止血带休克后主动脉收缩反应性及RAS成分的变化

发布时间：2018-02-25 16:40

  本文关键词： 止血带休克 主动脉 血管收缩反应性 肾素-血管紧张素系统　出处：《中国病理生理杂志》2016年03期 　论文类型：期刊论文

【摘要】：目的:通过观察止血带休克(tourniquet shock,TS)后主动脉收缩反应性及肾素-血管紧张素系统(renin-angiotensin system,RAS)的变化,探讨RAS稳态失衡在止血带休克后主动脉低反应性及损伤中的作用。方法:8月龄C57BL/6的雄性小鼠,分为对照组及6个模型组,每组6只。模型组进行止血带套扎双后肢阻断血流,2h后解套扎进行再灌注,分别于再灌注10 min、1 h、2 h、4 h、6 h和12 h后处死,对照组不进行套扎与再灌注,其余操作同模型组;多普勒血流仪测定肢体血流,颈动脉插管法测定平均动脉压(MAP),离体血管张力测定仪测定主动脉收缩反应性,HE染色结合透射电镜评价血管形态学损伤;Western blot检测血管组织中血管紧张素Ⅱ1型受体(AT1受体)、血管紧张素(1-7)受体(Mas受体)、血管紧张素转换酶(ACE)和ACE2蛋白的表达。采用ELISA检测血清中血管紧张素Ⅱ(AngⅡ)和血管紧张素(1-7)[Ang(1-7)]的含量。结果:与对照组相比,模型组出现下述变化:(1)随着再灌注时间的延长血流量逐渐减少;MAP在再灌注10 min明显升高,随后逐渐降低;血管对去甲肾上腺素的反应性在再灌注10 min升高随后下降,再灌注4 h的血管反应性最低;形态学损伤评分随再灌注时间延长逐渐增高;(2)主动脉AT1受体与ACE2蛋白表达逐渐下降,Mas受体与ACE蛋白表达逐渐升高;(3)血清中AngⅡ的含量整体呈升高趋势,Ang(1-7)的含量整体呈降低趋势。结论:主动脉收缩反应性在休克初期暂时升高,随后降低,其发生机制可能与血管形态学损伤及RAS失衡有关。
[Abstract]:Objective: to observe the changes of aortic contractile reactivity and renin-angiotensin system (RASs) after tourniquet shock in tourniquet TS. To investigate the role of RAS homeostasis in aortic hyporesponsiveness and injury after tourniquet shock. Methods male mice at the age of 8 months C57BL / 6 were divided into two groups: control group and 6 model groups. 6 rats in each group were treated with tourniquet ligation and ligation of hind limbs for 2 h, then released for reperfusion. The rats in the model group were killed at 10 min, 1 h, 2 h, 4 h, 4 h, 6 h and 12 h, respectively. The control group did not perform ligation and reperfusion, while the rest operated the same as the model group. The blood flow of limbs was measured by Doppler flow meter. The mean arterial pressure was measured by carotid artery catheterization, the vasoconstrictive reactivity of aorta was measured by in vitro vasotension apparatus, and the vascular morphological damage was evaluated by HE staining combined with transmission electron microscope. Western blot was used to detect angiotensin 鈪，

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