Objective To elucidate whether endoxin is one of important factors involved in myocardial ischemia reperfusion (MIR) injury, the change of myocardial endoxin level was determined in rats with MIR injury model and the ...Objective To elucidate whether endoxin is one of important factors involved in myocardial ischemia reperfusion (MIR) injury, the change of myocardial endoxin level was determined in rats with MIR injury model and the effects of anti-digoxin antiserum (ADA), an endoxin specific antagonist, on MIR injury were studied. Methods MIR injury model was obtained by ligating left anterior descending coronary artery 30 min followed by 45 min reperfusion. Sprauge Dawley rats were randomly divided into six groups of 10 rats, each. Sham group, MIR group, normal saline group, ADA 9, 18 and 36 mg/kg. ECG was continuously recorded. After reperfusion left ventricular myocardium samples of ischemic area were processed immediately. Myocardial endoxin level, Na++/K++-ATPase, Ca+{2+}-ATPase, Mg+{2+}-ATPase activities, and intramitochondrial Ca+{2+} content were measured. Results Myocardial endoxin level was significantly increased; Na++/K++-ATPase, Ca+{2+}- ATPase , and Mg+{2+}-ATPase activities were remarkably decreased; intramitochondrial Ca+{2+} content was remarkably raised; ST segments of ECG were significantly elevated and occurrence and scores of ventricular arrhythmias were significantly increased in early stage of reperfusion in rats with MIR. In all groups with ADA, myocardial endoxin level was remarkably decreased; Na++/K++-ATPase, Ca+{2+}-ATPase and Mg+{2+}-ATPase activities were drastically increased; intramitochondrial Ca+{2+} content was declined; ST segments and ventricular arrhythmias were improved. Conclusion Myocardial endoxin level was increased in MIR, which implies that the elevated endoxin may be one of major factors inducing MIR injury. This postulate is supported by the observation that ADA has protective and therapeutic effects against MIR injury probably by antagonizing the action of endoxin. The underlying mechanism may be ascribed to restoration of energy metabolism, and attenuation of intracellular Ca+{2+} overload.展开更多
文摘Objective To elucidate whether endoxin is one of important factors involved in myocardial ischemia reperfusion (MIR) injury, the change of myocardial endoxin level was determined in rats with MIR injury model and the effects of anti-digoxin antiserum (ADA), an endoxin specific antagonist, on MIR injury were studied. Methods MIR injury model was obtained by ligating left anterior descending coronary artery 30 min followed by 45 min reperfusion. Sprauge Dawley rats were randomly divided into six groups of 10 rats, each. Sham group, MIR group, normal saline group, ADA 9, 18 and 36 mg/kg. ECG was continuously recorded. After reperfusion left ventricular myocardium samples of ischemic area were processed immediately. Myocardial endoxin level, Na++/K++-ATPase, Ca+{2+}-ATPase, Mg+{2+}-ATPase activities, and intramitochondrial Ca+{2+} content were measured. Results Myocardial endoxin level was significantly increased; Na++/K++-ATPase, Ca+{2+}- ATPase , and Mg+{2+}-ATPase activities were remarkably decreased; intramitochondrial Ca+{2+} content was remarkably raised; ST segments of ECG were significantly elevated and occurrence and scores of ventricular arrhythmias were significantly increased in early stage of reperfusion in rats with MIR. In all groups with ADA, myocardial endoxin level was remarkably decreased; Na++/K++-ATPase, Ca+{2+}-ATPase and Mg+{2+}-ATPase activities were drastically increased; intramitochondrial Ca+{2+} content was declined; ST segments and ventricular arrhythmias were improved. Conclusion Myocardial endoxin level was increased in MIR, which implies that the elevated endoxin may be one of major factors inducing MIR injury. This postulate is supported by the observation that ADA has protective and therapeutic effects against MIR injury probably by antagonizing the action of endoxin. The underlying mechanism may be ascribed to restoration of energy metabolism, and attenuation of intracellular Ca+{2+} overload.
