摘要
目的 探讨前列环素 (PGI2 )和一氧化氮 (NO)在门静脉高压症高血流动力循环中的作用。 方法 66只雄性SD大鼠随机分成 :肝内型门静脉高压症组 (IHPH组 )、肝前型门静脉高压症组 (PHPH组 )和假手术组 (SO组 )。模型制备 1周后再随机分为 3个亚组 ,即对照组、一氧化氮合酶抑制剂L NNA组、消炎痛组。用药 1周后测定股动脉血浆 6 酮 前列腺素F1α(6 keto PGF1α)和NO2 - /NO3- 浓度 ,应用同位素微球技术行血流动力学研究 ,并对NO、PGI2 水平与血流动力学参数行Pearson相关分析。 结果 (1 )在基础状态下 ,血浆 6 keto PGF1α浓度 ,IHPH鼠 [(1 1 2 3 85± 1 53 64)pg/ml]和PHPH鼠 [(891 88± 83 1 1 )pg/ml]均显著地高于SO鼠 [(72 5 53± 1 0 5 54)pg/ml] ,P <0 0 5 ;血浆NO2 - /NO3- 浓度 ,IHPH鼠 [(73 34± 4 31 ) μmol/L]和PHPH鼠 [(75 2 1± 6 89) μmol/L]均显著高于SO鼠[(58 79± 8 47) μmol/L] ,P <0 0 5。 (2 )与对照组比较 ,L NNA与消炎痛均显著地降低IHPH与PHPH 2组鼠血浆 6 keto PGF1α和NO2 - /NO3- 的浓度 ,P <0 0 5 ;降低IHPH、PHPH 2组鼠的心脏指数 (CI)、门静脉压力 (FPP)和门静脉血流量 (PVI) ,P <0 0 5 ;显著地增高这 2组鼠的平均动脉压 (MAP)、总外周血管阻力 (TPR)和内脏血?
Objective To investigate the effects of prostacyclin (PGI 2) and nitric oxide (NO) in the development of hyperdynamic circulatory state on chronic portal hypertensive rats. Methods Sixty six male SD rats were divided into three groups, namely intrahepatic portal hypertension (IHPH) by injection of CCl 4, prehepatic portal hypertension (PHPH) by partial stenosis of the portal vein for 2 weeks and sham operated controls (SO). Animals in each group were divided further into 3 subgroups and received N ω nitro L arginine (L NNA), indomethacin and saline (as control), respectively. Splanchnic and systemic hemodynamics was measured using radioactive microsphere techniques. The NO concentation in serum was determined by nitrates intrites which were measured using a colorumetric method, and concentration of PGI 2 was determined using specific radioimmunoassay for its stable hydrolytic product, 6 keto PGF 1α . Results The concentrations of plasma 6 keto PGF 1α and serum nitrates+nitrites in IHPH rats(1 123 85±153 64; 73 34±4 31) and in PHPH rats (891 88±83 11; 75 21±6 89) were significantly higher than those of SO rats(725 53±105 54;58 79±8 47). L NNA and indomethacin could decrease the concentrations of plasma 6 keto PGF 1α and serum nitrates+nitrites in IHPH and PHPH rats ( P <0 05). At the same time, CI?FPP and PVI were lowered while MAP?TPR and SVR were increased( P <0 05). After deduction of NO action, there were no significant correlation between plasma PGI 2 level and hemodynamic parameters such as CI, TPR, PVI and SVR. However, after deduction of PGI 2 action, NO was still correlated highly with those hemodynamic parameters. Conclusion It is NO rether then PGI 2 that is a mediator in the formation and development of hyperdynamic circulatory state in chronic portal hypertensive rats.
出处
《中华外科杂志》
CAS
CSCD
北大核心
2003年第7期537-540,共4页
Chinese Journal of Surgery
