动物造模,2,3-丁二酮单肟,大鼠离体心脏钙反常损伤 z-bio 2022-01-12 370

　　Objective: To explore the effect of contracture inhibitor 2, 3-butanemonooctane (BDM) on the abnormal calcium in the isolated rat heart and its mechanism.

　　 Method: 32 SD male rats were randomly divided into 4 groups: normal control group, BDM control group, calcium abnormality group, and BDM intervention group. The taken out rat heart was perfused with Langendorff, the left ventricular pressure (left ventricular pressure, LVP) and left ventricular end diastolic pressure (left ventricular end diastolic pressure, LVEDP) were recorded, and the left ventricular developmental pressure (LVDP) was calculated as the calculated heart. Function; reperfusion measurement of lactate dehydrogenase (LDH) content in coronary effluent reflects myocardial injury; 2,3,5-chlorotriphenyltetrazolium (TTC) staining caused changes in the area of myocardial infarction; through TUNEL Methods To evaluate the apoptotic index of cardiomyocytes; Western blot method to detect the expression of caspase-3 and cytochrome c (chitochrome) protein.

　　 Results: Compared with the normal control group, the BDM (20 mmol/L) control group had no significant changes in left ventricular function, myocardial infarction area, apoptosis index, cleavedcaspase-3 and cytochrome c protein expression. \→ 0.05). In the calcium abnormal group, LVEDP was significantly increased, LVDP was 0, LDH content in coronary effluent was significantly increased (P\u003c0.01), caspase-3 and cytochrome c protein expression and apoptosis were lysed. u003c0.01). Heart tissue death (P\u003c0.01); BDM (20 mmol/L) intervention calcium abnormality group rats myocardial infarction area was significantly reduced (P\u003c0.01), LVEDP decreased, and part of LVDP (P reduced LDH release ( P \u003cu003c0.01), the expression of caspase-3 and cytochrome c protein and apoptosis index were significantly reduced (P \u003cu003c0.01).

　　 Conclusion: BDM can significantly inhibit contracture and apoptosis caused by acute calcium overload, improve cardiac function and reduce the damage of calcium overload in isolated rat hearts. This is a potential ischemia-reperfusion cardioplegia.