Liu D Q, Pang Z Q, Zhao D H, Sheng B H
Department of Pharmacology, Fourth Military Medical University, Xi-an, China.
Zhongguo Yao Li Xue Bao. 1991 May;12(3):253-6.
Acute myocardial ischemia and reperfusion in rats increased glutamic oxalacetic transaminase (GOT), non-esterified fatty acid (FFA), malondialdehyde (MDA) content. Furyl-dihydropyridines I 10 mg.kg-1 decreased the release of GOT, FFA, MDA of ischemic myocardium, and prevent ischemia-reperfusion arrhythmia. Furyl-dihydropyridines I increased Na, K-ATPase activity and N-acethylneuraminic acid (NANA) content of erythrocyte membranes, inhibited Ca-ATPase activity of erythrocyte membranes in rats. The results suggested that the mechanism of protecting the ischemic-reperfused myocardium might be associated with the inhibition of cellular lipid peroxidation and Ca-ATPase activity of cell membranes.
大鼠急性心肌缺血再灌注可使谷草转氨酶(GOT)、非酯化脂肪酸(FFA)、丙二醛(MDA)含量升高。呋喃二氢吡啶I 10毫克·千克⁻¹可降低缺血心肌中GOT、FFA、MDA的释放,并预防缺血再灌注心律失常。呋喃二氢吡啶I可提高大鼠红细胞膜的钠钾ATP酶活性和N-乙酰神经氨酸(NANA)含量,抑制红细胞膜的钙ATP酶活性。结果提示,其对缺血再灌注心肌的保护机制可能与抑制细胞脂质过氧化及细胞膜钙ATP酶活性有关。