The purpose of this study was to evaluate the effects of vascular and central α-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 α-adrenoceptors affect the distribution of regional microvascular and blood flow responses to hypoxia, and central α-adrenoceptors probably do not participate in this effect.
All Science Journal Classification (ASJC) codes
- Biochemistry, Genetics and Molecular Biology(all)
- Pharmacology, Toxicology and Pharmaceutics(all)