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Articles in PresS, published online ahead of print November 29, 2001
Am J Physiol Regu Physiol, 10.1152/ajpregu.00634.2001
Submitted on October 25, 2001
Accepted on November 23, 2001
1 Pediatrics, Research Institute GROW, Maastricht University, Maastricht, Netherlands
2 Pharmacology & Toxicology, Cardiovascular Research Institute Maastricht CARIM, Maastricht University, Maastricht, Netherlands
3 Physiology, University of Cambridge, Cambridge, United Kingdom
* To whom correspondence should be addressed. E-mail: amul{at}skin.azm.nl.
In response to an acute hypoxemic insult, the mammalian fetus shows a redistribution of the cardiac output in favor of 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) non-neurogenic via a direct effect of hypoxemia on chromaffin tissues. In the present study the effects of sympathetic blockade were studied on plasma catecholamine release and cardiac output distribution in response to acute hypoxemia 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 on the catecholaminergic response to acute hypoxemia becomes greater by the end of the incubation period.
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