administered to suppress arterial chemoreceptors. Increases in minute volume and decreases in arterial P(Co2) in response to norepinephrine and isoproterenol were blocked by breathing 100% oxygen. The decrease in minute volume during phenylephrine was not altered by 100% oxygen. THE RESULTS INDICATE THAT: (a) beta adrenergic receptors mediate the hyperventilatory response to norepinephrine and isoproterenol but not to hypoxia. (b) the pressor agents phenylephrine and angiotensin decrease ventilation, and (c) suppression of chemoreceptors blocks the ventilatory response to norepinephrine and isoproterenol but not to phenylephrine. Implications concerning the interaction of adrenergic receptors and chemoreceptors with respect to the hyperventilatory response to catecholamines are discussed.

Adult↗