The concentrations of plasma testosterone (T), estradiol (E_2), and serum luteinizing hormone (LH) and follicle-stimulating hormone (FSH) in 50 male patients with chronic cor pulmonale (CCP) and in 26 healthy men were detected by radioimmunoassay, and their responses to luteinizing hormone-releasing hormone (LRH) stimulating test were observed. The results showed that (1) during acute attack there was significantly low T value (P

Aim To investigate effects and the mechanism of endoxin special antagonist anti-digoxin antiserum on heart function in myocardial anoxia-reoxygenation injury in rats. Methods The isolated Langendorff perfused rat heart model was established. Sixty Sprague Dawley(SD) rats were randomly divided intosix groups and each group had 10 rats: control group, anoxia-reoxygenation group, verapamil group, low, middle, high dose anti-digoxin antiserum groups. ECG, HR, LVDP and ?dp/dtmax were continuously recorded. The endoxin levels and intramitochondrial Ca2+ contents in myocardial tissues and nitric oxide (NO) contents in coronary artery fluence were measured after reoxygenation. Structures of mitochondrial and endothelial cells were observed by microscope. Results The anoxia-reoxygenation group showed a remarkable increase in endoxin level and intramitochondrial Ca2+ content, an obvious decrease NO content, an obvious injury of mitochondrial and endothelial cell, an obvious inhibition of heart function. Middle, high dose of anti-digoxin antiserum group could remarkably decrease endoxin level and intramitochondrial Ca2+ content; increase NO content; obviously relieve the injury of mitochondrial and endothelial cells; remarkably improve the discovery of heart function. Conclusion Anti-digoxin antiserum could inhibit the failure of heart function induced by myocardial anoxia-reoxygenation injury. Its mechanism may be related to antagonize endoxin, relieve mitochondrial Ca2+ overload, increase NO contents, and protect the function of mitochondrial and endothelial cells.

Aim To research the changes of myocardial endoxin level in rats with myocardial ischemia reperfusion (MIR) and the protevtive effects of anti digoxin antiserum, an endoxin specific antagonist, on MIR injury. Methods Myocardial ischemia reperfusion injury models were obtained by ligating left anterior descending coronary artery 30 min followed by 45 min reperfusion. Sprauge Dawley rats were randomly divided into seven groups each with 10 rats. There were sham group, MIR group, normal saline group, verapamil group, low dose anti digoxin antiserum group, middle dose anti digoxin antiserum group, and high dose anti digoxin antiserum group. After reperfusion of left ventricular myocardium, sample of ischemia were processed immediately. Myocardial endoxin levels, Na +, K + ATPase activities, and intramitochondrial Ca 2+ contents were measured. The myocardial morphology were observed. Results Myocardial endoxin levels were significantly increased; Na +, K + ATPase activities were remarkably decreased; intramitochondrial Ca 2+ contents were remarkably raised. Meanwhile, myocardial morphology injury were remarkable in light microscope and electric microscope. Middle and high dose of anti digoxin antiserum intervention, myocardial endoxin levels were remarkably decreased; Na +, K + ATPase activities were drastically increased; intramitochondrial Ca 2+ declined. The myocardial histological morphology was significantly improved. Conclusion Antidigoxin antiserum, an endoxin antagonist, had protective effect against MIR. The mechanism maybe related to antagonizing endoxin, restoring energy metabolism, attenuating intracellular Ca 2+ overload.