The purpose of this study was to evaluate the effects of vascular and central alpha-
adrenoceptor blockade on cerebral blood flow (CBF) and utilization of brain arteriolar and capillary reserve in conscious rats during normoxia and
hypoxia (8% O2 in N2). Animals were divided into three groups and administered either saline,
N-methyl chlorpromazine (does not cross the blood-brain barrier), or
phenoxybenzamine (crosses the blood-brain barrier) in equipotent doses. Neither agent affected regional CBF and the utilization of brain microvascular reserve during normoxia. CBF increased from 70.9 +/- 2.9 (SEM) ml/min/100 g in the control normoxic group to 123.8 +/- 4.2 ml/min/100 g in control hypoxic animals. In control, hypoxic flow to pons and medulla of the brain was higher than to cortex, hypothalamus or thalamus. The percent of arterioles/mm2 perfused increased from 49.6 +/- 2.0% during control normoxia to 65.6 +/- 3.0% during control
hypoxia. The percentage of capillaries/mm2 perfused changed similarly. Hypoxic CBF was increased similarly after administration of
N-methyl chlorpromazine or
phenoxybenzamine. Administration of
N-methyl chlorpromazine or
phenoxybenzamine eliminated regional differences in hypoxic CBF and the utilization of arterioles, and did not affect capillary response. There was no difference between the effect of
N-methyl chlorpromazine and
phenoxybenzamine on cerebral microvascular and blood flow responses to
hypoxia. It was concluded that peripheral alpha-
adrenoceptors affect the distribution of regional microvascular and blood flow responses to
hypoxia, and central alpha-
adrenoceptors probably do not participate in this effect.