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聚腺苷二磷酸核糖基聚合酶在大鼠失血性休克后血管低反应性发生中的作用
引用本文:周学武,刘建仓,廖自福,王丽亭,刘良明. 聚腺苷二磷酸核糖基聚合酶在大鼠失血性休克后血管低反应性发生中的作用[J]. 中国危重病急救医学, 2008, 20(3): 148-150
作者姓名:周学武  刘建仓  廖自福  王丽亭  刘良明
作者单位:第三军医大学大坪医院野战外科研究所二室,创伤、烧伤和复合伤国家重点实验室,重庆,400042
基金项目:国家重点基础研究发展规划(973计划) 
摘    要:目的 研究聚腺苷二磷酸核糖基聚合酶(PARP)在大鼠失血性休克后血管低反应性发生中的作用.方法 将SD大鼠随机分为休克组、PARP抑制剂3-氨基苯甲酰胺(3-AB)预处理+休克组和假手术对照组,采用股动脉放血复制失血性休克模型.在体观察给予3 μg/kg去甲肾上腺素(NE)升高血压的幅度;离体测定肠系膜上动脉血管环对NE的反应性;硝酸还原酶法测定血浆和肠系膜上动脉血管环组织匀浆中一氧化氮(NO)的含量.结果 休克模型完成后即刻静脉给NE,休克组血压升高幅度显著低于假手术对照组(P<0.01);回输血1 h后再次静脉给NE,休克组血压显著低于3-AB预处理+休克组和假手术对照组(P<0.05和P<0.01).假手术对照组最大收缩张力[(0.367 1±0.221 3)g/mm]>3-AB预处理+休克组C(0.286 4±0.153 2)g/mm]>休克组C(0.185 6±0.11 3)g/mm,P<0.05或P<0.01];与休克组比较,3-AB预处理+休克组量一效曲线左移,在NE终浓度为10-7、10-6和10-5 mol/L时其收缩力显著增加(P均<0.05).3组间血浆NO含量差异均无统计学意义,3-AB预处理+休克组血浆和肠系膜上动脉组织匀浆中NO含量虽较休克组稍有降低,但两组问比较差异无统计学意义.结论 PARP参与了大鼠失血性休克后血管低反应性的发生.

关 键 词:聚腺苷二磷酸核糖基聚合酶  失血性休克  血管低反应性

Effect of poly-adenosine diphosphate ribosyl-polymerase on vascular hyporeactivity in rats with hemorrhagic shock
ZHOU Xue-wu,LIU Jian-cang,LIAO Zi-fu,WANG Li-ting,LIU Liang-ming. Effect of poly-adenosine diphosphate ribosyl-polymerase on vascular hyporeactivity in rats with hemorrhagic shock[J]. Chinese critical care medicine, 2008, 20(3): 148-150
Authors:ZHOU Xue-wu  LIU Jian-cang  LIAO Zi-fu  WANG Li-ting  LIU Liang-ming
Affiliation:State Key Laboratory of Trauma, Burns and Combined Injury, Department 2, Research Institute of Surgery, Daping Hospital, The Third Military Medical University, Chongqing, China. zhouxw@cta.cq.cn
Abstract:OBJECTIVE: To study the effects of poly-adenosine diphosphate ribosyl-polymerase (PARP) on vascular hyporeactivity during hemorrhagic shock in rats. METHODS: Sprague-Dawley (SD) rats were randomly divided into three groups: shock, 3-aminobenzamide (3-AB) pretreatment+shock, and sham operation. Bleeding from the femoral artery to induce hemorrhagic shock model. The blood pressure changes following 3 microg/kg norepinephrine (NE) injection were observed in vivo. The response of vascular rings of superior mesenteric artery (SMA) to NE was determined ex vivo. The nitrogen monoxidum (NO) contents of plasma and tissue homogenate of SMA were measured using the assay kit based on the nitrate reductase reaction. RESULTS: The maximum increase of mean arterial pressure in response to NE immediately following shock in the shock group was significantly lower than in the sham operation group (P<0.01) and the value at 1 hour after blood reinfusion in the shock group was obviously lower than in the 3-AB pretreatment+shock group (P<0.05) and in the sham operation group (P<0.01). The maximum concentration force in the sham operation group [(0.367 1+/-0.221 3)g/mm] was significantly increased than in the 3-AB pretreatment+shock group [(0.286 4+/-0.153 2) g/mm, P<0.05] and in the shock group [(0.185 6+/-0.111 3)g/mm, P<0.01]. The cumulative dose-response curves of SMA to NE shifted to the left, and the contraction force was markedly increased as NE concentration reaching 10(-6), 10(2+) and 10(-5) mol/L in the 3-AB pretreatment+shock group compared to the shock group (all P<0.05). There were no significant difference on plasma NO content among the three groups. However, the NO contents of plasma and tissue homogenate of SMA in the 3-AB pretreatment+ shock group were slightly lower than in the shock group (P>0.05). CONCLUSION: PARP is involved in the vascular hyporeactivity in hemorrhagic-shocked rats.
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