失血性休克血管反应性变化与Rho激酶的关系  

Relationship of Rho kinase and vascular reactivity following hemorrhagic shock

作　　者：李涛[1] 明佳[1] 徐竞[1] 杨光明[1] 刘良明[1] 

机构地区：[1]第三军医大学附属大坪医院野战外科研究所,创伤、烧伤与复合伤国家重点实验室,重庆400042

出　　处：《中华创伤杂志》2008年第2期146-150,共5页Chinese Journal of Trauma

基　　金：国家自然科学基金资助项目（30370563,30600288,30625037）;国家重点基础研究发展规划资助项目（2005CB522601）;重庆市自然科学基金资助项目（CSTC2007BB5078）

摘　　要：目的观察休克后血管反应性变化与Rho激酶的关系。方法分别从整体动物，离体血管环和原代血管平滑肌细胞（vascular smooth muscle cell，VSMC），观察Rho激酶活性调节剂对失血性休克后大鼠平均动脉压（MAP）、肠系膜上动脉血管管径对去甲肾上腺素（NE）收缩反应性、离体血管环和VSMC收缩反应性的影响。结果失血性休克后大鼠对NE的升压反应和肠系膜上动脉对NE的收缩反应明显降低（P〈0．05或P〈0．01），Rho激酶激动剂精氨酸血管加压素（arginine vasopressin，AVP，0．4U／kg）可增加失血性休克大鼠对NE的升压反应和肠系膜上动脉对NE的收缩反应（P〈0．05或P〈0．01），Rho激酶抑制剂Y-27632（3μg／100g）可拮抗由AVP引起NE的升压反应和肠系膜上动脉对NE收缩反应的升高。休克2h和VSMC缺氧90min后，血管环和VSMC对NE收缩反应性明显降低（P〈0．01）。Rho激酶激动剂血管紧张素Ⅱ（angiotensin Ⅱ，Ang—Ⅱ，10^-9mol／L）可明显升高休克2h血管环和VSMC缺氧90min对NE反应性（P〈0．05或P〈0．01），而Y-27632（10^-5mol／L）可拮抗由Ang—Ⅱ引起的休克2h血管环和VSMC缺氧90min对NE反应性的增高。结论Rho激酶可明显升高休克后血管反应性。Objective To observe the relationship of Rho-kinase and vascular reactivity following hemorrhagic shock in rats. Methods An observation from angles of integrity, ex vivo circulus vasculosus and vascular smooth muscle cell （VSMC） was done on the effect of Rho kinase regulating agents on mean arterial pressure （MAP） and the effect of caliber of superior mesenteric artery （SMA） on norepinephrine（NE） contractile response, ex vivo circulus vasculosus and VSMC contractile response after hemorrhagic shock. Results NE-induced the pressor response and contraction of SMA following hemorrhagic shock were significantly decreased （ P 〈 0.05 or P 〈 0.01 ）. Arginine vasopressin （ AVP, 0.4 U/kg） increased the pressor response of NE and NE induced contraction of SMA （P 〈 0.05 or P 〈 0.01 ） ,Y-27632 （3μg/100 g） could depress the increase of AVP-induced pressor response of NE and NE-induced SMA contractile response. After 2 hours of shock and 90 minutes of VSMC hypoxia, the vascular reactivity of circulus vasculosus and VSMC to NE was decreased significantly （P 〈 0.01 ）. Aangiotensin Ⅱ （ Ang- Ⅱ , 10^ -9 mol/L） could increase the vascular reactivity of SMA and contractile response of VSMC to NE （ P 〈 0.05 or P 〈 0.01 ）, while Y-27632 （ 10 ^-5 mol/L） abolished Ang- Ⅱ -induced increase of the vascular reactivity of SMA and the contractile response of VSMC to NE after 2 hours of shock and 90 minutes of VSMC hypoxia. Conclusion Rho kinase can increase vascular reactivity following hemorrhagic shock.

关 键 词：休克 血管紧张素Ⅱ Rho-激酶 血管反应性 

分 类 号：R686[医药卫生—骨科学]