Tamaki F, Oguchi T, Kashimoto S, Nonaka A, Kumazawa T
Department of Anesthesiology, Yamanashi Medical University, Japan.
Jpn Heart J. 2001 Mar;42(2):193-206. doi: 10.1536/jhj.42.193.
The aim of the present study was to investigate whether clinical doses of propofol and thiamylal affect oxygen free radical production and intracellular calcium concentration ([Ca2+]i) in the post-ischemic reperfused heart. Forty-eight rat hearts were perfused with a Langendorff system and loaded with Fura-2 / AM as a [Ca2+]i marker. The hearts were divided into 6 groups as follows (each group: n = 8); Group S (saline), Group TL (thiamylal 100 microM), Group TH (thiamylal 300 microM), Group I (Intralipid), Group PL (propofol 3 microM), and Group PH (propofol 10 microM). All hearts were initially perfused for 5 min as control aerobic perfusion. Afterwards, no-flow ischemia was induced for 15 min, followed by reperfusion for 20 min. The formation of hydroxyl radicals in the coronary effluent was measured with high performance liquid chromatography using salicylic acid. At the beginning of the ischemia and reperfusion periods, increases in systolic and diastolic [Ca2+]i were observed in all groups except Group TH. The high dose of thiamylal significantly suppressed this initial increase in cytosolic [Ca2+]i (Group S 1.30+/-0.15; Group TL 0.99+/-0.17; Group TH 0.70+/-0.09, at 1 min after reperfusion; systolic [Ca2+]i : p < 0.05). Total DHBAs in the coronary effluent of all groups increased significantly 1 min after reperfusion, however, there were no significant differences among the groups. Clinical doses of propofol had no significant effect on myocardial function and [Ca2+]i before and after ischemia, whereas thiamylal suppressed the increase in [Ca2+]i during ischemia and reperfusion. However, free radical formation during reperfusion was unaffected by thiamylal and propofol.
本研究的目的是调查临床剂量的丙泊酚和硫喷妥钠是否会影响缺血再灌注心脏中氧自由基的产生和细胞内钙浓度([Ca2+]i)。48只大鼠心脏用Langendorff系统灌注,并加载Fura-2 / AM作为[Ca2+]i标记物。心脏分为以下6组(每组:n = 8);S组(生理盐水)、TL组(硫喷妥钠100微摩尔)、TH组(硫喷妥钠300微摩尔)、I组(脂质乳剂)、PL组(丙泊酚3微摩尔)和PH组(丙泊酚10微摩尔)。所有心脏最初作为对照有氧灌注灌注5分钟。之后,诱导无血流缺血15分钟,然后再灌注20分钟。使用水杨酸通过高效液相色谱法测量冠状动脉流出液中羟自由基的形成。在缺血和再灌注期开始时,除TH组外,所有组均观察到收缩期和舒张期[Ca2+]i升高。高剂量硫喷妥钠显著抑制了细胞溶质[Ca2+]i的这种初始升高(再灌注1分钟时,S组1.30±0.15;TL组0.99±0.17;TH组0.70±0.09;收缩期[Ca2+]i:p < 0.05)。再灌注1分钟后,所有组冠状动脉流出液中的总二羟基苯甲酸(DHBAs)均显著增加,然而,各组之间无显著差异。临床剂量的丙泊酚对缺血前后的心肌功能和[Ca2+]i无显著影响,而硫喷妥钠抑制缺血和再灌注期间[Ca2+]i的升高。然而,再灌注期间的自由基形成不受硫喷妥钠和丙泊酚的影响。