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

Effect of poly-adenosine diphosphate ribosyl-polymerase on vascular hyporeactivity in rats with hemorrhagic shock

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3μg／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1h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[（0.3671士0.2213）g／mm]〉3-AB预处理＋休克组[（0.2864±0.1532）g／mm]〉休克组[（0.1856士0.1113）g／mm，P〈0.05或P〈0.01]；与休克组比较，3-AB预处理＋休克组量-效曲线左移，在NE终浓度为10^-7、10^-6和10^-5mol／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，但两组间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。

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 μg/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 [（0.3671±0.2213）g/mm] was significantly increased than in the 3-AB pretreatmentd-shock group [（0.286±0.1532） g/mm, P〈0.05] and in the shock group [（0.185±0.1113）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^-7, 10^-6 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.