摘要
严重创伤性休克等临床重症晚期血管低反应性表现为血管对血管活性物质的反应性降低或不反应,脓毒性休克或失血性休克后血管反应性呈时间和器官差异,且存在年龄和性别差异。诱发休克血管低反应性因素包括有酸中毒、能量代谢以及细胞因子等,引起血管低反应性发生的机制以前认为与血管平滑肌细胞受体失敏、膜超极化有关,近年发现休克后血管平滑肌细胞钙失敏在休克血管低反应性的发生中具有重要作用,此外也存在非肌球蛋白轻链(MLC20)磷酸化依赖的调节途径在休克血管低反应性发生中起着作用。目前针对现有血管低反应性诱发因素以及发生机制的防治措施对恢复休克血管低反应性有一定作用。
Vascular reactivity to vasoconstrictors and vasodilators is greatly reduced after severe trauma,shock or sepsis.Acidosis,cytokine release and energy medtabolism dysfunction are the main factors causing vascular hyporeactivity.Studies have shown that it may be related to the membrane hyperpolarization and calcium desensitization of vascular smooth muscle cells（VSMCs）.And our studies demonstrated that non-myosin light chain phosphorylation（MLC20）-pathway also participated in the occurrence process of vascular hyporeactivity following shock.At present,preventive measures referring the causative factor and mechanism of hyporeactivity are significant to restore the vascular hyporeactivity after shock.
出处
《创伤外科杂志》
2012年第2期181-183,共3页
Journal of Traumatic Surgery
关键词
休克
血管
低反应
平滑肌细胞
shock
vessel
hyporeactivity
smooth muscle cell
