Résumé
AIM: To study the effects of quateranary ammonium salt derivative (F2) of haloperidol on ischemia and reperfusion injury in rat hearts. METHODS: Ischemia and reperfusion injury in rat hearts was induced by occluding the left anterior descending coronary artery for 30 min and restoring blood reperfusion for 30 min. F2(1, 2, 4 mg·kg-1, respectively) was intravenously injected before heart ischemia. Plasma creatine kinase (CK), creatine kinase isoenzyme MB(CK-MB), lactate dehydrogenase(LDH), α-Hydroxybutyrate dehydrogenase (HBDH), grutamicoxalacetic transaminase(GOT), superoxide dismutase (SOD) activity and malondiadehyde (MDA) contents were measured. The pathologic changes of ischemia and reperfusion myocardium were observed on the transmission electron microscopy. RESULTS: F2 reduced the release of CK, CK-MB LDH, HBDH, GOT from I/R rat hearts, increased the activity of SOD and decreased the MDA contents. In F2(1mg·kg-1) group, the serum CK-MB LDH HBDH concentration was lowered significantly (vs I/R group P<0.01 or P<0.05). In F2(2 and 4 mg·kg-1) groups serum CK CK-MB LDH HBDH GOT concentration and MDA contents were decreased significantly (vs I/R group P<0.01), and SOD increased significantly (vs I/R group P<0.01). The decrease of CK, CK-MB, LDH, HBDH, MDA in F2(4 mg·kg-1) group was more remarkable than that in F2(2 mg·kg-1) group (P<0.01). CK-MB in F2(4 mg·kg-1) group was lowered than that in Verapamil (2 mg·kg-1) 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 modified these changes. CONCLUSION: F2 may play an apparent role against rat heart ischemia/reperfusion injury in dose-dependent manner.
Résumé
AIM To study the effects of quateranary ammonium salt derivative (F 2) of haloperidol on ischemia and reperfusion injury in rat hearts. METHODS Ischemia and reperfusion injury in rat hearts was induced by occluding the left anterior descending coronary artery for 30 min and restoring blood reperfusion for 30 min. F 2 (1, 2, 4 mg?kg -1 , respectively) was intravenously injected before heart ischemia. Plasma creatine kinase (CK), creatine kinase isoenzyme MB(CK MB), lactate dehydrogenase(LDH),? Hydroxybutyrate dehydrogenase (HBDH), grutamic oxalacetic transaminase(GOT), superoxide dismutase (SOD) activity and malondiadehyde (MDA) contents were measured. The pathologic changes of ischemia and reperfusion myocardium were observed on the transmission electron microscopy. RESULTS F 2 reduced the release of CK,CK MB LDH,HBDH,GOT from I/R rat hearts, increased the activity of SOD and decreased the MDA contents. In F 2 (1mg?kg -1 ) group, the serum CK MB LDH HBDH concentration was lowered significantly (vs I/R group P