机构地区:[1]哈尔滨医科大学附属第二临床医学院消化内科,黑龙江省哈尔滨市150000 [2]哈尔滨医科大学附属第二临床医学院超声诊断科,黑龙江省哈尔滨市150000 [3]哈尔滨医科大学附属第三临床医学院重症监护病房,黑龙江省哈尔滨市150000 [4]哈尔滨医科大学附属第一临床医学院心血管内科,黑龙江省哈尔滨市150000
出 处:《世界华人消化杂志》2010年第33期3508-3514,共7页World Chinese Journal of Digestology
摘 要:目的:比较经门静脉和股静脉注入扩血管药物后对肝硬化大鼠门脉血流动力学紊乱的差异,从而寻找更合适的途径降低门脉压力,改善肝脏血流.方法:采用酒精联合CCl4法建立肝硬化门脉高压大鼠模型,42只大鼠随机化平均分成6组,分别为硝酸甘油门脉组和硝酸甘油股静脉组(NG门和NG股)、前列腺素E1门脉组和前列腺素E1股静脉组(PGE1门和PGE1股)、生理盐水门脉组和生理盐水股静脉组(NaCl门和NaCl股).使用超声多普勒测定给药前后不同时间段门静脉内径(PVD)、门静脉血流速度(PFR)和肝门静脉血流量(PVF)的变化情况.结果:NaCl门组和NaCl股组给药前后PVD、PFR、PVF均无显著性差异(P=0.1742,P=0.2372,P=0.6566),而NG门、NG股和PGE1门、PGE1股4组给药后PVD均明显扩张,但不同给药方式和不同药物之间无显著差异(P=0.0516,P=0.1225);给药后PVF增加,NG股和PGE1股组增加量明显大于NG门和PGE1门组,且差异具有显著性(P<0.0001);较给药前,给药后10、20minNG股和PGE1股组PFR明显增加,而NG门和PGE1门组却显著减少,差异具有显著性[NG股:4.98mm/(s*100g)±0.62mm/(s*100g),4.31mm/(s*100g)±0.46mm/(s*100g)vs3.62mm/(s*100g)±0.38mm/(s*100g);PGE1股:3.96mm/(s*100g)±0.56mm/(s*100g),4.18mm/(s*100g)±0.50mm/(s*100g)vs3.63mm/(s*100g)±0.47mm/(s*100g),P<0.0001;NG门:2.93mm/(s*100g)±0.22mm/(s*100g),3.13mm/(s*100g)±0.21mm/(s*100g)vs3.70mm/(s*100g)±0.48mm/(s*100g);PGE1门:3.65mmmm/(s*100g)±0.22mm/(s*100g),3.36mm/(s*100g)±0.21mm/(s*100g)vs3.84mm/(s*100g)±0.19mm/(s*100g),P<0.001].结论:硝酸甘油和前列腺素E1可以明显增加经门静脉入肝血流量,但门静脉直接注药方式并不优于股静脉注药方式.To compare the effects ot temoral versus portal vein administration of vasodilators on portal hemodynamics in rats with liver cirrhosis.METHODS: Forty-two male Wistar rats with liver cirrhosis induced with carbon tetrachloride and alcohol were divided randomly and equally into six groups, which underwent femoral or portal vein injection of nitroglycerol (NG), pros- taglandin E1 (PGE1) or isotonic sodium chloride (NaCI), respectively. Hemodynamic parameters, including portal vein diameter (PVD), portal flow rate (PFR) and portal vein inflow (PVF), were measured after drug injection. RESULTS: There were no significant differences in PVD, PVF and PFR between rats undergoing femoral and portal vein injection of NaC1 (P = 0.1742, 0.2372 and 0.6566). PVD was increased significantly in cirrhotic rats that were given vasodilator agents, however, there were no significant differences in PVD changes between rats undergoing portal and femoral vein administration (P = 0.0516 and 0.1225). PVF was less increased in rats under- going portal vein administration of NG and PGE1 than in those undergoing femoral vein administration of NG and PGE1 (P 〈 0.0001). Comparing with pre-injection, PFR increased in rats undergoing femoral vein administra- tion of NG and PGEυ, but decreased in rats un- dergoing portal vein administration NG and PGE1 after dosed 10, 20 min [NGf: 4.98 rnm/(s . 100 g) +- 0.62 mm/(s,100 g), 4.31 mm/(s,100 g) +- 0.46 mm/(s.100 g) vs 3.62 mm/(s.100 g) +- 0.38 mm/(s.100 g); PGE1f: 3.96 mm/(s.100 g) + 0.56 mm/(s.100 g), 4.18 mm/(s.100 g) + 0.50 mm/(s.100 g) vs 3.63 mm/(s;100 g) + 0.47 mm/(s.100 g) P 〈 0.0001; NGp: 2.93 mm/(s. 100 g) + 0.22 mm/(s.100 g), 3.13 mm/(s.100 g) + 0.21 mm/(s.100 g) vs 3.70 mm/(s.100 g) +- 0.48 mm/(s.100 g); PGE1p: 3.65 mm mm/(s. 100 g) + 0.22 mm/(s.100 g), 3.36 mm/(s.100 g) + 0.21 mm/(s.100 g) vs 3.84 mm/(s.100 g) + 0.19 mm/�
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