ISOFLURANE PRODUCES ENDOTHELIUM-INDEPENDENT RELAXATION IN CANINE MIDDLE CEREBRAL-ARTERIES
ISOFLURANE PRODUCES ENDOTHELIUM-INDEPENDENT RELAXATION IN CANINE MIDDLE CEREBRAL-ARTERIES
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DOI：
10.1097/00000542-199203000-00021
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发表时间：
1992-03-01
期刊：
影响因子：
8.8
通讯作者：
KAMPINE, JP
中科院分区：
文献类型：
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作者：
FLYNN, NM;BULJUBASIC, N;KAMPINE, JP
尽管人们普遍认为异氟烷可引起脑血管舒张，但脑血管对这种麻醉剂的敏感性仍存在争议。此外，异氟烷对脑血管系统产生直接影响的机制仍不清楚。本研究的目的是确定异氟烷诱导的犬大脑中动脉松弛是否具有剂量依赖性和/或内皮依赖性。在另外一系列实验中，在吲哚美辛抑制前列环素释放的情况下研究了异氟烷诱导的舒张，并用硝普钠检查了内皮依赖性舒张。在用 300-mu-M N(G)-单甲基-L-精氨酸 (LnMMA)（一种内皮依赖性血管舒张抑制剂）预处理之前和之后，检查大脑中动脉对异氟烷的反应。将血管环（长2.5毫米，直径600-800微米）悬浮在组织浴中并记录等长张力。这些环用 0.2-μm 5-羟色胺或 5-μm 前列腺素 F2-α 收缩，随后暴露于浓度不断增加的异氟烷 (0.65-4.9%)。在单独的实验中，在有内皮和无内皮的血管中重复该过程。异氟烷在所有血管中产生剂量依赖性松弛。这种松弛不受 LnMMA 抑制，也不受内皮缺失的影响。异氟烷反应与环氧合酶抑制无关。这些结果表明，异氟烷引起的犬大脑中动脉松弛：1）是剂量依赖性的； 2) 不是通过内皮源性舒张因子的调节或前列环素的释放介导的； 3) 不依赖于内皮细胞。
Although it is generally accepted that isoflurane can cause cerebral vasodilation, the sensitivity of the cerebral vessels to this anesthetic agent remains controversial. Furthermore, the mechanism by which isoflurane produces its direct effects on the cerebral vasculature remains unknown. The purpose of this study was to determine if isoflurane-induced relaxation of canine middle cerebral arteries is dose-dependent and/or endothelium-dependent. In an additional series of experiments, isoflurane-induced relaxation was studied in the presence of indomethacin to inhibit prostacyclin release, and endothelium-independent relaxation was examined with sodium nitroprusside. The response to isoflurane was examined in middle cerebral arteries prior to and following pretreatment with 300-mu-M N(G)-monomethyl-L-arginine (LnMMA), an inhibitor of endothelium-dependent vasodilation. Vascular rings (2.5 mm in length and 600-800-mu-m in diameter) were suspended in tissue baths and isometric tension recorded. The rings were constricted with either 0.2-mu-m 5-hydroxytryptamine or 5-mu-m prostaglandin F2-alpha and subsequently exposed to increasing concentrations of isoflurane (0.65-4.9%). In separate experiments the procedure was repeated in vessels with and without endothelium. Isoflurane produced a dose-dependent relaxation in all vessels. This relaxation was not inhibited by LnMMA and was unaffected by the absence of endothelium. The isoflurane response was independent of cyclooxygenase inhibition. These results demonstrate that isoflurane-induced relaxation of canine middle cerebral arteries: 1) is dose-dependent; 2) is not mediated by modulation of endothelium-derived relaxing factor or a release of prostacyclin; and 3) is endothelium-independent.