机构地区:[1]贵州医科大学附属医院麻醉科,贵州省贵阳市550004 [2]贵州省骨科医院麻醉科
出 处:《中国煤炭工业医学杂志》2015年第10期1721-1723,共3页Chinese Journal of Coal Industry Medicine
基 金:贵州省教育厅自然科学研究项目[编号:黔教科(2011)38号]
摘 要:目的 探讨重度失血性休克期阻断缝隙连接对缺血性肺损伤的影响。方法 健康家兔24只,体重1.5~2.2kg,按照Wiggers改良法制作重度失血性休克模型,随机分为二组,每组12只:传统治疗组(A组)静脉输注乳酸钠林格1.5ml/(kg·min)30min;辛醇组(B组)静脉输注乳酸钠林格液1.5ml/(kg·min)30min,同时腹腔注射99.5%辛醇5mmol/kg。然后二组回输全部放血及等放血量的乳酸钠林格液后静脉输注乳酸钠林格液2.5ml/(kg·h)150min。于放血前(T1)、失血性休克模型制备成功后即刻(T2)、容量复苏30min(T3)、容量复苏180min(T4)时记录MAP、HR,记录容量复苏期间兔的病死情况。于实验兔容量复苏死亡或复苏结束时取右上肺置于-80℃冰箱内用于检测髓过氧化物酶(MPO)、总超氧化物歧化酶(T-SOD)、丙二醛含量(MDA)等生化指标,右下肺置于甲醛溶液中固定作肺多形核粒细胞(PMNs)计数。结果 1肺组织总超氧化物歧化酶(T-SOD)活力:A组较B组显著降低(P〈0.01);2肺组织丙二醛(MDA)含量:A组含量较B组显著升高(P〈0.01);3肺组织髓过氧化物酶(MPO):A组较B组显著升高(P〈0.01);4HE染色肺多形核粒细胞(PMNs)计数:A组显著高于B组(P〈0.01)。结论 兔失血性休克诱发肺损伤时阻断缝隙连接可减轻肺组织损伤程度。Objective To investigate the effects of the lung injury induced by hemorrhagic shock by blocking intercellular gap junction in rabbits. Methods Twenty- four healthy rabbits of both sexes weighing 1.5- 2.2 kg were used in this study. The animals were anesthetized with iv 3 % Pentobarbital 30mg/kg, tracheostomized and mechanically ventilated. Femoral artery was cannulated for MAP monitoring, blood- letting, blood sampling and fluid infusion. Twenty- four healthy rabbits of both sexes weighing 1.5-2.2kg were used in this study. The animals were anesthetized with iv 3% pentobarbital 30 mg/kg, tracheostomized and mechanically ventilated. Femoral artery was cannulated for MAP monitoring, bloodletting, blood sampling and fluid infusion. Severe hemorrhagic shock was induced according to the method described by Wiggers. MAP was maintained at 35-40mm Hg for 60 min. The animals were then randomly divided into 2 groups (n= 12 each): traditional treatment group (group A) and octanol group (group B). Both groups received rapid iv infusion of lactated Ringer's solution (LR solution) 1.5/(ml · kg · min). In group B of 99.5% octanol (a specific gap junction inhibitor) 5 mmol/kg was injected intraperitoneally (IP) in ad- dition to iv LR solution infusion. Thirty minutes later the animals were resuscitated with infusion of the blood withdrawn and LR solution (the volume was equal to the volume of blood loss). Then LR solution was infused iv at 2. 5ml/(kg · h) for 150min. MAP and HR were recorded before blood letting (T1), immediately after successful establishment of the model (T2), and at 30 and 180min (T3-4) of resuscitation. The mortality during resuscitation was calculated. The animals were killed at the end of resuscitation. Results The T- SOD activity, as compared to the values in group A, the T- SOD activity was significantly high in group B(P〈0. 01). The ratio of MDA: as compared to the values in group B, the ratio of MDA was significantly high in group A(P〈
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