We report a case of intravenous(IV) amiodarone drug induced liver injury(DILI).The patient received IV N-acetylcysteine(NAC) which resulted in a rapid improvement in liver enzymes.While the specific mechanisms for the...We report a case of intravenous(IV) amiodarone drug induced liver injury(DILI).The patient received IV N-acetylcysteine(NAC) which resulted in a rapid improvement in liver enzymes.While the specific mechanisms for the pathogenesis of IV amiodaroneDILI and the therapeutic action of IV NAC are both unknown, this case strongly implies at least some commonality.Because IV amiodarone is indicated for the treatment of serious cardiac arrhythmias in an intensive care unit setting, some degree of ischemic hepatitis is likely a cofactor in most cases.展开更多
AIM:To study the effect of cerebral ischemia-reperfusion(CI /RP)injury on the function and cycle of T cells in ra t.METHODS:Using animal model of brain ischemia-reperfusion injury,H-TdR incorporation and flow cytom et...AIM:To study the effect of cerebral ischemia-reperfusion(CI /RP)injury on the function and cycle of T cells in ra t.METHODS:Using animal model of brain ischemia-reperfusion injury,H-TdR incorporation and flow cytom eter to detect the change of T cell function a nd cell cycle.RESULTS:After CI /RP,the proliferation ability,clon e formation rate and IL-2production ability of T cells of experimental group were apparently lower than those of contr ol group(P<0.01),and it more apparent with prolonged ischemia time;with CI /RP the recovery of 3-hour gro up was more rapid than that of 6-hour group;after CI /RP injury,the proliferation cycle of T cells in each grou ps changed,the cells in G 0 /G 1 stage were more than those of control group(P<0.01);while the cells in S +G 2 +M stages were few than those of contr ol group(P<0.01);when CI /RP,amount of cells in G 0 /G 1 stage decrease gradually and that of cells in S +G 2 +M stages increase gradual-ly.CONCLUSION:after CI /RP,the function of rat sple en T cells decrease and the proliferation and different iation of cells were inhibited.Early-stage reperfusion can recover damaged immune function as soon as possible.展开更多
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We report a case of intravenous(IV) amiodarone drug induced liver injury(DILI).The patient received IV N-acetylcysteine(NAC) which resulted in a rapid improvement in liver enzymes.While the specific mechanisms for the pathogenesis of IV amiodaroneDILI and the therapeutic action of IV NAC are both unknown, this case strongly implies at least some commonality.Because IV amiodarone is indicated for the treatment of serious cardiac arrhythmias in an intensive care unit setting, some degree of ischemic hepatitis is likely a cofactor in most cases.
文摘AIM:To study the effect of cerebral ischemia-reperfusion(CI /RP)injury on the function and cycle of T cells in ra t.METHODS:Using animal model of brain ischemia-reperfusion injury,H-TdR incorporation and flow cytom eter to detect the change of T cell function a nd cell cycle.RESULTS:After CI /RP,the proliferation ability,clon e formation rate and IL-2production ability of T cells of experimental group were apparently lower than those of contr ol group(P<0.01),and it more apparent with prolonged ischemia time;with CI /RP the recovery of 3-hour gro up was more rapid than that of 6-hour group;after CI /RP injury,the proliferation cycle of T cells in each grou ps changed,the cells in G 0 /G 1 stage were more than those of control group(P<0.01);while the cells in S +G 2 +M stages were few than those of contr ol group(P<0.01);when CI /RP,amount of cells in G 0 /G 1 stage decrease gradually and that of cells in S +G 2 +M stages increase gradual-ly.CONCLUSION:after CI /RP,the function of rat sple en T cells decrease and the proliferation and different iation of cells were inhibited.Early-stage reperfusion can recover damaged immune function as soon as possible.
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.
