[Animal Modeling] The effect and mechanism of 2,3-butanedione monooxime in improving calcium abnormalities in isolated rat hearts

  Objective: To explore the effect and mechanism of contracture inhibitor 2,3-butanone oxime (BDM) in improving calcium ion abnormalities in isolated rat hearts.

  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 emption pressure, LVP) and left ventricular end diastolic pressure (left ventilability end diastolic pressure, LVEDP) were recorded, and the left ventricular developmental pressure (LVDP) was calculated as the calculated heart. Be evaluated. Function; The content of lactate dehydrogenase (LDH) in coronary effluent reflects myocardial injury; 2,3,5-triphenyltetrazolium chloride (TTC) staining to evaluate the changes of myocardial infarction area; TUNEL method to detect myocardial cell apoptosis index ; Western blot method cleaved caspase-3 and detection of cytochrome c (shell pigment) protein expression.

  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 (P\→ 0.05) . In the calcium abnormal group, LVEDP was significantly increased, LVDP was 0, LDH content in coronary effluent was significantly increased (Pu003c0.01), cleaved caspase-3 and cytochrome c protein expression and apoptosis index were significantly increased ( Pu003c0.01). u003c0.01). Heart tissue death (Pu003c0.01); BDM (20 mmol/L) intervention calcium abnormality group rats myocardial infarction area was significantly reduced (Pu003c0.01), LVEDP decreased, LVDP partially decreased (P) u003c0.01), LDH release decreased (Pu003c0.01), cleavedcaspase-3 and cytochrome c protein expression and apoptosis index were significantly reduced (Pu003c0.01).

  Conclusion: BDM significantly inhibits contracture and cell apoptosis caused by acute calcium overload, improves cardiac function, and reduces calcium overload injury in the isolated rat heart. This is a potential ischemia-reperfusion cardioplegia.