摘要
离体大鼠心脏经低灌(0.17 ml·min^(-1))60min后,用正常K-H液复灌20min,可导致严重的心肌损伤,赛庚啶(2.5和5 μmol·L^(-1))对上述心肌损伤有明显的保护作用,表现为明显改善心脏复灌时的心功能,抑制心律失常的发生和降低心脏停搏的发生率,减少心肌细胞内CK和LDH的漏出,提高心肌组织SOD和GSH-Px活性,抑制MDA的升高。
The protective effects of cypro-heptadine (Cyp), an antiserotonin-antihist-aminic agent with calcium channel blocker activity, on myocardial reperfusion injury in isolated Langendorff heart of rats were studied. After a low perfusion [0. 17 ml·min-1, standard Krebs-Henseleit (K-H) buffer without glucose, gassed with 95 % O2+ 5 % CO2] of 60 min followed by a normal K-H buffer perfusion of 20 min, an extensive and severe myocardial injury appeared: a release of lac-tate dehydrogenase (LDH) and creatine kinase (CK), a decrease of superoxide dismutase (SOD) and glutathion peroxidase (GSH-Px) activities, and an increase of malondialdehyde (MDA) content. Serious inhibition of cardiac functions and appearence of arrhythmia, even asystole, were also elicited in the injuried hearts. Cyp (2. 5 and 5 μmol·L-1) effectively antagonized the damage. The results suggested that the protective effects of Cyp on the ischemia-reperfusion injury may be related to its actions of blocking the calcium channel, scavenging the oxygen free radicals , protecting the antioxygen free radical enzymes, and inhibiting the lipid peroxidation in the
myocardium.
出处
《中国药理学报》
CSCD
1994年第3期253-257,共5页
Acta Pharmacologica Sinica
关键词
赛庚啶
心肌
再灌注损伤
丙二醛
cyproheptadine
myocardial reperfusion injury
creatine kinase
lactate dehydrogenase
superoxide dismutase
glutathione peroxidase
malondialdehyde