Postconditioning of sevoflurane and propofol is associated with mitochondrial permeability transition pore
Postconditioning of sevoflurane and propofol is associated with mitochondrial permeability transition pore
复制标题
七氟烷和丙泊酚后处理与线粒体通透性转变孔相关
DOI：
10.1631/jzus.b0710586
复制
发表时间：
2008-02-01
影响因子：
5.1
通讯作者：
Yan, Min
中科院分区：
文献类型：
--
作者：
He, Wei;Zhang, Feng-Jiang;Yan, Min
背景：七氟醚和异丙酚是有效的心脏保护麻醉剂，尽管异丙酚的心脏保护作用尚未在人类身上显示出来。它们在麻醉后处理中的作用和潜在机制尚不清楚。线粒体通透性转换孔(MPTP)开放是缺血再灌注损伤的主要原因。在这里，我们研究了七氟醚和异丙酚诱导的后处理及其与MPTP的关系。方法：大鼠离体心缺血40min，再灌流1h。再灌流前15min分别给予对照缓冲液(CTRL组)、含20μμ/L苍术油苷缓冲液(ATR组)、3%(v/v)七氟醚缓冲液(SPC组)、50 Mol/L丙泊酚缓冲液(PPC组)、苍术苷复合麻醉药组(SPC+ATR组和PPC+ATR组)。心肌梗死面积通过将左心室总坏死面积除以左心室切片总面积(坏死面积百分比)来确定。结果：与对照组相比，使用七氟醚或异丙酚的心脏表现出更好的冠状动脉流量、舒张末压力、左心室发展压和导数的恢复。七氟醚对血流动力学的保护作用在再灌流的大部分时间点均强于异丙酚。这些改善与减少乳酸脱氢酶释放和缩小心肌梗死面积(SPC vs CTRL：(17.48±2.70)%vs(48.47±6.03)%，P<；0.05；PPC vs CTRL：(35.60±2.10)%vs(48.47±6.03)%，P<；0.05)平行。SPC组心肌梗死面积小于PPC组[(17.48±2.70)%vs(35.60±2.10)%，P<0.05]。白术苷合用可减弱或完全阻断七氟醚和异丙酚的后处理心脏保护作用。结论：七氟醚、异丙酚后处理对心脏缺血再灌注损伤有保护作用，其机制可能与抑制MPTP开放有关。与异丙酚相比，七氟醚在功能恢复和心肌梗死面积方面具有更好的保护作用。
Background: Sevoflurane and propofol are effective cardioprotective anaesthetic agents, though the cardioprotection of propofol has not been shown in humans. Their roles and underlying mechanisms in anesthetic postconditioning are unclear. Mitochondrial permeability transition pore (MPTP) opening is a major cause of ischemia-reperfusion injury. Here we investigated sevoflurane-and propofol-induced postconditioning and their relationship with MPTP. Methods: Isolated perfused rat hearts were exposed to 40 min of ischemia followed by 1 h of reperfusion. During the first 15 min of reperfusion, hearts were treated with either control buffer (CTRL group) or buffer containing 20 μmol/L atractyloside (ATR group), 3% (v/v) sevoflurane (SPC group), 50 μmol/L propofol (PPC group), or the combination of atractyloside with respective anesthetics (SPC+ATR and PPC+ATR groups). Infarct size was determined by dividing the total necrotic area of the left ventricle by the total left ventricular slice area (percent necrotic area). Results: Hearts treated with sevoflurane or propofol showed significantly better recovery of coronary flow, end-diastolic pressures, left ventricular developed pressure and derivatives compared with controls. Sevoflurane resulted in more protective alteration of hemodynamics at most time point of reperfusion than propofol. These improvements were paralleled with the reduction of lactate dehydrogenase release and the decrease of infarct size (SPC vs CTRL: (17.48±2.70)% vs (48.47±6.03)%, P<0.05; PPC vs CTRL: (35.60±2.10)% vs (48.47±6.03)%, P<0.05). SPC group had less infarct size than PPC group (SPC vs PPC: (17.48±2.70)% vs (35.60±2.10)%, P<0.05). Atractyloside coadministration attenuated or completely blocked the cardioprotective effect of postconditioning of sevoflurane and propofol. Conclusion: Postconditioning of sevoflurane and propofol has cardioprotective effect against ischemia-reperfusion injury of heart, which is associated with inhibition of MPTP opening. Compared to propofol, sevoflurane provides superior protection of functional recovery and infarct size.