Adrenal lipid profiles of chemically sympathectomized normoxic and hypoxic neonatal rats

Neonatal hypoxia is a common condition that elicits a coordinated endocrine response. In the neonatal rat, hypoxia induces an ACTH-independent increase in corticosterone which can be partially blocked by chemical sympathectomy. The present study sought to characterize the effects of sympathectomy on the adrenal lipid profile, since previous work suggested that augmented plasma corticosterone during hypoxia may be due to changes in adrenal lipid metabolism. Newborn rats were exposed to normoxia or hypoxia from birth to seven days of age, and guanethidine was used to produce the sympathectomy. Plasma epinephrine and norepinephrine were not significantly affected by hypoxia, while guanethidine decreased plasma norepinephrine in normoxic and hypoxic pups. Hypoxia alone increased the concentration of cholesterol esters in the adrenal gland; this increase was due to increases in cholesterol ester-associated oleic (18:1n9), docosahexaenoic (22:6n3), arachidonic (20:4n6), and adrenic (22:4n6) acids. Hypoxia also increased diglyceride-associated adrenic acid. Guanethidine treatment attenuated the hypoxia-induced increase in cholesterol ester-bound arachidonic and adrenic acids. Guanethidine also decreased saturated fatty acid concentrations and increased n3 fatty acid-enriched triglycerides. The results support the idea that the ACTH-independent corticosterone response to hypoxia in the neonatal rat is mediated by specific, sympathetically driven alterations in the adrenal lipid profile.