Antishock effect of arginine vasopressin and its relationship with Rho kinase

方玉强; 李涛; 刘良明

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Antishock effect of arginine vasopressin and its relationship with Rho kinase

更新时间：2026-01-09

- Antishock effect of arginine vasopressin and its relationship with Rho kinase
- Journal of Army Medical University Vol. 30, Issue 13, Pages: 1223-1226(2008)
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  CLC： R363;R605.971;972.5
- Published：2008
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方玉强,李涛,刘良明.精氨酸血管加压素抗失血性休克作用及其与Rho kinase的关系[J].陆军军医大学学报(原第三军医大学学报),2008,30(13):1223-1226.

　FANG Yu-qiang,LI Tao,LIU Liang-ming.Antishock effect of arginine vasopressin and its relationship with Rho kinase[J].J Amry Med Univ (J Third Mil Med Univ),2008,30(13):1223-1226.
方玉强,李涛,刘良明.精氨酸血管加压素抗失血性休克作用及其与Rho kinase的关系[J].陆军军医大学学报(原第三军医大学学报),2008,30(13):1223-1226. DOI：

　FANG Yu-qiang,LI Tao,LIU Liang-ming.Antishock effect of arginine vasopressin and its relationship with Rho kinase[J].J Amry Med Univ (J Third Mil Med Univ),2008,30(13):1223-1226. DOI：

摘要

目的观察精氨酸血管加压素（arginine vasopressin

AVP）抗失血性休克作用与Rho kinase的关系。方法采用大鼠失血性休克模型，整体动物观察AVP对失血性休克大鼠去甲肾上腺素（NE）的升压反应和对肠系膜上动脉收缩反应性的影响，同时观察Rho kinase在其中的作用；离体血管环观察AVP对失血性休克大鼠肠系膜上动脉反应性和钙敏感性的影响，并观察Rho kinase在其中的作用。结果失血性休克后大鼠对NE的升压反应性和肠系膜动脉对NE的收缩反应性明显降低，AVP 0.4 U/kg可明显增加休克大鼠NE升压反应和肠系膜动脉的收缩反应性，Rho kinase特异性抑制剂Y-27632可明显拮抗由AVP引起的休克大鼠血管反应性的增加。在离体血管环研究表明，休克后血管反应性和钙敏感性明显降低，AVP在浓度为5 nmol/L和0.5 nmol/L可明显增加休克后血管反应性和钙敏感性，Y-27632可明显拮抗由AVP引起的血管反应性和钙敏感性的增加。结论 AVP可通过增加休克血管平滑肌细胞的钙敏感性和血管反应性发挥抗休克作用，通过激活Rho kinase发挥其抗休克作用。

Abstract

Objective To investigate the relationship of antishock effect of arginine vasopressin (AVP) on hemorrhagic shock and its relationship with Rho kinase. Methods Hemorrhagic shock (40 mmHg for 2 h) Wistar rats were treated respectively by AVP (0.4 U/kg)

Rho kinase specific inhibitor

Y-27632 (30 μg/kg)

or these 2 reagents. The pressor effect of norepinephrine (NE) on these rats and the contractility of their isolated superior mesenteric artery (SMA) were observed. Isolated SMAs from hemorrhagic shock rats were adopted to observe the effects of AVP on vascular reactivity and calcium sensitivity and its relationship to Rho kinase with an isolated organ perfusion system. Results AVP at the concentration of 0.4 U/kg significantly improved the pressor effect of NE and the contractile response of SMA. While

Y-27632 (30 μg/kg) abolished these beneficial effects of AVP. The vascular reactivity and calcium sensitivity of SMA were significantly decreased following hemorrhagic shock. AVP at the concentration of 0.5 and 5 nmol/L significantly increased the decreased vascular reactivity and calcium sensitivity. These effects of AVP were abolished by Y-27632 (10 μmol/L). Conclusion Rho kinase may take part in the action of AVP on hemorrhagic shock via improving shock induced vascular hyporeactivity and calcium desensitization.

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