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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.
RESUMO
AIM To evaluate the changes of serum and brain tissue endoxin in model of bilateral cerebral hemisphere ischemic reperfusion injury, and effect of anti digoxin antiserum (an antagonist of endoxin). METHODS The bilateral cerebral hemisphere ischemic model was prepared by ligating three vascular by Kameyama's manner. SD rats were randomly divided into 7 groups and each group had 8 rats. Sham group, ischemic reperfusion group, negative control group, nimodipine group, low concentration anti digoxin antiserum group, middle concentration anti digoxin antiserum group, high concentration anti digoxin antiserum group. The blood was collected at the end of reperfusion, meanwhile rats were killed, and the bilateral cerebral hemisphere were took out and used to prepare encephlon homogenate and made into samples of light microscope. RESULTS Compared with sham group, the serum CK content increased; Brain tissue SOD activity reduced and MDA content increased importantly in ischemia reperfusion group; The levels of serum and brain tissue endoxin in ischemia reperfusion group were significantly higher, while ATPase activity in brain tissue decreased; Mitochondrial Ca 2+ content in brain tissue increased significantly and Mg 2+ content decreased significantly. In brain tissue,there was some inflammatory change and local necrosis;The rank order and structure of cell wasn't clear;The morphology of pyramidal cell was abnormal. Compared with ischemic reperfusion group, Anti digoxin antiserum reduced serum CK content; It antagonized lowering of SOD activity and increase of MDA content in brain tissue; It remarkably reduced the level of brain tissue endoxin; It reduced abnormal ion content of brain tissue mitochondrion induced by cerebral ischemic reperfusion injury; The high and middle concentration anti digoxin antiserum had a significant effect on raising brain tissue ATPase activity. It reduced neuron denaturation. CONCLUSION Cerebral ischemic reperfusion can increase the level of brain tissue and serum endoxin and higher endoxin can promote brain injury. Endoxin is a major factor involved in cerebral ischemic reperfusion injury. Anti digoxin antiserum can reduce brain tissue injury and had a protective and treatment effect on cerebral ischemic reperfusion injury by antagonizing the effect of endoxin.
RESUMO
Aim To evaluate the protective effect of anti_digoxin antiserum on hypoxic injury myocardium and its mechanism. Methods It was observed that different concentration anti_digoxin antiserum effect on endogenous digitalis_like factor and cell membrane ATPase activity in hypoxic myocardium model. Results The level of endogenous digitalis_like factor was remarkably higher, cell membrane ATPase activity were remarkably lower in hypoxic group than those of normal group; anti_digoxin antiserum can resume membrane ATPase activity.Conclusion Rise of endogenous digitalis_like factor was basic of molecular biology of myocardial damage during myocardial hypoxia. Anti_digoxin antiserum has lightened myocardial injury and has protective effect on hypoxic myocardium by against effect of endogenous digitalis_like factor.
RESUMO
To evaluate the protective effect of anti-digoxin antiserum on hypoxic injury myocardium and its mechanism.Methods It was observed that different concentration anti-digoxin antiserum effect on endogenous digitalis-like factor and cell membrane ATPase activity in hypoxic myocardium model.Results The level of endogenous digitalis-like factor was remarkably higher,cell membrane ATPase activity were remarkably lower in hypoxic group than those of normal group;anti-digoxin antiserum can resume membrane ATPase activity.Conclusion Rise of endogenous digitalis-like factor was basic of molecular biology of myocardial damage during myocardial hypoxia.Anti-digoxin antiserum has lightened myocardial injury and has protective effect on hypoxic myocardium by against effect of endogenous digitalis-like factor.
RESUMO
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.
