摘要
目的探讨生长抑素对内毒素诱导感染性休克大鼠血清炎症介质的影响。方法用24只健康 Wistar 雄性大鼠建立内毒素诱导感染性休克大鼠动物模型。随机分为对照组及生长抑素干预组,观察0、30、90和360 min 4个时间点的生命体征及白细胞介素6(IL-6)和肿瘤坏死因子(TNF-α)水平。结果生长抑素可有效抑制感染性休克大鼠血压的下降,360 min 为(34±48)mm Hgvs(86±20)mm Hg(1 mm Hg=0.133 kPa),P<0.05;降低 IL-6水平,360 min:(230±92)mg/L vs(217±26)mg/L(P<0.05)及 TNF-α水平,360 min:(474±219)mg/L vs(440±49)mg/L(P<0.05);对照组在30~90 min 之间死亡2只,90~360 min 之间死亡4只,施他宁干预组均存活,时序检验 P=0.0054。结论生长抑素可通过抑制感染性休克大鼠的炎症反应而改善预后,降低死亡率。
Objective To explore the effect of somatostatin on serum interleukin (IL)-6 and tumor necrosis factor (TNF)-α in lipopolysaccharide (LPS)-induced septic shock. Methods 24 male Wistar rats were randomly divided into 2 groups: intervention group ( injected with LPS of Escherichia coli via femoral vein to induce septic shock) and control group ( injected with LPS of Escherichia coli and then injected with somatostatin). The mean arterial pressure (MAP), heart rate, respiration rater, and mortality rate were observed before the injection of LPS, and 30, 90, and 360 min after the injection, and the serum IL-6 and TNF-α level were detected before the injection of LPS, 30, 90, and 360 min after the injection, or after the death. Results The IL-6 levels 30 min, 90 min, and 360 min after the injection of the somatostatin intervention group were 233 ± 47, 212 ± 33, and 217 ± 26 mg/L respectively, all significantly lower then those of the control group (308 ± 56, 260 ± 32, and 230 ± 92 mg/L, all P 〈 0.05 ). The TNF-α level 30 min, 90 min, and 360 min after the injection of the somatostatin intervention group were 450 ± 82, 417 ± 92, and 440 ±49 mg/L, all significantly lower than those of the control group (607 ± 149, 517 ±74, and 474 ± 219 mg/L, all P 〈 0.05). In addition, compared with the control group, the MAP of the somatostatin intervention group increased after 90 min. Two rats in the control group died 30 to 90 min latei" and 4 rats died 90 to 360 min later, however, 360 min later all rats in the somatostatin intervention group were alive (P = 0.0054). Conclusion Somatostatin can inhibit the level of serum IL-6 and TNF-α in septic shock induced by LPS and improve the survival rate.
出处
《中华医学杂志》
CAS
CSCD
北大核心
2007年第5期345-347,共3页
National Medical Journal of China