摘要
目的在四氯化碳(CCl4)诱导大鼠肝硬化模型中,观察内脏血红素氧合酶(HO)活性的变化。方法用CCl4制备大鼠肝硬化模型,采用动脉插管生理多导仪记录心率、平均动脉压的变化,门静脉插管测定门静脉压力,用联二亚硫酸盐还原法测定血浆一氧化碳(CO)水平,用胆红素生成量反映组织HO的活性。结果与正常对照组相比,肝硬化组平均动脉压显著降低[(15.92±0.74)对(18.93±0.71)kPa,P<0.01],门脉压力显著增高[(16.67±0.63)对(8.82±0.29)cmH2O,P<0.01];血浆CO水平显著上升[(18.69±1.86)对(10.27±1.21)μmol/L,P<0.01];脾脏、小肠、肠系膜HO活性显著增加[分别为(6.55±1.12)对(11.87±1.49),(1.29±0.36)对(2.59±0.28),(1.20±0.33)对(5.18±1.08)nmol/(mg蛋白.h),P<0.01],而肝脏HO活性差异无统计学意义[(2.64±0.33)对(2.73±0.28)nmol/(mg蛋白.h,P>0.05]。结论内脏HO活性增加可能是肝硬化血流动力学紊乱的原因之一。
Objective To explore the heme oxygenase activity in splanchnic organs from CCl4-induced cirrhotic rats.Methods Liver cirrhosis was induced by the s.c.administration of carbon tetrachloride in rats.Mean arterial pressure(MAP,kPa) 、heart rate(HR,b/min) 、portal pressure(PP,cm/H2O) were measured by indwelling catheter.Plasma CO was determined by Chalmers method and heme oxygenase activity in the tissues was analyzed by the rate of bilirubin formation.Results Compared with the control,mean arterial pressure of animals with liver cirrhosis was significantly reduced(15.92±0.74 vs.18.93±0.71 kPa;P〈0.01),portal pressure(16.67±0.63 vs.8.82±0.29 cmH2O;P〈0.01) and plasma CO level(18.69±1.86 vs.10.27±1.21 μmol / L;P〈0.01) were significantly increased.The HO activity in the spleens,intestines,and mesenteries from cirrhotic rats significantly increased(6.55±1.12 vs.11.87±1.49;1.29±0.36 vs.2.59±0.28;1.20±0.33 vs.5.18±1.08 nmol bilirubin/mg protein/h;P〈0.01;respectively) in comparison with controls.No differences were observed regarding the liver HO activity(2.64±0.33 vs.2.73±0.28 nmol bilirubin/mg protein/h;P〉0.05).Conclusion These results demonstrate that HO activity was increased in splanchnic organs of cirrhotic rats,suggesting its key role in the development of the hemodynamic disturbance of liver cirrhosis.
出处
《肝脏》
2011年第1期45-47,共3页
Chinese Hepatology