摘要
目的 研究大剂量肝素对门静脉高压症鼠血浆前列环素 (PGI2 )、一氧化氮 (NO)水平及血流动力学的影响。方法 4 5只雄性 SD大鼠随机分成 IHPH (CCl4 肌肉注射法 )、PHPH (部分门静脉缩窄法 )和 SO(假手术 )三组。动物模型制备后两周 ,三组鼠再随机分成二个亚组 ,即生理盐水对照组和大剂量肝素组。肝素通过鼠尾静脉用微量注射器以 2 0 0 IU / Kg/ m in的速度持续静脉输注 1小时 ,然后用同位素微球技术行血流动力学研究。用放射免疫法测股动脉血浆 6- keto- PGF1α浓度。用还原法测股动脉血浆 NO2 / NO3浓度。结果 与 SO鼠比较 ,IHPH、PHPH两组鼠的 TPR与 SVR均显著降低 (P<0 .0 5 ) ,CI与 PVI均显著升高 (P<0 .0 5 )。应用大剂量肝素后 ,血浆 6- keto- PGF1α浓度 (pg/ m l)在 IHPH、PHPH和 SO鼠分别为 2 3 90 .61± 14 0 0 .3 8、2 766.4 7± 5 0 6.95和 3 965 .96± 976.82 ,均显著地高于生理盐水对照组中三组鼠的浓度 (分别为 112 3 .85± 15 3 .64;891.88± 83 .11;72 5 .5 3± 10 5 .5 4 ) ;相反 ,血浆 NO2 / NO3浓度 (μmol/ L )在 IHPH、PHPH和 SO鼠分别为 5 4 .0 2± 11.89、62 .0 6± 3 .5 6和 4 5 .2 8± 4 .3 9,均显著地低于生理盐水对照组中三组鼠的浓度 (分别为 73 .3 4± 4 .3 1;75 .2
Objective To evaluate the effects of high dose heparin on the production of NO and PGI 2 and on the hemodynamics of portal hypertensive rats. Methods Forty five male SD rats were divided into three groups named by intrahepatic portal hypertension (IHPH) by injection of CCl 4, prehepatic portal hypertension (PHPH) by patial stenosis of the portal vein after 2wk and sham-operated controls (SO). Animals of each group were received high-dose heparin (200IU/Kg/min, iv) with saline as control. Serum concentation of NO was determined by nitrates/nitrites which were measured by colorumetric method, and that of PGI 2 was done by a specific radioimmunoassay for its stable hydrolysis products 6 keto PGF 1α . Splanchnic and systemic hemodynamics was measured by radioactive microsphere techniques. Results The concentrations of plasma 6 keto PGF 1α and serum nitrates/nitrites in IHPH and PHPH rats were significantly higher than those of SO rats. After the administration of high dose heparin, plasma 6 keto PGF 1α concentrations (pg/ml) of IHPH rats (2390.6±1400.38), PHPH rats (2766.47±506.95) and SO rats (3965.96±976.82) were significantly higher than those administrated with saline (1123.85±153.64;891.88±83.11;725.53±105.54 respectively) (P<0.05); On the contrary, serum nitrates/nitrites (μmol/L) concentrations of IHPH rats (54.02±11.89), PHPH rats (62.06±3.56) and SO rats (45.28±4.39) were significantly lower than those administrated with saline (73.34±4.31; 75.21±6.89; 58.79±8.47 respectively) (P<0.05). There was the characteristics of hyperdynamic circulatory state in IHPH and PHPH rats. Compared with those rats administrated with saline, the hemodynamic parameters of portal hypertensive rats such as CI and PVI declined significantly after the administration of high dose heparin (P<0.05), while the hemodynamic parameters such as TPR and SVR increased significantly (P<0.05). Conclusion High-dose heparin extenuates the hyperdynamic circulatory state of portal hypertensive rats presumably by reducing the production of NO. High dose heparin can also increase the production of PGI 2, which indicates that PGI 2 is not a mediator in the formation and the development of hyperdynamic circulation in portal hypertensive rats.
出处
《肝胆外科杂志》
2003年第2期138-140,共3页
Journal of Hepatobiliary Surgery
