Department of Anesthesiology and Pain Medicine, Gyeongsang National University College of Medicine, Jinju, Korea.
Korean J Anesthesiol. 2010 Apr;58(4):378-82. doi: 10.4097/kjae.2010.58.4.378. Epub 2010 Apr 28.
It is well known that propofol protects myocardium against myocardial ischemia/reperfusion injury in the rat heart model. The aim of this study was to investigate whether propofol provides a protective effect against a regional myocardial ischemia/reperfusion injury in an in vivo rat heart model after 48 h of reperfusion.
Rats were subjected to 25 min of left coronary artery occlusion followed by 48 h of reperfusion. The sham group received profopol without ischemic injury. The control group received normal saline with ischemia/reperfusion injury. The propofol group received profopol with ischemia/reperfusion injury. The intralipid group received intralipid with ischemia/reperfusion injury. A microcatheter was advanced into the left ventricle and the hemodynamic function was evaluated. The infarct size was determined by triphenyltetrazolium staining. The serum level of cardiac troponin-I (cTn-I) was determined by ELISA (enzyme-linked immunosorbent assay).
Propofol demonstrated protective effects on hemodynamic function and infarct size reduction. In the propofol group, the +dP/d(tmax) (P = 0.002) was significantly improved compared to the control group. The infarct size was 49.8% of the area at risk in the control group, and was reduced markedly by administration of propofol to 32.6% in the propofol group (P = 0.014). The ischemia/reperfusion-induced serum level of cTn-I was reduced by propofol infusion during the peri-ischemic period (P = 0.0001).
Propofol, which infused at clinically relevant concentration during the peri-ischemic period, has delayed myocardial protective effect after regional myocardial ischemia/reperfusion injury in an in vivo rat heart model after 48 h of reperfusion.
众所周知,丙泊酚在大鼠心脏模型中对心肌缺血/再灌注损伤具有保护作用。本研究旨在探讨丙泊酚在缺血后 48 小时的体内大鼠心脏模型中是否对局部心肌缺血/再灌注损伤具有保护作用。
大鼠接受 25 分钟的左冠状动脉闭塞,随后进行 48 小时的再灌注。假手术组给予丙泊酚而无缺血损伤。对照组给予缺血/再灌注损伤的生理盐水。丙泊酚组给予丙泊酚加缺血/再灌注损伤。脂肪乳组给予脂肪乳加缺血/再灌注损伤。将微导管推进左心室,评估血流动力学功能。通过三苯基四氮唑染色测定梗死面积。通过酶联免疫吸附试验(ELISA)测定血清中心肌肌钙蛋白 I(cTn-I)的水平。
丙泊酚对血流动力学功能和梗死面积缩小具有保护作用。与对照组相比,丙泊酚组的+dP/d(tmax)(P=0.002)显著改善。对照组的梗死面积为危险区的 49.8%,丙泊酚组的梗死面积明显减少至 32.6%(P=0.014)。丙泊酚在缺血期输注可降低缺血/再灌注诱导的 cTn-I 血清水平(P=0.0001)。
在缺血期以临床相关浓度输注的丙泊酚在缺血后 48 小时的体内大鼠心脏模型中对局部心肌缺血/再灌注损伤具有延迟的心肌保护作用。