硝苯地平恶化低钾状态下心脏缺血再灌注后舒张功能

Nifedipine worsens recovery of diastolic function after ischemia/reperfusion in heart perfused with low K^+ buffer

目的评价钙通道阻断剂硝苯地平对低钾状态下心脏功能的影响。方法离体大鼠心脏接受低钾KH液灌注,其中K+浓度为3.1 mmol/L,实验全程记录左室发展压(LVDP)、左室舒张末压(LVEDP)和左室内压变化速率(dp/dt)的变化。结果 1 h全心缺血和1 h再灌注处理后,LVDP、dp/dt均较缺血前显著降低,LVEDP显著升高;与对照组相比,再灌注开始后前15 min使用含0.5 mmol/L Ca2+的KH灌注,检测指标均明显改善,但是再灌注开始后前10 min给予1 mol/L硝苯地平显著升高LVEDP。结论钙稳态失衡是低钾灌注心脏缺血再灌注后功能损伤的重要原因,硝苯地平恶化心脏舒张功能,其机制有待进一步研究。

Objective The purpose of this study was to evaluate the effect of nifedipine, the calcium channel blocker, on myo- cardial contractile changes induced by low K^＋ perfusion. Methods Isolated rat hearts were perfused with modified KH solution can- taining 3.1 mmol/L K^＋. The left ventricular developed pressure （LVDP）, left ventricular end - diastolic pressure （LVEDP）, and dp/dt of left ventricle were monitored. Results After 1 h ischemia/1 h reperfusion, there were a marked decrease in LVDP and dp/ dt, and an increase in LVEDP. Perfusion with 0.5 mmol/L Ca^2＋during the first 15 min reperfusion significantly improved the contrac- tile dysfunction. However, nifedinpine, which was given during the first 10 min reperfusion, significantly increased the level of LV- EDP. In addition, nifedinpine produced a trend of decrease in LVDP and dp/dt, although no statistical significance. Conclusion Those results confirmed that calcium overload mediates ischemia/reperfusion - induced contractile dysfunction in heart perfusing with low potassium, and also suggested that nifedipine produces exacerbated effect on the ischemic heart.