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The effects of propofol, a novel intravenous anesthetic agent, an regulation of vascular tone in isclateo rabbit pulmonary arteries

新型静脉麻醉剂异丙酚对兔伊斯骨肺动脉血管张力的调节作用

基本信息

批准号：
10671437
负责人：
KATSUYA Hirotada
金额：
$ 0.45万
依托单位：
Nagoya City University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1998
资助国家：
日本
起止时间：
1998 至 1999
项目状态：
已结题

项目摘要

By measuring isometric contractions, intracellular concentration of CaィイD12+ィエD1([CaィイD12+ィエD1]ィイD2iィエD2) and membrane potential changes, we found that propofol had many actions on agonist-induced CaィイD12+ィエD1-mobilization mechanisms in smooth muscle cells of rabbit mesenteric arteries : (1) inhibition of CaィイD12+ィエD1 influxes through L-type CaィイD12+ィエD1 channels, (2) inhibition of agonist-induced CaィイD12+ィエD1 release from intracellular CaィイD12+ィエD1 storage sites, (3)inhibition of [CaィイD12+ィエD1]ィイD2iィエD2 removal mechanisms. In addition, propofol inhibits the synthesis of prostacyclin, but not of EDHF, in endothelial cells of these arteries. Propofol is known to be a scavenger against reactive oxygen species (ROS). However, the physiological function of these ROS has not been clarified in resistance vessels. Therefore, the effect of HィイD22ィエD2OィイD22ィエD2, one of major ROS in vascular tissues, was first examined on regulation of vascular tones in rabbit mesenteric arteries. As a result, we found that (1) HィイD22ィエD2OィイD22ィエD2 attenuated the contraction induced by norepinephrine in endothelium-intact and -denuded preparations, (2) HィイD22ィエD2OィイD22ィエD2 increases the synthesis of prostanoids (PGEィイD22ィエD2, PGIィイD22ィエD2) in both preparations, (3) HィイD22ィエD2OィイD22ィエD2 hyperpolarizes a smooth muscle cell membrane through an activation of glibenclamide-sensitive KィイD2ATPィエD2 channels. Now, we are trying to examine the action of propofol on these HィイD22ィエD2OィイD22ィエD2-induced responses in rabbit mesenteric arteries. In a future, using rabbit intrapulmonary arteries, we are planning to clarify the physiological and pathophysiological roles of HィイD22ィエD2OィイD22ィエD2 and also to examine the action of propofol on the HィイD22ィエD2OィイD22ィエD2-induced responses.

通过测定等长收缩、细胞内钙ィイD12+ィエD1([CaィイD12+ィエD1]ィイD2iィエD2)浓度和膜电位的变化，我们发现异丙酚对激动剂诱导的兔肠系膜动脉平滑肌细胞CaィイD12+ィエD1-动员机制有许多作用：(1)抑制钙ィイD12+ィエD1通过L型钙ィイD12+ィエD1通道内流；(2)抑制激动剂诱导的CaィイD12+ィエD1从细胞内钙ィイD12+ィエD1储存部位释放。(3)[CaィイD12+ィエD1]ィイD2iィエD2清除的抑制机制。此外，异丙酚抑制血管内皮细胞合成前列环素，但不抑制EDHF的合成。丙泊酚是已知的清除活性氧自由基(ROS)的清除剂。然而，这些ROS在抗性维管束中的生理功能尚不清楚。因此，首次研究了血管组织中的主要ROS之一H-ィイD22-ィエ-D2O-ィイ-D22-ィエ-D2对兔肠系膜动脉张力的调节作用。结果，我们发现(1)HィイD22ィエD2OィイD22ィエD2可减弱去甲肾上腺素对内皮完整和去内皮标本的收缩作用，(2)HィイD22ィエD2OィイD22ィエD2增加两种制剂中前列腺素(PGEィイD22ィエD2，PGIィイD22ィエD2)的合成，(3)HィイD22ィエD2OィイD22ィエD2通过激活格列本脲敏感的KィイD2ATPィエD2通道使平滑肌细胞膜超极化。现在，我们试图研究异丙酚对H-ィイD22-ィエ-D2O-ィイ-D22-ィエ-D2诱导的兔肠系膜动脉反应的影响。在未来，我们计划利用兔肺内动脉，阐明HィイD22ィエD2OィイD22ィエD2的生理和病理生理学作用，并研究异丙酚对HィイD22ィエD2OィイD22ィエD2诱导的反应的作用。