Singh R C, Srivastava V K, Tayal G, Srivastava R K, Prasad D N
Indian J Physiol Pharmacol. 1978 Jan-Mar;22(1):61-5.
Interaction of insulin with beta-adrenoceptor antagonists was studied in conscious rabbits. Propranolol and metoprolol did not modify the peak of insulin hypoglycaemia but delayed its recovery. Practolol, sotalol and 1-INPEA enhanced the peak effect and delayed the recovery of insulin-induced hypoglycaemia. H 35/25 and d-INPEA did not modify insulin hypoglycaemia. The beta-blockers did not produce significant hypoglycaemia per se. Since sotalol, 1-INPEA (specific beta-adrenoceptor antagonists devoid of local anaesthetic activity); practolol and metoprolol (selective cardiac beta-1 adrenoceptor antagonists) enhanced hypoglycaemic action of insulin and H 35/25 (a selective beta-2 adrenoceptor antagonist) failed to affect it, it seems that selective beta-adrenoceptor blockade (similar to cardiac beta-1 adrenoceptors) mediates enhancement of insulin hypoglycaemia. Caution should, therefore, be exercised in administering beta-adrenoceptor antagonists and insulin together. A reduction in the dose of insulin may be necessary.
在清醒兔中研究了胰岛素与β-肾上腺素能受体拮抗剂的相互作用。普萘洛尔和美托洛尔未改变胰岛素低血糖的峰值,但延迟了其恢复。普拉洛尔、索他洛尔和1-INPEA增强了峰值效应并延迟了胰岛素诱导的低血糖的恢复。H 35/25和d-INPEA未改变胰岛素低血糖。β-阻滞剂本身未产生明显的低血糖。由于索他洛尔、1-INPEA(无局部麻醉活性的特异性β-肾上腺素能受体拮抗剂);普拉洛尔和美托洛尔(选择性心脏β-1肾上腺素能受体拮抗剂)增强了胰岛素的低血糖作用,而H 35/25(选择性β-2肾上腺素能受体拮抗剂)未能影响它,似乎选择性β-肾上腺素能受体阻滞(类似于心脏β-1肾上腺素能受体)介导了胰岛素低血糖的增强。因此,联合使用β-肾上腺素能受体拮抗剂和胰岛素时应谨慎。可能需要减少胰岛素的剂量。