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Sevoflurane as opposed to propofol anesthesia preserves mitochondrial function and alleviates myocardial ischemia/reperfusion injury
背景与目的
麻醉药物可减轻心肌缺血再灌注（I/R）损伤，而七氟醚和丙泊酚可通过不同分子机制产生心肌保护作用。本研究旨在验证，不同于丙泊酚，七氟醚通过线粒体机制发挥抗I/R损伤的心肌保护作用这一假设。
方 法
雄性新西兰大白兔(n=42)，冠状动脉结扎30min，再灌注3h。戊巴比妥钠诱导麻醉后，吸入七氟醚或静脉注射丙泊酚维持全身麻醉。使用TTC染色法测定心肌梗死面积。分离心肌线粒体并用Clark电极测定线粒体耗氧量。线粒体呼吸链复合体活性(I~IV)采用特异性分析。实验数据用平均值±标准差表示。
结 果
与丙泊酚相比，七氟醚麻醉显著减少了心肌梗死面积(p= 0.0275 vs. 丙泊酚组)。丙泊酚麻醉组线粒体呼吸控制率显著降低(p=0.01909 vs. 假手术组)，呼吸链复合体I (p=0.0147 vs. 假手术组；p<0.01 vs.七氟醚组)和复合体IV(p=0.0181 vs. 假手术组)的活性受损。而七氟醚麻醉组并无线粒体功能障碍。此外，七氟醚麻醉组的呼吸链复合体I在I/R损伤期间失活比例明显更高。
结 论
与丙泊酚麻醉相比，七氟醚可保留线粒体呼吸作用，并对I/R损伤产生心肌保护作用。
原始文献来源及摘要
Lotz C, Stumpner J, Smul TM. Sevoflurane as opposed to propofol anesthesia preserves mitochondrial function and alleviates myocardial ischemia/reperfusion injury.Biomed. Pharmacother. 2020,20:129.
Abstract
BACKGROUND: Pharmacological interventions reducing myocardial ischemia and reperfusion (I/R) injury include the administration of anesthetics. Both sevoflurane as well as propofol have been shown to elicit cardiac protection via distinct molecular mechanisms. We investigated the hypothesis that sevoflurane in contrary to propofol anesthesia elicits cardiac protection against I/R-injury via mitochondrial mechanisms of disease.
METHODS: Male New Zealand white rabbits (n = 42) were subjected 30 min of coronary artery occlusion followed by 3 h of reperfusion. After induction with pentobarbital, the animals either received sevoflurane or propofol to maintain general anesthesia. Infarct size was determined gravimetrically after triphenyltetrazolium chlorid-staining. Cardiac mitochondria were isolated and mitochondrial oxygen consumption was measured using a Clark electrode. Mitochondrial respiratory chain complex activities (I-IV) were analyzed utilizing specific assays. Data are mean ± SD.
RESULTS: Sevoflurane anesthesia significantly decreased the resulting myocardial infarct size compared to propofol anesthesia (p= 0.0275 vs. propofol). Mitochondria from animals receiving propofol anesthesia showed a significantly reduced mitochondrial respiratory control ratio (p= 0.01909 vs. sham) and impaired activities of respiratory complex I (p= 0.0147 vs. sham; p < 0.01 vs. sevoflurane) as well as respiratory complex IV (p= 0.0181 vs. sham). Mitochondrial dysfunction was absent in sevoflurane anesthesized animals. Furthermore, a significantly higher portion of complex I was found to be in its deactive form during I/R-injury in animals receiving sevoflurane anesthesia (p= 0.0123 vs. propofol).
CONCLUSIONS: Sevoflurane as opposed to propofol anesthesia preserved mitochondrial respiration and elicited cardiac protection against I/R-injury
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