Klein M, Stupienski R F, Nettler S, Smith T, Oshiro G
Department of Pharmacology, Ayerst Laboratories Research, Princeton, New Jersey.
J Cardiovasc Pharmacol. 1989 Jan;13(1):118-24.
Epinephrine-induced hypokalemia is a beta 2-adrenoceptor-mediated effect known to occur in patients after acute myocardial infarction. Cetamolol and atenolol are beta-adrenoceptor antagonists that possess cardioselectivity. They were studied for their ability to inhibit epinephrine- and isoproterenol-induced hypokalemia in anesthetized dogs at equipotent beta 1-adrenoceptor blocking doses. Cetamolol was able to block epinephrine-induced hypokalemia completely, in a dose-related manner, and to block isoproterenol-induced hypokalemia partially. On the other hand, atenolol could produce only partial blockade of epinephrine-induced hypokalemia in a dose-related manner and had essentially no effect on isoproterenol-induced hypokalemia. These results showed that cetamolol was less cardioselective than atenolol and suggest cetamolol would be more beneficial than atenolol in preventing epinephrine-induced hypokalemia in patients who have an acute myocardial infarction.
肾上腺素诱发的低钾血症是一种已知在急性心肌梗死后患者中出现的β2 -肾上腺素能受体介导的效应。塞他洛尔和美托洛尔是具有心脏选择性的β -肾上腺素能受体拮抗剂。在麻醉犬中,以等效的β1 -肾上腺素能受体阻断剂量研究了它们抑制肾上腺素和异丙肾上腺素诱发低钾血症的能力。塞他洛尔能够以剂量相关的方式完全阻断肾上腺素诱发的低钾血症,并部分阻断异丙肾上腺素诱发的低钾血症。另一方面,美托洛尔只能以剂量相关的方式对肾上腺素诱发的低钾血症产生部分阻断作用,而对异丙肾上腺素诱发的低钾血症基本没有影响。这些结果表明,塞他洛尔的心脏选择性低于美托洛尔,并提示在预防急性心肌梗死患者的肾上腺素诱发低钾血症方面,塞他洛尔比美托洛尔更有益。