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机构地区:[1]无锡市第四人民医院麻醉科,无锡214062 [2]江苏省麻醉学重点实验室,徐州221002
出 处:《重庆医科大学学报》2010年第6期877-880,共4页Journal of Chongqing Medical University
摘 要:目的:探讨HSPTX(7%、5%氯化钠+己酮可可碱)对失血性休克大鼠肺损伤的保护作用。方法:24只雄性SD大鼠随机分为3组:假失血性休克(Sham)组,仅接受动静脉插管操作,不放血及复苏、大容量等张乳酸钠林格氏液(RL)复苏组,接受32ml/kgRL、小容量高张(7%、5%氯化钠)液+PTX复苏组,接受4ml/kg7.5%NaCl+25mg/kgPTX,每组8只。测定各组动脉血氧分压(PaO2)、pH值、二氧化碳分压(PaCO2)、肺湿/干重比值、测定血清丙二醛(Malondialdehyde)含量以及超氧化物歧化酶(Superoxide dismutase)活性;检测支气管肺泡灌洗液(Bronchoalveolor lavage fluid)中性粒细胞比例及肺通透性指数,采用ELISA法测定灌洗液上清中TNF-α、IL-1β含量;采用Western blot技术检测肺组织NF-κB蛋白表达。结果:与RL组相比,HSPTX组PaO2和pH值升高、PaCO2降低(P<0.01),HSPTX组大鼠肺湿/干重(W/D)、支气管肺泡灌洗液中上清中TNF-α、IL-1β含量均低于RL组(P<0.01),同时HSPTX组肺组织中核因子κB蛋白(NF-κB)表达显著低于RL组。结论:HSPTX复苏通过抑制核因子κB蛋白的表达减少失血性休克大鼠炎性细胞因子的表达,减轻由失血性休克诱发的急性肺损伤。Objective:To explore the effects of hypertonic saline and pentoxifylline resuscitation on pulmonary inflammation following hemorrhagic shock in rats. Methods:Controlled hemorrhagic shock was induced by blood withdrawal (MAP,40 mmHg)and maintained for 60 min. Animals were randomly divided into 3 groups:① Sham animals(n=8)underwent cannulation without shock or resuscitation and served as negative controls;②RL-resuscitated animals (n=8)received 32 ml/kg RL;③HSPTX group received 4 ml/kg of 7.5% NaCl+25 mg/kg of PTX. PaO2,pH,PaCO2,wet/dry lung weight ratio(W/D),and lung penetrating index were determined. The percentages of neutrophil in bronchoalveolar lavage fluid,the levels of malonadialdehyde (MDA)and superoxide dismutase (SOD)were measured. The tumor necrosis factor-α(TNF-α)and interleukin 1β(IL-1β)in the supernatant of bronchoalveolor lavage fluid were determined by ELISA method,and the expression of NF-κB in the lung tissues was quantified by Western blot. Results:PaO2 and pH were increased whereas PaCO2 was decreased in HSPTX group when compared with that in RL group (P〈0.01). The wet/dry lung weight ratio and the percentages of neutrophil in the supernatant of bronchoalveolar lavage fluid were significantly lower than that in RL group(P〈0.01). The content of tumor TNF-αand IL-1βin HSPTX group was significantly reduced when compared with that in RL group(P〈0.01). The protein expression of NF-κB in HSPTX group was significantly decreased than that in RL group (P〈0.01). Conclusion: Attenuation of hemorrhagic shock-induced pulmonary inflammation with HSPTX is associated with HSPTX-induced inhibition of neutrophil activation and production of inflammatory cytokines via inhibiting the expression of NF-κB.
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