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1,6-二磷酸果糖对体外循环促炎性细胞因子释放的影响 被引量:1

Effects of Fructose 1,6-diphosphate on the Release of Proinflammatory Cytokine after Cardiopulmonary Bypass
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摘要 目的探讨1,6-二磷酸果糖(FDP)对体外循环术后促炎性细胞因子释放的影响。方法将20例二尖瓣瓣膜置换术的风湿性心脏病患者随机分为实验组10例,对照组10例。实验组在体外循环前及体外循环中分别静脉注射FDP200mg/kg,对照组不用FDP。于手术开始前1h、CPB结束后即刻、CPB结束后1h分别抽取桡动脉血,测定血浆肿瘤坏死因子(TNF-α)、白介素-6(IL-6)、白介素-8(IL-8)。结果外循环前两组TNF-α、IL-6、IL-8水平均无差异,体外循环后即刻及后1h,两组患者TNF-α、IL-6、IL-8水平显著升高(P<0.05),但实验组低于对照组(P<0.01)。结论在CPB时静注FDP可明显减少体外循环术后患者血中TNF-α、IL-6、IL-8的释放,表明FDP可减轻体外循环术后患者全身炎症反应。 Objective To investigate the effect of fructose 1,6-diphosphate(PDF) on the release of proinflammatory cytokine after cardiopulmonary bypass(CPB).Methods 20 patients scheduled for cardiac surgery under CPB were randomly divided into two groups. In treatment group (n=10), FDP(200 mg/kg) was injected intravenously before and during CPB respectively, but in control group (n=10) no FDP was used. Blood samples were drawn from the radial artery at the following time points: 1 hour before CPB, 0 and 1 hour after CPB. The plasma levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and interleukin-8 (IL-8) were measured.Results There was no difference between two groups before CPB. 0 and 1 hour after CPB, the levels of TNF-α, IL-6, IL-8 in two groups were increased significantly(P<0.05). But the indexes above of treatment group were lower than those of control group(P<0.01).Conclusion Intravenous injection of FDP during CPB can release the concentration of TNF-α, IL-6, IL-8 in plasma after CPB. FDP can alleviate the systemic inflammatory response after CPB.
出处 《医学文选》 2005年第3期305-306,共2页 Anthology of Medicine
基金 广西壮族自治区卫生厅课题(Z2002030)
关键词 1 6-二磷酸果糖 体外循环 细胞因子 炎症反应 Fructose-1,6-diphosphate Cardiopulmonary bypass Cytokine Inflammatory response
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  • 1Akao T, Takeyoshi I, Totsuka O, et al. Effect of the free radical scavenger MCI-186 on pulmonary ischemia-reperfusion injury in dogs. J Heart Lung Transplant, 2006, 25 : 965-971.
  • 2Nimata M, Okabe TA, Hattori M, et al. MCI-186 (edara vone), a novel free radical scavenger, protects against acute autoimmune myocarditis in rats. Am J Physiol Heart Circ Physiol, 2005,289 : 2514-2518.

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