Endothelium-dependent effects of halothane, enflurane, and isoflurane on isolated rat aortic vascular rings.
Endothelium-dependent effects of halothane, enflurane, and isoflurane on isolated rat aortic vascular rings.
复制标题
氟烷、安氟烷和异氟烷对离体大鼠主动脉血管环的内皮依赖性影响。
DOI：
10.1097/00000542-198907000-00021
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发表时间：
1989
期刊：
影响因子：
8.8
通讯作者：
Johns,RA
中科院分区：
文献类型：
--
作者：
Stone,DJ;Johns,RA
为了确定氟烷、安氟醚和异氟醚的内皮依赖性血管效应，在悬浮于Kreb缓冲液中并用95%O2/5%CO2通气的大鼠胸主动脉的隔离环制备物中记录等长张力。一组环具有完整的内皮，另一组环具有机械剥脱的内皮。用苯乙醯胺（1 × 10（-6）M）使环预收缩。在含和不含吲哚美辛（28 μ M）的制剂中，将氟烷、恩氟烷或异氟烷气体以递增浓度（0.5-5.0%）鼓泡通过水浴。内皮完整的环表现出显着的（P <0.05）血管收缩，在低浓度的异氟烷和安氟烷，然后在较高浓度的血管舒张。氟烷也引起某些环的血管收缩，但其平均效应与对照组无显著差异。停止麻醉气体后，内皮完整的环表现出反弹血管收缩超过以前的最大水平的所有三种麻醉剂。当吲哚美辛加入浴中时，血管收缩增强，并且对所有三种麻醉剂都具有统计学意义。这些结果表明，在低浓度下，安氟醚和异氟醚通过抑制基础EDRF产生和/或刺激内皮源性收缩因子的释放而引起血管收缩。在较高的麻醉剂浓度下，麻醉剂的直接血管舒张作用占主导地位。在吲哚美辛存在下的血管收缩增强表明，这些挥发性麻醉剂刺激血管舒张性前列腺素类从内皮释放。
To determine the endothelium-dependent vascular effects of halothane, enflurane, and isoflurane, isometric tension was recorded in isolated ring preparations of rat thoracic aorta suspended in Kreb's buffer and aerated with 95% O2/5% CO2. One set of the rings had intact endothelium and the other set of the rings had the endothelium mechanically denuded. The rings were precontracted with phenylephrine (1 x 10 (-6) M). Halothane, enflurane, or isoflurane gas was bubbled through the baths at increasing concentrations (0.5-5.0%) in preparations with and without indomethacin (28 microM). Endothelium-intact rings demonstrated significant (P less than 0.05) vasoconstriction at low concentrations of both isoflurane and enflurane followed by vasodilation at higher concentrations. Halothane also induced vasoconstriction in some rings, but its mean effect was not significantly different from control. After discontinuation of the anesthetic gas, endothelium-intact rings demonstrated a rebound vasoconstriction above previous maximal levels for all three anesthetics. When indomethacin was added to the baths, the vasoconstriction was potentiated and was statistically significant for all three anesthetics. These results suggest that at low concentrations, enflurane and isoflurane cause vasoconstriction through inhibition of basal EDRF production and/or stimulation of the release of an endothelium-derived constricting factor. At higher anesthetic concentrations, a direct vasodilating effect of the anesthetic predominates. The potentiation of vasoconstriction in the presence of indomethacin suggests that these volatile anesthetics stimulate the release of a vasodilating prostanoid from endothelium.