摘要
目的探讨氨甲酰化促红细胞生成素(CEPO)抗慢性心力衰竭(CHF)的作用及其可能的机制。方法 90只Wistar大鼠随机分为心衰组、干预组及对照组。心衰组及干预组均采用腹腔注射异丙肾上腺素(ISO)法建立大鼠CHF模型,干预组予以CEPO干预4周后,测定各组大鼠血流动力学指标、血清诱生型一氧化氮合酶(iNOS)及超氧化物歧化酶(SOD)水平。结果心衰组及干预组左室内压峰值(LVSP)、左室内压上升/下降最大速率(±dp/dtmax)及血清SOD水平较对照组均显著降低(P<0.05),而左室舒张末压(LVEDP)、心率(HR)及血清iNOS水平均显著增高(P<0.05);干预组LVSP、±dp/dtmax及血清SOD水平较心衰组均显著增高(P<0.05),而LVEDP、HR及血清iNOS水平均显著降低(P<0.05)。结论 CEPO具有抗CHF的作用,可能与抑制过度的NO释放及清除氧自由基有关。
Objective To observe the value of carbamylated erythropoietin(CEPO) on rats with chronic heart failure(CHF) and its possible mechanism.Methods Ninty Wistar rats were randomly divided into intervention,CHF and control group.Both intervention group and CHF group were established models of CHF by intraperitoneal injection of isoproterenol.The intervention group were received CEPO.After 4 weeks,rats were observed changes in hemodynamics,inducible nitric oxide synthase(iNOS) and superoxide dismutase(SOD).Results Compared with control group,left ventricular systolic pressure(LVSP) and maximal rate of rise/decline of left ventricular pressure(±dp/dtmax) were lower(P〈0.05),whereas left ventricular end-diastolic pressure(LVEDP) and heart rate(HR) were higher(P〈0.05),the level of iNOS increased(P〈0.05),the level of SOD decreased(P〈0.05) in both CHF group and intervention group.Compared with CHF group,intervention group had higher LVSP,±dp/dtmax and SOD levels(P〈0.05),lower LVEDP,HR and iNOS levels(P〈0.05).Conclusion CEPO has the role of against CHF by inhibiting the excessive release of nitric oxide and scavenging oxygen free radicals.
出处
《山东医药》
CAS
北大核心
2011年第28期31-33,共3页
Shandong Medical Journal
基金
甘肃省新药临床前研究重点实验室开放基金项目(GSKFKT-0707)