氯化钾和前列腺素F2α预收缩的离体犬脑动脉和肠系膜动脉对巴比妥类药物的反应。

Responses to barbiturates of isolated dog cerebral and mesenteric arteries contracted with KCl and prostaglandin F2 alpha.

作者信息

Moriyama S, Nakamura K, Hatano Y, Harioka T, Mori K

机构信息

Department of Anesthesia, Kyoto University Hospital, Japan.

出版信息

Acta Anaesthesiol Scand. 1990 Oct;34(7):523-9. doi: 10.1111/j.1399-6576.1990.tb03138.x.

DOI:10.1111/j.1399-6576.1990.tb03138.x

PMID:2244437

Abstract

In helical strips of dog cerebral and mesenteric arteries previously contracted with KCl or prostaglandin F2 alpha (PGF2 alpha), the addition of pentobarbital (10(-5) to 10(-3) mol.l-1) caused dose-related relaxation, whereas thiamylal and thiopental in a low concentration (10(-5) to 10(-4) mol.l-1) caused further contraction and in a high concentration (10(-3) mol.l-1) profound relaxation. Thiobarbiturate-induced contractions were greater in mesenteric than in cerebral arteries previously contracted with PGF2 alpha. In cerebral and mesenteric arteries exposed to Ca(++)-free media for 60 min and treated with KCl or PGF2 alpha, reintroduction of Ca++ produced a transient contraction, a transient relaxation and a persistent contraction. The Ca(++)-induced persistent contraction was attenuated by pretreatment with pentobarbital (10(-4) to 10(-3) mol.l-1) and thiamylal (10(-3) mol.l-1); the attenuation was greater in arteries treated with KCl than with PGF2 alpha. The Ca(++)-induced contractions of mesenteric artery treated with PGF2 alpha were potentiated by 10(-4) mol.l-1 thiamylal. It is concluded that pentobarbital possesses only a vasodilator effect, whereas thiamylal and thiopental have both constrictor and dilator effects on vascular smooth muscle. The vasodilator effect of barbiturates is associated in part with inhibition of transmembrane influx of Ca++; the inhibition is more predominant on the influx evoked by KCl-induced depolarization than by a stimulation of PGF2 alpha receptors. Thiamylal in low concentrations appears to enhance Ca++ influx through a receptor-operated Ca++ channel for PGF2 alpha.

摘要

在预先用氯化钾或前列腺素F2α（PGF2α）收缩的犬脑动脉和肠系膜动脉螺旋条中，加入戊巴比妥（10⁻⁵至10⁻³mol·L⁻¹）会引起剂量相关的舒张，而低浓度（10⁻⁵至10⁻⁴mol·L⁻¹）的硫喷妥钠和硫戊巴比妥会引起进一步收缩，高浓度（10⁻³mol·L⁻¹）则引起深度舒张。硫代巴比妥酸盐诱导的收缩在肠系膜动脉中比在预先用PGF2α收缩的脑动脉中更大。在暴露于无钙培养基60分钟并用氯化钾或PGF2α处理的脑动脉和肠系膜动脉中，重新引入钙离子会产生短暂收缩、短暂舒张和持续收缩。钙离子诱导的持续收缩通过预先用戊巴比妥（10⁻⁴至10⁻³mol·L⁻¹）和硫喷妥钠（10⁻³mol·L⁻¹）预处理而减弱；在用氯化钾处理的动脉中，这种减弱比用PGF2α处理的动脉中更大。用PGF2α处理的肠系膜动脉的钙离子诱导收缩被10⁻⁴mol·L⁻¹硫喷妥钠增强。结论是戊巴比妥仅具有血管舒张作用，而硫喷妥钠和硫戊巴比妥对血管平滑肌既有收缩作用又有舒张作用。巴比妥酸盐的血管舒张作用部分与抑制钙离子跨膜内流有关；这种抑制在由氯化钾诱导的去极化引起的内流上比在PGF2α受体刺激引起的内流上更占优势。低浓度的硫喷妥钠似乎通过PGF2α的受体操纵性钙离子通道增强钙离子内流。