BETA-RECEPTOR-MEDIATED INCREASE IN CEREBRAL BLOOD-FLOW DURING HYPOGLYCEMIA
BETA-RECEPTOR-MEDIATED INCREASE IN CEREBRAL BLOOD-FLOW DURING HYPOGLYCEMIA
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DOI:
10.1152/ajpheart.1987.253.4.h949
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发表时间:
1987-10-01
影响因子:
--
通讯作者:
BRYAN, RM
中科院分区:
文献类型:
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作者:
HOLLINGER, BR;BRYAN, RM
We tested the hypothesis that .beta.-adrenergic receptor stimulation is involved with the increase in regional cerebral blood flow (rCBF) during hypoglycemia. Rats were surgically prepared with the use of halothane-nitrous oxide anesthesia. A plaster restraining cast was placed around the hindquarters, and anesthesia was discontinued. Hypoglycemia was produced by an intravenous injection of insulin (15 U/kg); normoglycemic control rats were given saline. Propranolol (1.5 mg/kg) was administered to some control and some hypoglycemic rats to block the .beta.-adrenergic receptors. Regional CBF was measured using 4-[N-methyl-14C]iodoantipyrine. Plasma glucose in the normoglycemic and hypoglycemic groups was .apprx.6 and 1.4 .mu.g/ml respectively. Regional CBF increased during hypoglycemia in rats that were not treated with propranolol. The increase varied from .apprx.60 to 200% depending on the brain region. During hypoglycemia, propranolol abolished the increase in rCBF in the hypothalamus, cerebellum, and pyramidal tract. In other regions the increase in rCBF was only 33-65% of the increase in hypoglycemic rats that were not treated with propranolol. We conclude that .beta.-receptor stimulation plays a major role in the increase in rCBF during hypoglycemia.