首页> 外文期刊>American Journal of Physiology >Left ventricular mechanoenergetics after hyperpolarized cardioplegic arrest by nicorandil and after depolarized cardioplegic arrest by KCl.
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Left ventricular mechanoenergetics after hyperpolarized cardioplegic arrest by nicorandil and after depolarized cardioplegic arrest by KCl.

机译:尼可地尔超极化心脏停搏后和氯化钾消极心脏停搏后左心室机械能。

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We hypothesized that there are no differences in left ventricular (LV) mechanoenergetics between after hyperpolarized cardioplegic arrest by nicorandil (nicorandil arrest) and after depolarized one by high potassium chloride (KCl arrest). The aim of the present study was to test this hypothesis using LV curved end-systolic pressure-volume relation (ESPVR) and linear pressure-volume area (PVA)-myocardial oxygen consumption per beat (VO2) relation. All hearts underwent 30 min global ischemia (30 degrees C) after infusion of 5 ml of cardioplegia. Cardioplegia consisted of either 30 mmol/l KCl (7 hearts) or nicorandil (100 micromol/l) in Tyrode solution (6 hearts). After a 30-min blood reperfusion, ESPVR and VO2-PVA relation were assessed again. Mean end-systolic pressure (ESP(mLVV)) and mean PVA at midrange LV volume (PVA(mLVV)) significantly (P < 0.05) decreased to 79.1 +/- 13.4% and 85.4 +/- 17.1% of control after KCl arrest and to 85.3 +/- 14.8% and 86.4 +/- 16.9% of control after nicorandil arrest. There were no significant differences in both decreases of mean ESP(mLVV) and PVA(mLVV) between each arrest. The slopes of VO2-PVA relations were also unchanged after each arrest. There was a significant (P < 0.005) difference in the decreases of mean VO2 intercepts of VO2-PVA relations between post-KCl arrest (73.9 +/- 8.2% of control) and post-nicorandil arrest (99.2 +/- 10.1% of control), however. Proteolysis of alpha-fodrin due to Ca2+ overload was significantly marked after KCl arrest. The present results indicate that the total calcium handling in excitation-contraction coupling is transiently impaired after KCl arrest, whereas it is unchanged after nicorandil arrest. This suggests the possibility that nicorandil is a better cardioplegia than KCl.
机译:我们假设在尼古地尔超极化心脏停搏后(尼可地尔停滞)与高氯化钾去极化后的左心室(LV)机械能之间没有差异。本研究的目的是使用LV弯曲末期收缩期压力-容积关系(ESPVR)和线性压力-容积面积(PVA)-每搏心肌耗氧量(VO2)关系来检验该假设。输注5 ml心脏麻痹后,所有心脏均经历30分钟的整体缺血(30摄氏度)。心律失常由在Tyrode溶液(6个心脏)中的30 mmol / l KCl(7个心脏)或尼可地尔(100 micromol / l)组成。血液再灌注30分钟后,再次评估ESPVR和VO2-PVA的关系。在KCl停止后,平均收缩末压(ESP(mLVV))和中程左室容积的平均PVA(PVA(mLVV))显着(P <0.05)降至对照的79.1 +/- 13.4%和85.4 +/- 17.1%尼可地尔停滞后达到控制的85.3 +/- 14.8%和86.4 +/- 16.9%。每个逮捕之间的平均ESP(mLVV)和PVA(mLVV)下降均无显着差异。每次逮捕后,VO2-PVA关系的斜率也保持不变。在KCl停止后(占对照组的73.9 +/- 8.2%)和尼可地尔后停止(占99.2 +/- 10.1%)之间,VO2-PVA关系的平均VO2截距的减少存在显着差异(P <0.005)。控制)。 KCl被捕后,由于Ca2 +超载导致的α-fodrin蛋白水解显着。目前的结果表明,在兴奋-收缩偶联中的总钙处理在KCl停止后暂时受损,而在尼可地尔停止后不变。这表明尼可地尔比KCl有更好的心脏停搏的可能性。

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