多巴酚丁胺联合加压素对感染性休克大鼠肠损伤的影响

目的观察不同强效升压药对感染性休克大鼠肠损伤的影响。方法健康雄性SD大鼠50只,体重250～300g,随机均分为五组:生理盐水组(NS组)、去甲肾上腺组(NE组)、多巴胺组(DA组)、精氨酸加压素组(AVP组)及多巴酚丁胺联合精氨酸加压素组(DOB+AVP组)。股静脉注射内毒素15mg/kg建立感染性休克模型后,静脉输注生理盐水10ml·kg-1·h-1进行容量复苏,同时分别输注等容NS、NE1μg·kg-1·min-1、DA10μg·kg-1·min-1、AVP0.04U·kg-1·min-1和DOB10μg·kg-1·min-1联合AVP0.04U·kg-1·min-1。调整实验组升压药剂量使MAP维持在90mmHg左右,4h后取肠组织测定TNF-α、IL-6、IL-10水平;显微镜下观察肠组织及线粒体的损伤程度。结果 DOB+AVP组和NE组肠组织中TNF-α、IL-6含量低于NS组、DA组和AVP组(P<0.05)。IL-10含量各组之间差异无统计学意义。DOB+AVP组肠组织和线粒体损伤程度轻于其它四组。结论 DOB联合AVP治疗感染性休克时,可减轻肠组织炎症反应、缓解肠组织和线粒体损伤。

Effects of dobutamine combined with vasopressin on intestinal injury in rats with septic shock

Objective To observe the effects of different potent vasopressor agents on intestinal injury in rats with septic shock.Methods Fifty healthy male SD rats weighing 250-300 g,were randomized into 5 groups:normal saline group(NS group),noradrenaline group(NE group),dopamine group(DA group),arginine vasopressin group(AVP group),and dobutamine combined with arginine vasopressin group(DOB+AVP group).After establishing the septic shock model via the injection of lipopolysaccharide 15 mg/kg,normal saline 10 ml·kg-1·h-1 was intravenously infused for volume resuscitation together with the same volume of NS,NE 1 μg·kg-1·min-1,DA 10 μg·kg-1·min-1,AVP 0.04 U·kg-1·min-1,or DOB 10 μg·kg-1·min-1 combined with AVP 0.04 U·kg-1·min-1.The doses of vasopressor were adjusted to maintain mean arterial pressure(MAP) around 90 mm Hg.Four hours later,intestinal tissue was obtained to detect the levels of TNF-α,IL-6,and IL-10,and to observe the injury degree of intestinal tissue and mitochondria.Results The levels of intestinal TNF-α and IL-6 were significantly lower in DOB + AVP group and NE group than NS group,DA group,or AVP group(P<0.05.There was no significant difference in IL-10 between any two groups.DOB+AVP group had milder injury of intestinal tissue and mitochondria than the other 4 groups.Conclusion DOB combined with AVP may reduce the intestinal inflammatory responses and relieve the injury of intestinal tissue and mitochondria in septic shock.