肿瘤坏死因子和丙二醛对内毒素休克新生大鼠心肌改变的影响

THE EFFECTS OF TUMOR NECROSIS FACTOR-α AND MALONDIALDEHYDE ON MYOCARDIAL INJURY IN NEONATAL RATS WITH ENDOTOXIC SHOCK

目的 :通过测定内毒素休克时新生大鼠血清TNF -α ,心肌丙二醛 (MDA) ,超氧化物歧化酶 (SOD)及观察心肌细胞超微结构的变化 ,探讨内毒素休克新生大鼠心肌改变的部分发生机制。方法 :健康 7d龄新生大鼠12 6只随机分为 3组 ,每组 4 2只。对照组 :腹腔注入与其它 2组等量的 0 .9%氯化钠液 0 .1ml;内毒素 (LPS)组 :腹腔注射LPS(5mg/mg) ;治疗组 :于注入内毒素后立即分别注入地塞米松 (Dex) 10mg/kg。于 0 ,1,2 ,4 ,6及 2 4h随机选取 7只断头取血 ,测定血清TNF -α ,心肌MDA及SOD的浓度 ,用透射电镜观察心肌细胞超微结构的变化。结果 :与对照组相比 ,LPS组血清TNF -α ,心肌MDA明显升高 (P <0 .0 1) ,SOD明显降低 (P <0 .0 1)。电镜下可见心肌细胞空泡变性 ,心肌纤维断裂。Dex组血清TNF -α ,心肌MDA升高程度明显低于B组 (P <0 .0 1) ,SOD部分降低 ,心肌损害明显减轻。结论 :TNF -α ,MDA及SOD均参与了内毒素休克心肌损害的病理变化过程 ,Dex能抑制TNF -α及MDA的产生 ,提高SOD的活性 ,对心肌细胞起保护作用。

Objective:To investigate the mechanism of myocardial injury in neonatal rats with endotoxic shock, the concentration of tumor necrosis factor (TNF-α) in serum malondialdehyde(MDA) and superoxide dismutase (SOD) in myocardial tissues were measured. The superstructure of cardiacmyocytes under the electric microscope were observed.Methods:Seven day old healthy newbom Wistar rats were randomly divided into 3 groups. In control group, animals were intraperitoneally injected with the same amount of 0.9% sodium chloride as the other 2 groups. In LPS group, a rat model of endotoxic shock was reproduced by a single bolus injection of lipopolysaccharide (Stag/kg). In treatment group(Dex group), animals received intraperitoneally with dexamethasone ( 10mg/kg )after endotoxin challenge. At the designed time point (0,1,2,4,6,24h postinjection), seven newborn rats were killed. All blood sample were spun in a microcentrifuge ,and the organisms were stored at-80℃ until ready for detecting the concentration of TNF- α, MDA and SOD.The superstructure of cardiac myocytes under the electric microscope were observed.Results:In group LPS, the concentration of TNF-α in serum and MDA in myocardial tissues markedly elevated compared with control group, the levels of SOD decreased . In group Dex , the concentration of TNF-α and MDA increased compared with control group, but the levels markedly decreased compared with group LPS( P <0.01).In group LPS and group Dex ,the levels of SOD decreased compared with control group ( P <0.01), but the decreased levels of SOD in group Dex were less than group LPS( P <0.01). Under the electric microscope, the partial mitochondrias within cardiac myocytes appeared necrosis .In group Dex, mitochondrias within cardiac myocytes were injured slightly and a few of mitochondrias appeared necrosis.Conclusions:TNF-α, MDA and SOD are involved in the pathophysiological alterations of endotoxic shock in neonatal rats. Dexamethasone may prevents myocardial of neonatal rats from injury in endotoxic shock.