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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Mitochondrial role in ischemia-reperfusion of rat hearts exposed to high-K+ cardioplegia and clonazepam: energetic and contractile consequences.
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Mitochondrial role in ischemia-reperfusion of rat hearts exposed to high-K+ cardioplegia and clonazepam: energetic and contractile consequences.

机译：线粒体在暴露于高K +心脏停搏和氯硝西am的大鼠心脏缺血-再灌注中的作用：能量和收缩力的后果。

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摘要

The role of the mitochondrial Na/Ca-exchanger (mNCX) in hearts exposed to ischemia-reperfusion (I/R) and pretreated with cardioplegia (CPG) was studied from a mechano-calorimetric approach. No-flow ischemia (ISCH) and reperfusion (REP) were developed in isolated rat hearts pretreated with 10 micromol/L clonazepam (CLZP), an inhibitor of the mNCX, and (or) a high K+ - low Ca2+ solution (CPG). Left ventricular end diastolic pressure (LVEDP), pressure development during beats (P), and the steady heat release (Ht) were continuously measured and muscle contents of ATP and PCr were analyzed at the end of REP. During REP, Ht increased more than P, reducing muscle economy (P/Ht) and the ATP content. CPG induced an increase in P recovery during REP (to 90% +/- 10% of preISCH) with respect to nonpretreated hearts (control, C, to 64% +/- 10%, p < 0.05). In contrast, CLZP reduced P recovery of CPG-hearts (50% +/- 6.4%, p < 0.05) and increased LVEDP in C hearts. To evaluate effects on sarcoplasmic reticulum (SR) function, ischemic hearts were reperfused with 10 mmol/L caffeine -36 mmol/L Na (C - caff - low Na). It increased LVEDP, which afterwards slowly relaxed, whereas Ht increased (by about 6.5 mW/g). CLZP sped up the relaxation with higher DeltaHt, C - caff - low Na produced higher contracture and lower Ht in perfused than in ischemic hearts. Values of DeltaHt were compared with reported fluxes of Ca2+-transporters, suggesting that mitochondria may be in part responsible for the DeltaHt during C - caff - low Na REP. Results suggest that ISCH-REP reduced the SR store for the recovery of contractility, but induced Ca2+ movement from the mitochondria to the SR stores. Also, mitochondria and SR are able to remove cytosolic Ca2+ during overloads (as under caffeine), through the mNCX and the uniporter. CPG increases Ca2+ cycling from mitochondria to the SR, which contributes to the higher recovery of P. In contrast, CLZP produces a deleterious effect on ISCH-REP associated with higher heat release and reduced resynthesis of high energy phosphates, which suggests the induction of mitochondrial Ca cycling and uncoupling.
机译：通过机械量热方法研究了线粒体Na / Ca交换子（mNCX）在暴露于缺血再灌注（I / R）并经心脏停搏（CPG）预处理的心脏中的作用。在用10μmol/ L氯硝西am（CLZP），mNCX抑制剂和（或）高K +-低Ca2 +溶液（CPG）预处理的离体大鼠心脏中发展了无血流缺血（ISCH）和再灌注（REP）。连续测量左心室舒张末期压力（LVEDP），搏动过程中的压力发展（P）和稳定的热量释放（Ht），并在REP结束时分析ATP和PCr的肌肉含量。在REP期间，Ht比P增加更多，从而降低了肌肉经济性（P / Ht）和ATP含量。与未经预处理的心脏相比，CPG引起REP期间P恢复的增加（至preISCH的90％+/- 10％）（对照组，C，至64％+/- 10％，p <0.05）。相反，CLZP降低了CPG心脏的P恢复（50％+/- 6.4％，p <0.05），并增加了CVE心脏的LVEDP。为了评估对肌质网（SR）功能的影响，将缺血性心脏再灌注10 mmol / L咖啡因-36 mmol / L Na（C-caff-低钠）。它增加了LVEDP，此后缓慢放松，而Ht增加了（约6.5 mW / g）。 CLZP促进了松弛，其DeltaHt较高，C-caff-低Na在灌注时比在缺血性心脏中产生更高的挛缩和Ht更低。将DeltaHt的值与报告的Ca2 +转运通量进行了比较，这表明线粒体可能是C-咖啡因-低Na REP期间DeltaHt的部分原因。结果表明，ISCH-REP减少了SR存储库以恢复收缩力，但诱导了Ca2 +从线粒体到SR存储库的移动。同样，线粒体和SR能够通过mNCX和单向转运蛋白在超负荷（如在咖啡因中）去除胞浆中的Ca2 +。 CPG增加了从线粒体到SR的Ca2 +循环，这有助于P的更高回收。相反，CLZP对ISCH-REP产生有害作用，与更高的热量释放和高能磷酸盐的再合成有关，这表明线粒体的诱导Ca循环和解偶联。

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