Intracellular mechanisms of halothane's effect on isolated aortic strips of the rabbit.
Intracellular mechanisms of halothane's effect on isolated aortic strips of the rabbit.
复制标题
氟烷对兔离体主动脉条作用的细胞内机制。
DOI：
10.1097/00000542-198909000-00017
复制
发表时间：
1989
期刊：
影响因子：
8.8
通讯作者：
Zhang,CC
中科院分区：
文献类型：
--
作者：
Su,JY;Zhang,CC
氟烷作用的细胞内机制在主动脉的血管平滑肌中进行了检查。将来自兔的主动脉的中间层固定在光电二极管张力传感器上，拉伸至20 mg静息张力，并用皂苷”剥皮”。然后将去皮的纤维制品浸入浴溶液中，以研究氟烷（0.5-2%）对收缩蛋白的Ca 2+激活以及使用咖啡因诱导的张力瞬变从肌浆网（SR）摄取和释放Ca 2+的影响。为了进行比较，将分离的完整主动脉环安装在Blink的双组织浴上并连接到力传感器上。用40 mM KCl或去甲肾上腺素（NE）收缩制剂，然后用乙酰胆碱（ACh）或硝普钠（SNP）诱导松弛。在稳态收缩或舒张时，研究了氟烷（1-3%）的作用。氟烷给药期间的稳态张力表示为氟烷给药前稳态张力的百分比。在离体完整主动脉环中，氟烷（1-3%）对KCl诱导的张力产生双相效应，即最初轻微增加，随后降低，与内皮无关。氟烷明显增加紧张的乙酰胆碱或SNP放松状态。这些效应具有剂量依赖性。在皮肤的主动脉条，氟烷略有下降的最大Ca 2+激活的张力发展的收缩蛋白。氟烷以剂量依赖性方式减少SR中的Ca 2+积累并增加SR中的Ca 2+释放。氟烷诱导的钙释放增加的SR被阻止ryanodine，SR钙释放通道阻滞剂。可以得出结论，氟烷直接导致血管收缩或舒张，这取决于条件，氟烷的SR的影响可能发挥作用。
The intracellular mechanisms of halothane action were examined in vascular smooth muscle from the aorta. Medial layers of the aorta from rabbits were mounted on photodiode tension transducers, stretched to 20 mg resting tension, and" skinned" with saponin. The skinned fiber preparations were then immersed in bathing solutions to study the effects of halothane (0.5-2%) on Ca2+ activation of the contractile proteins, and Ca2+ uptake and release from the sarcoplasmic reticulum (SR) using caffeine-induced tension transients. For comparison, isolated intact aortic rings were mounted on Blinks' dual tissue bath and attached to force transducers. The preparations were contracted with either 40 mM KCl, or norepinephrine (NE) followed by acetylcholine (ACh)-or sodium nitroprusside (SNP)-induced relaxation. At steady state contraction or relaxation, the effects of halothane (1-3%) were studied. The steady state tension during halothane was expressed as a percentage of the steady state tension before administration of halothane. In the isolated intact aortic rings, halothane (1-3%) produced biphasic effects on KCl-induced tension, ie, an initially slight increase followed by decreases, independent of endothelium. Halothane markedly increased tension in the ACh-or SNP-relaxed state. The effects were dose-dependent. In the skinned aortic strips, halothane slightly decreased maximum Ca2+-activated tension development of the contractile proteins. Halothane decreased Ca2+ accumulation in the SR and increased Ca2+ release from the SR in a dose-dependent manner. The halothane-induced increases in Ca2+ release from the SR were blocked by ryanodine, an SR Ca2+ release channel blocker. It is concluded that halothane directly causes vascular contraction or relaxation, depending on the condition, and that halothane's effects on the SR may play a role.