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

Abstract

In response to an acute hypoxemic insult, the mammalian fetus shows a redistribution of the cardiac output in favor of the heart and brain. Peripheral vasoconstriction contributes to this response and is partly mediated by the release of catecholamines. Two mechanisms of catecholamine release in the fetus are reported: 1) neurogenic sympathetic stimulation and 2) a nonneurogenic mechanism via a direct effect of hypoxemia on chromaffin tissues. In the present study, the effects of sympathetic blockade on plasma catecholamine release and cardiac output distribution in response to acute hypoxemia were studied in the chick embryo at different stages of incubation. Only at the end of the incubation period, sympathetic blockade markedly attenuated the increase in plasma catecholamine concentrations and resulted in a greater fraction of the cardiac output distributed to the carcass. However, these effects did not prevent a significant increase in cardiac output to the brain and heart during acute hypoxemia. These data imply that in the chick embryo the contribution of neurogenic mechanisms to the catecholaminergic response to acute hypoxemia becomes greater by the end of the incubation period. fetus; hexamethonium; hypoxia; catecholamines; avian HYPOXEMIA IN THE FETUS, resulting largely from placental dysfunction or umbilical blood flow impairment, has been postulated to be a major cause of neurological damage and neonatal morbidity (20,30). During gestation, fetal cardiovascular responses develop to maintain organ blood flow and minimize damage of sensitive tissues during episodes of hypoxemia (for review see Refs. 11,12,and 14). The mechanisms mediating the fetal cardiovascular response to hypoxemia are triggered by carotid chemoreceptor stimulation, which elicits bradycardia, hypertension, and a redistribution of the cardiac output in favor of the adrenal gland, the heart, and the brain (10). Neural sympathetic stimulation and endocrine vasopressor substances, such as catecholamines, contribute to peripheral vasoconstriction, prioritizing the fetal cardiac output away from the periphery to the more vital organs (11,12,14). 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).In fetal sheep (4, 5, 27) and neonatal rats (29), at least two mechanisms mediating catecholamine release in response to hypoxemia have been described. First, before functional innervation of the adrenal glands, hypoxemia may stimulate chromaffin cells directly to promote catecholamine release into the circulation. Second, after the establishment of innervation to the adrenal gland, hypoxemia may stimulate adren...

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

“…The partial restoration of HR under hypoxia on D10 and D14 that followed its decrease may have been related to an increase in the catecholamine content of the blood under hypoxia resulting from stimulation of the adrenal glands [33]. However, we did not find published data on the effect of 10% hypoxia on the catecholamine content of the blood during the studied period of chick embryogenesis.…”

“…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.…”

Impact of Hypoxia on Early Chick Embryo Growth and Cardiovascular Function

“…Of note, cardiac output is initially disproportionately distributed to extraembryonic vessels early in development and the proportion of cardiac output distributed to the embryo increases commensurate with increasing metabolic demand (18,19). During the second half of gestation, compensatory mechanisms such as activation of the autonomic nervous system and catecholamine release redistribute cardiac output to the heart and brain in response to hypoxia (19,20).…”

“…Most studies of the detrimental effects of hypoxia on CV morphogenesis and function have focused on late gestation (6,19,20). The current study was designed to investigate the CV response to hypoxia during early embryogenesis and to test the hypothesis that hypoxia alters both embryonic ven-tricular and vascular function in the early embryo.…”