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全球缺血及损伤后硫喷妥钠治疗对猴子脑血流和代谢的影响

Brain blood flow and metabolism after global ischemia and post-insult thiopental therapy in monkeys.

作者信息

Kofke W A, Nemoto E M, Hossmann K A, Taylor F, Kessler P D, Stezoski S W

出版信息

Stroke. 1979 Sep-Oct;10(5):554-60. doi: 10.1161/01.str.10.5.554.

Abstract

We measured total and regional cerebral blood flow (CBF, rCBF) and cerebral metabolic rate (CMR) of oxygen (O2), glucose (G), and lactate (L) levels for 4 h after 16 min global brain ischemia in rhesus monkeys with and without post-insult thiopental therapy. Eleven monkeys weighing 4-5 kg anesthetized with 1 percent halothane, 66 percent nitrous oxide and 33 percent oxygen, were subjected to 16 min global brain ischemia by a combination of trimethaphan hypotension (to a mean arterial pressure of 50 torr) and a high pressure (1500 torr) neck tourniquet. Post-ischemia, 7 monkeys were untreated (controls) and 4 received thiopental 90 mg/kg infused intravenously over 60 min, beginning at 5 min post-ischemia. Total CBF and rCBF were measured by continuous monitoring of cerebral venous (torcula) and parietal-occipital (external scintillation) 133Xe activity, respectively, after intra-innominate artery injection of 500 micronCi 133Xe in saline. In control monkeys, hyperemia in rCBF, but not in total CBF was observed at 6-7 min post-ischemia, whereas both total CBF and rCBF increased in thiopental treated monkeys. The hyperemia in thiopental treated monkeys coincided with an increase in CMRG without a proportional increase in CMRO2 or lactate levels. Indeed, CMRO2 was depressed in the first 30 min post-ischemia. At 30 min post-ischemia, CMRO2 rose to twofold greater than pre-ischemia in control monkeys, but only to pre-ischemic levels in thiopental treated monkeys. The data suggest that thiopental therapy improves distribution of brain blood flow and brain glucose uptake early post-ischemia and depresses CMRO2 later post-ischemia.

摘要

我们在有或没有缺血后硫喷妥钠治疗的恒河猴全脑缺血16分钟后,测量了4小时内的全脑和局部脑血流量(CBF、rCBF)以及氧(O2)、葡萄糖(G)和乳酸(L)水平的脑代谢率(CMR)。11只体重4 - 5千克的猴子,用1%氟烷、66%氧化亚氮和33%氧气麻醉,通过三甲噻方低血压(平均动脉压降至50托)和高压(1500托)颈部止血带联合作用使其经历16分钟全脑缺血。缺血后,7只猴子未接受治疗(对照组),4只在缺血后5分钟开始,60分钟内静脉输注90毫克/千克硫喷妥钠。在无名动脉内注射500微居里溶于生理盐水的133Xe后,分别通过连续监测脑静脉(窦汇)和顶枕部(外部闪烁)的133Xe活性来测量全脑CBF和rCBF。在对照猴子中,缺血后6 - 7分钟观察到rCBF充血,但全脑CBF未出现充血,而在硫喷妥钠治疗的猴子中,全脑CBF和rCBF均增加。硫喷妥钠治疗的猴子中的充血与CMRG增加同时出现,而CMRO2或乳酸水平没有成比例增加。实际上,缺血后最初30分钟CMRO2降低。缺血后30分钟,对照猴子的CMRO2升至缺血前的两倍以上,但硫喷妥钠治疗的猴子仅升至缺血前水平。数据表明,硫喷妥钠治疗可改善缺血后早期脑血流分布和脑葡萄糖摄取,并在缺血后期降低CMRO2。

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