Chronic episodic hypoxia produces a wide array of cardiovascular dysfu
nctions in rats, including increases in blood pressure, heart rate, an
d sympathetic nerve activity. The action of episodic hypoxia might be
related to low oxygen itself (hypoxemia) and/or combined with low CO2
(hypocapnia) resulting from hyperventilation. It is unknown whether or
not the cardiovascular abnormalities are related to alterations in th
e central nervous system (CNS) that may be manifested as neurotransmit
ter and/or behavioral changes. In this study, we investigated effects
of episodic eucapnic and hypocapnic hypoxia on monoamine metabolism in
both CNS and adrenal glands, and on motor behavioral activity. Thirty
-five male rats were divided into 3 groups. Experimental rats were exp
osed 8 h daily to varying fractional concentrations of inspired oxygen
(FiO(2)) and carbon dioxide (FiCO(2)) for 35 days. These consisted of
brief exposures (3-6 s) of episodic (twice every min) eucapnic (3.5%
FiO(2) and 10% FiCO(2), n = 6) or hypocapnic (3.5% FiO(2) and 0% FiCO(
2), n = 14) hypoxia, or room air (21% FiO(2) and 0.03% FiCO(2), n = 15
). Norepinephrine, dopamine, serotonin, and their metabolites in the h
ypothalamus, hippocampus, and adrenal glands were measured by high-per
formance liquid chromatography (HPLC). spontaneous behavioral activity
was assessed for 30 min by automated activity monitors. Episodic hypo
capnic hypoxia produced a decrease in dopamine turnover and eucapnic h
ypoxia increased norepinephrine levels in the hypothalamus. Animals ex
posed to hypocapnic hypoxia also exhibited a consistent increase in ho
rizontal (walking) and vertical (rearing) activity, as well as in tota
l activity time. From these results, it is concluded that episodic euc
apnic and hypocapnic hypoxia may affect metabolism of different neurot
ransmitters in the CNS.