Adrenomedullary function in the neonatal rat: responses to acute hypoxia.

Publisher Website
Google Scholar
Abstract
The mechanism of release of catecholamines from the adrenal medulla of neonatal rats was examined, together with the role of these amines in the ability of the organism to withstand acute O2 deprivation. Splanchnic innervation of the rat adrenal is non-functional until the end of the 1st postnatal wk. Hypoxia caused depletion of adrenal catecholamines in 1-day-old rats as well as in 8-day-old animals. Pre-treatment with cholinergic receptor blocking agents did not prevent the catecholamine response at 1 day but did in older animals. The depletion mechanism is not neurogenic in 1-day-old animals but is neurogenic in 8-day-old animals. The proportions of noradrenaline [norepinephrine] and adrenaline [epinephrine, EP] released by hypoxic stress also differed at the 2 ages, with preferential release of EP by the neurogenic mechanism but not by the non-neurogenic one. The ontogenetic replacement of non-neurogenic adrenomedullary responses by the neurogenic mechanism was directly related to the onset of splanchnic nerve function. Treatments which accelerated the development of neuronal connections caused premature loss of the non-neurogenic response. Prior to the development of sympathetic nerve function, adrenal catecholamines play a predominant role in enabling the neonate to survive hypoxia. Interference with the release of adrenal amines invariably increased mortality during hypoxia. Interference with sympathetic neural release of catecholamines did not affect the ability of 1-day-old rats to withstand hypoxia, indicating that survival during low PO2 [partial pressure of O2] conditions is not dependent on the sympathetic innervation at that stage od development. After functional development of the sympathetic nerves and disappearance of non-neurogenic adrenomedullary responses, the neonatal rats became partially dependent upon catecholamines derived from sympathetic terminals; administration of bretylium at 8 days significantly compromised survival during hypoxia. Interference with adrenergic receptor function also interfered with the ability of neonatal rats to withstand low PO2. At 1 day of age, either phenoxybenzamine or ICI-118551 [erythro-DL-1(7-methylindan-4-yloxy)-3-isopropylaminobutan-2-ol] but not atenolol, shortened the survival time during hypoxia. At 8 days, only phenoxybenzamine did so. The ability of the neonatal rat to survive acute hypoxia depends upon the release of catecholamines and their subsequent actions at peripheral .alpha.- and .beta.2-adrenergic receptors; in the absence of a functional sympathetic innervation, the amines are released from the adrenal medullae by some other mechanism, which disappears shortly after birth.