α-Adrenergic contribution to the cardiovascular response to acute hypoxemia in the chick embryo

Abstract

Fetal responses to acute hypoxemia include bradycardia, increase in blood pressure, and peripheral vasoconstriction. Peripheral vasoconstriction contributes to the redistribution of the cardiac output away from ancillary vascular beds toward myocardial, cerebral, and adrenal circulations. We investigated the effect of alpha-adrenergic receptor blockade on this fetal response. Fluorescent microspheres were used to measure cardiac output distribution during basal and hypoxemic conditions with and without phentolamine treatment. Phentolamine altered basal cardiac output distribution, indicating a basal alpha-adrenergic tone, but this was mainly noted at the earlier stages of incubation. During hypoxemia, phentolamine prevented vasoconstriction in the carcass. At day 19 of incubation, the percent cardiac output distributed to the carcass increased by 20% compared with a decrease in the control group by 17%. Phentolamine markedly attenuated the subsequent redistribution of the cardiac output toward the brain (from +102% in the control group to -25% in the phentolamine-treated group) and the heart (from +196% in the control group to +69% in the phentolamine-treated group). In the chick embryo, alpha-adrenergic mechanisms contribute to the maintenance of basal vascular tone and to the redistribution of the cardiac output away from the peripheral circulations toward the brain and heart during hypoxemic conditions.

Effect of Acute Hypoxia on the Motor Activity and Heart Rate of the 10- and 14-Day Chick Embryo

“…It was earlier demonstrated to depend on the age of the chick embryo and it includes a complex changes in the different functional systems [29][30][31][32][33][34][35]. Our study has added data on the changes in embryonic motor activity to the general picture of the integrated response.…”

“…It was demonstrated that it induced a rapid, integrated response, numerous functional systems being involved in the prevention of damage to the embryo. This response includes a decrease in the PO 2 of the blood; an increase in the blood catecholamine level; hypotensive bradycardia; redistribution of blood flow to vital organs, such as the brain, adrenals, and heart; and a decrease in the frequency of the amniotic contraction [29][30][31][32][33][34][35]. At the same time, changes in embryonic motility during acute hypoxia have been poorly studied.…”

Sympathetic control of the cardiovascular response to acute hypoxemia in the chick embryo

“…On days 11,15, and 19 of incubation, 10 chick embryos were randomly assigned to a control group and 10 to an experimental group. Cardiac output distribution was determined by injection of 15-m fluorescent microspheres (Fluospheres, Molecular Probes, Eugene, OR) suspended in saline and 0.05% Tween 80 (1 ϫ 10 6 spheres/ml), as previously described (22,23). Before injection, the microspheres were thoroughly mixed and vortexed.…”

“…Previous studies from our laboratory have demonstrated the importance of catecholamine release in the cardiovascular response to an episode of acute hypoxemia in the chick embryo. At the end of the incubation period, plasma concentrations of catecholamines increase markedly in response to acute hypoxemia (21), and treatment of the chick embryo with the ␣-adrenergic receptor antagonist phentolamine prevented the redistribution of the cardiac output away from the peripheral circulations (22).…”

Impact of Hypoxia on Early Chick Embryo Growth and Cardiovascular Function

“…Hypoxia produced by 10% oxygen reduces HR in the d 7 chick embryo (42), even though the parasympathetic and sympathetic limbs of the autonomic nervous system are not functional in the chick embryo before d 12 and 20, respectively (40). Thus, hypoxia does not trigger HR compensation via baroreflex, chemoreceptor reflexes, or autonomic innervation in avian embryos until the last third of gestation (20,40,43,44). Effects of hypoxia on ventricular function.…”