Anesthetic choice of halothane versus propofol - Impact on experimental perioperative stroke
Anesthetic choice of halothane versus propofol - Impact on experimental perioperative stroke
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DOI：
10.1161/01.str.32.8.1920
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发表时间：
2001-08-01
期刊：
影响因子：
8.3
通讯作者：
Kirsch, JR
中科院分区：
文献类型：
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作者：
Bhardwaj, A;Castro, AF;Kirsch, JR
背景和目的：目前尚不清楚缺血前暴露于麻醉剂是否会影响停止麻醉后发生的短暂局灶性缺血的损伤量。我们比较了先前暴露于氟烷或异丙酚对苏醒动物短暂性大脑中动脉闭塞（MCAO）后梗死面积的影响，以验证麻醉类型和暴露时间独立影响脑损伤量的假设。方法：雄性Wistar大鼠（体重200 ~ 300 g）用氟烷短暂麻醉放置血流动力学仪器。二十四小时后。对大鼠进行短时间（约1小时）或长时间（8小时）吸入氟烷（1%至2%）或静脉注射异丙酚（10mg /kg， 30mg /kg每小时输注）治疗。每个队列（每组n = 8）然后通过腔内缝合技术进行2小时MCAO。达到MCAO后停止所有麻醉。在再灌注22小时测量梗死体积。在第二个队列中，在短时间氟烷（n=5）或短时间异丙酚（n=5）麻醉组和相应的手术假组（各n=3）末闭塞时测量区域脑血流量（[C-14]碘安替比林放射自显影）。结果：颅周温度，Pao(2), Paco(2)。治疗前后血压均得到控制，各组间无明显差异。MCAO导致清醒动物在停止麻醉后激光多普勒血流信号的立即减少。与短时间异丙酚暴露的大鼠（皮质，177.5 +/- 16.9 mm(3)）相比，暴露于短时间氟烷的大鼠皮质（87.5 +/- 16.6 mm）（平均+/- SEM）和尾丘门（38.3 +/- 13.7 mm(3)）的梗死体积较小；尾突门，47.8±2.9 mm(3))。长时间氟烷治疗与长时间异丙酚治疗的梗死体积没有差异。短时间氟烷或短时间异丙酚治疗的绝对皮质或尾核脑缺血CBF无差异。结论：这些数据表明，与异丙酚相比，苏醒动物在MCAO前短时间暴露氟烷可减少梗死体积。氟烷的这种保护作用不是通过缺血脑血流的保存来介导的。长时间的氟烷暴露可能激活继发性损伤通路，从而抵消短期氟烷缺血前治疗的保护作用。
Background and Purpose-It is not known whether preischemic exposure to anesthetic agents affects the amount of damage from transient focal ischemia that occurs after cessation of the anesthetic. We compared the effect of prior exposure to halothane or propofol on infarction size after transient middle cerebral artery occlusion (MCAO) induced in the awakening animal to test the hypothesis that anesthetic type and exposure duration would independently affect the amount of brain injury.Methods-Male Wistar rats (weight, 200 to 300 g) were anesthetized briefly with halothane for placement of hemodynamic instrumentation. Twenty-four hours later. rats were treated with either a short (approximately I hour) or long (8 hours) duration of inhaled halothane (1% to 2%) or intravenous propofol (10 mg/kg bolus, 30 mg/kg per hour infusion). Each cohort (n = 8 per group) was then subjected to 2-hour MCAO by the intraluminal suture technique. All anesthesia was discontinued once MCAO was achieved. Infarct volume was measured at 22 hours of reperfusion. In a second cohort, regional cerebral blood flow (CBF) was measured ([C-14]iodoantipyrine autoradiography) at end-occlusion in short-duration halothane (n=5) or short-duration propofol (n=5) anesthesia groups and in corresponding surgical shams (n=3 each).Results-Pericranial temperature, Pao(2), Paco(2). and blood pressure were controlled and not different among groups before or during occlusion. MCAO resulted in a similar immediate reduction in laser-Doppler flow signal after discontinuation of anesthesia in the awakening animals. Infarct volume was smaller in rats exposed to short-duration halothane in cortex (87.5 +/- 16.6 mm(3)) (mean +/- SEM) and caudoputamen (38.3 +/- 13.7 mm(3)) compared with rats exposed to short-duration propofol (cortex, 177.5 +/- 16.9 mm(3); caudoputamen, 47.8 +/-2.9 mm(3)). Infarct volume was not different in long-duration halothane versus long-duration propofol treatment. Absolute cortical or caudoputamen intraischemic CBF was not different between short-duration halothane or short-duration propofol treatment.Conclusions-These data demonstrate that short-duration halothane exposure before MCAO in the awakening animal attenuates infarction volume compared with propofol. This protection by halothane is not mediated through preservation of intraischemic CBF. Longer durations of halothane exposure may activate secondary injury pathways, which negate the protective effects of short-term halothane preischemic treatment.