Kokita N, Hara A, Abiko Y, Arakawa J, Hashizume H, Namiki A
Department of Anesthesiology, Sapporo Medical University School of Medicine, Japan.
Anesth Analg. 1998 Feb;86(2):252-8. doi: 10.1097/00000539-199802000-00006.
Propofol attenuates mechanical dysfunction, metabolic derangement, and lipid peroxidation by exogenous administration of H2O2 in the Langendorff rat heart. In this study, we examined the effects of propofol on mechanical and metabolic changes, as well as on lipid peroxidation induced by ischemia-reperfusion, in isolated, working rat hearts. Rat hearts (in control-modified Krebs-Henseleit bicarbonate buffer) were treated with two doses (25 microM and 50 microM) of propofol in an intralipid vehicle. In the first protocol, propofol was administered during the preischemic and reperfusion period, whereas in the second, it was only administered during the reperfusion period. Ischemia (15 min) decreased peak aortic pressure (PAOP), heart rate (HR), rate-pressure product (RPP), coronary flow (CF), and tissue concentrations of adenosine triphosphate (ATP) and creatine phosphate. After postischemic reperfusion (20 min), the CF and tissue concentration of ATP recovered incompletely; however, PAOP, HR, and RPP did not. Ischemia-reperfusion also increased the tissue concentration of malondialdehyde (MDA). In both protocols, both doses of propofol enhanced recovery of PAOP, HR, RPP, CF, and tissue concentration of ATP during reperfusion, and inhibited the tissue accumulation of MDA. These results indicate that propofol improves recovery of mechanical function and the energy state in ischemic reperfused isolated rat hearts, and the mechanism may involve the reduction of lipid peroxidation during postischemic reperfusion.
We evaluated the possible cardioprotective effects of propofol in isolated, working rat hearts subjected to 15-min ischemia, followed by 20-min reperfusion. We observed that propofol attenuated mechanical dysfunction, metabolic derangement, and lipid peroxidation during reperfusion. This latter finding seems to be one mechanism for cardioprotective effects of propofol.
在Langendorff大鼠心脏中，通过外源性给予过氧化氢，丙泊酚可减轻机械功能障碍、代谢紊乱和脂质过氧化。在本研究中，我们检测了丙泊酚对离体工作大鼠心脏中由缺血再灌注诱导的机械和代谢变化以及脂质过氧化的影响。大鼠心脏（置于对照改良的Krebs-Henseleit碳酸氢盐缓冲液中）用两种剂量（25微摩尔/升和50微摩尔/升）的丙泊酚于脂质乳剂载体中进行处理。在第一个方案中，丙泊酚在缺血前期和再灌注期给药，而在第二个方案中，仅在再灌注期给药。缺血（15分钟）使主动脉峰值压力（PAOP）、心率（HR）、速率压力乘积（RPP）、冠脉流量（CF）以及三磷酸腺苷（ATP）和磷酸肌酸的组织浓度降低。缺血后再灌注（20分钟）后，CF和ATP的组织浓度未完全恢复；然而，PAOP、HR和RPP未恢复。缺血再灌注还增加了丙二醛（MDA）的组织浓度。在两个方案中，两种剂量的丙泊酚均增强了再灌注期间PAOP、HR、RPP、CF和ATP组织浓度的恢复，并抑制了MDA的组织蓄积。这些结果表明，丙泊酚可改善缺血再灌注离体大鼠心脏的机械功能恢复和能量状态，其机制可能涉及缺血后再灌注期间脂质过氧化的减少。
我们评估了丙泊酚对经历15分钟缺血、随后20分钟再灌注的离体工作大鼠心脏可能的心脏保护作用。我们观察到丙泊酚减轻了再灌注期间的机械功能障碍、代谢紊乱和脂质过氧化。后一发现似乎是丙泊酚心脏保护作用的一种机制。
