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作 者:赵志斌[1] 陈莺[1] 高新跃[2] 曾因明[3]
机构地区:[1]连云港市第一人民医院麻醉科,江苏222002 [2]江苏省无锡市第四人民医院麻醉科,214062 [3]徐州医学院江苏省麻醉医学研究所,221002
出 处:《中国危重病急救医学》2006年第9期551-553,共3页Chinese Critical Care Medicine
摘 要:目的观察羟乙基淀粉(HES)对失血性休克血管反应性的影响,并探讨其机制。方法40只SD大鼠,雌雄不限,按照随机数字表法分为正常组、休克组、复方氯化钠(即林格液,SC)组、HES130/0.4组和HES200/0.5组,每组8只。股动脉放血至大鼠平均动脉压(MAP)为40mm Hg(1mm Hg=0.133kPa),维持30min后分别输注溶液,使MAP升至70mm Hg,并维持60min;观察各用药组在60min内维持MAP70mm Hg所需补液量。分别在休克前及休克30、60和90min静脉注射去甲肾上腺素(NE)2μg/kg,观察液体对NE升压反应的影响;取动脉血测定血浆一氧化氮(NO)和一氧化氮合酶(NOS)含量。结果各用药组之间维持MAP70mm Hg所需补液量比较差异均有显著性(P均<0.01),其中HES200/0.5组所需补液量最少,HES130/0.4组次之,SC组最多。休克90min时,HES130/0.4组、HES200/0.5组MAP升高幅度均明显高于SC组(P均<0.05),血浆NO和NOS含量均明显低于SC组(P<0.05或P<0.01)。结论HES130/0.4和HES200/0.5可通过降低血浆NO和NOS含量,从而改善休克大鼠的血管反应性。Objective To study the effect of hydroxyethyl starch (HES) on vascular reactivity of rat during hemorrhagic shock and its mechanism. Methods Forty SD rats were randomly divided into 5 groups: normal control group, shock group, sodium chloride (SC) group, HES 130/0.4 group and HES 200/0.5 group with 8 rats in each group. Rats were hemorrhaged and maintained mean arterial pressure (MAP) at 40 mm Hg (1 mm Hg= 0.133 kPa) for 30 minutes, then rats were infused with fluids to restore and maintain MAP at 70 mm Hg for 60 minutes. The infusion volumes of each fluid to maintain MAP were recorded. The responses of MAP to norepinephrine (NE) were measured before shock, at 30, 60 and 90 minutes during hemorrhagic shock. Concentrations of nitric oxide (NO) and nitric oxide synthase (NOS) of plasma were measured at 90 minutes during hemorrhagic shock. Results The infusion volumes of each fluid to maintain MAP were significantly different (all P〈0. 01). HES 200/0.5 group〈HES 130/0. 4 group〈SC group. In HES 130/0. 4 group and HES 200/0.5 group at 90 minutes during hemorrhagic shock, the responses of MAP to NE were improved significantly compared with those of SC group (both P〈0. 05), plasma contents of NO and NOS were reduced markedly compared with those of SC group (P〈0. 05 or P〈0. 01). Conclusion HES can improve vascular reactivity during hemorrhagic shock by inhibiting plasma contents of NO and NOS.
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