[Protective effects of cyproheptadine on myocardial reperfusion injury in isolated rat hearts].
The protective effects of cyproheptadine (Cyp), an antiserotonin-antihistaminic 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 lactate 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 appearance of arrhythmia, even asystole, were also elicited in the injured hearts. Cyp (2.5 and 5 mumol.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.
Xin
H B
HB
Department of Pharmacology, School of Basic Medical Sciences, Beijing Medical University, China.
Zhang
B H
BH
Shen
H J
HJ
D000818:Animals; D003402:Creatine Kinase / Q000097:blood; D003533:Cyproheptadine / Q000627:therapeutic use*; D005979:Glutathione Peroxidase / Q000378:metabolism; D066298:In Vitro Techniques; D007770:L-Lactate Dehydrogenase / Q000097:blood; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D015428:Myocardial Reperfusion Injury / Q000378:metabolism / Q000517:prevention & control*; D009206:Myocardium / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D013482:Superoxide Dismutase / Q000378:metabolism
D003533:Cyproheptadine; D008315:Malondialdehyde; D007770:L-Lactate Dehydrogenase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D003402:Creatine Kinase