CAJ | 학술논문

目的:研究氟哌啶醇季铵盐衍生物(F2)对大鼠心肌缺血再灌注损伤保护作用的影响.方法:大鼠冠状动脉左前降支结扎30min 后恢复血液灌注30min,于缺血前舌下静脉注射不同剂量F2(1mg/kg,2mg/kg,4mg/kg).测定血清CK,CK*MB、LDH、HBDH、GOH、SOD、MDA的含量;观察心肌病理形态学改变.结果:F2能降低由于缺血再灌注引起的心肌损害心肌酶CK、CK-MB、LDH、HBDH、GOT的释放,保护SOD的活性,降低脂质过氧化物MDA的产生,并呈量效关系;透视电子显微镜下可观察到F2能较好减轻缺血再灌注心肌的形态学改变.结论:F2 对大鼠心肌缺血再灌注损伤具有保护作用.
목적:연구불고정순계안염연생물(F2)대대서심기결혈재관주손상보호작용적영향.방법:대서관상동맥좌전강지결찰30min 후회복혈액관주30min,우결혈전설하정맥주사불동제량F2(1mg/kg,2mg/kg,4mg/kg).측정혈청CK,CK*MB、LDH、HBDH、GOH、SOD、MDA적함량;관찰심기병리형태학개변.결과:F2능강저유우결혈재관주인기적심기손해심기매CK、CK-MB、LDH、HBDH、GOT적석방,보호SOD적활성,강저지질과양화물MDA적산생,병정량효관계;투시전자현미경하가관찰도F2능교호감경결혈재관주심기적형태학개변.결론:F2 대대서심기결혈재관주손상구유보호작용.
Objective:To study the effect of quaternary ammonium salt derivative(F2)of haloperidol on rat heart ischemia/reperfusion(I/R)injury.Methods:Rat heart I/R injury was induced by occluding the left anterior descending coronary artery for 30 minutes and restoring blood perfusion for 30 minutes.Three dosages (1mg/kg,2mg/kg,4mg/kg,respectively)of F2 were intravenously injected before heart ischemia.Plasma creatine kinase (CK),creatine kinase isoenzyme MB(CK-MB),lactate dehydrogenase (LDH),α-Hydroxybutyrate dehydrogenase(HBDH),grutamic-oxalacetic transaminase(GOT),malondiadehyde(MDA) concentrations and superoxide dismutase(SOD)activity were measured.The pathologic changes of I/R myocardium were observed on the transmission electron microscopy.Results:F2 reduced the release of CK,CK-MB,LDH,HBDH and GOT from I/R rat hearts,increased the activity of SOD and decreased the MDA product.In F2 (1mg/kg)group,the serum CK-MB,LDH and HBDH concentrations were lowered significantly(vs I/R group P＜0.01 or P＜0.05).In F2(2mg/kg and 4mg/kg)groups,serum CK,CK-MB,LDH,HBDH and GOT concentrations and MDA content were decreased significantly (vs I/R group P＜0.01),and SOD activity increased significantly(vs I/R group P＜0.01).The decrease of CK,CK-MB,LDH,HBDH and MDA in F2 (4mg/kg) group was more remarkable than that in F2(2mg/kg) group(P＜0.01).CK-MB in F2 (4mg/kg) group was lower than that in Verapamil(2mg/kg) group(P＜0.05).For morphology,myocytes of I/R heart showed intracellular edema,disarrangement and rapture of myocardial fiber,damaged mitochondria,marginated and concentrated nucleus.F2 mollified these changes.Conclusion:F2 may exert an apparent role against rat heart ischemia/reperfusion injury in dose-dependent manner.