门静脉高压犬肝缺血再灌注时肺循环血液动力学及NO／ET和PGI2／TXA2的变化

Changes in pulmonary hemodynamics and pulmonary circulation NO/ET and PGI2/TXA2 during liver ischemia-reperfusion in portal hypertension canines

目的评价门静脉高压犬肝缺血再灌注时肺循环血液动力学及肺循环一氧化氮（NO）／内皮素（ET）和前列腺素I2（PG12）／血栓素A2（TXA2）的变化。方法健康家犬12只，雌雄不拘，体重10-18kg，随机分为2组（n=6）：对照组和模型组。模型组采用部分结扎门静脉的方法建立犬门静脉高压模型，12周后完全阻断门静脉、肝后下腔静脉30min，再灌注60min制备肝缺血再灌注模型。于第2次麻醉后即刻、肝缺血前即刻、缺血5、30min、再灌注前即刻、再灌注5、10、15、30和60min（T1-10）时记录心率（HR）、心输出量（CO）、中心静脉压（CVP）、肺动脉楔压（PAWP）和平均肺动脉压（MPAP），计算心脏指数（CI）、肺血管阻力（PVR）和肺血管阻力指数（PVRI），并计算T2。时CI、CVP、MPAP、PAWP和PVRI相对于T1的变化幅度；于T2、T4和T9时测定肺动脉血浆NO、ET、IXA2和PGI2的浓度，并计算NO／ET和PGI2／TXA2比值。结果两组肝缺血时CI、CVP、PVRI、PAWP和MPAP均降低，且模型组CI、CVP、PAWP、MPAP降低幅度低于对照组，两组再灌注时CVP、PAWP、MPAP和PVRI均升高，且模型组PAWP和PVRI升高幅度高于对照组（P〈0．05或0．01）；模型组肝缺血再灌注时肺动脉血浆NO浓度、NO／ET比值和肝缺血时肺动脉血浆TXA2浓度、PGIdTX＆比值均低于对照组（P〈0．01）。模型组PVR与肺动脉血浆NO浓度呈负相关（r=-0．567，P〈0．05）。结论门静脉高压犬肝缺血再灌注时肺动脉压升高，可能与肺循环NO水平降低、NO与ET失衡有关。

Objective To investigate the changes in pulmonary hemodynamics and pulmonary circulation NO/ET and PGI2/TXA2 during liver ischemia-reperfusion （I/R） in portal hypertension canines. Methods Twelve healthy canines of both Sexes weighing 10-18 kg were randomly divided into 2 groups （ n = 6 each） ： control group and model group. Anesthesia was performed with iv injection of pentobarbital sodium 30 mg/kg. Portal hypertension was produced by partial ligation of portal vein in model group. Portal vein was isolated but not ligated in control group. Twelve weeks later, I/R was produced by complete ligation of portal vein and post-hepatic inferior vena cava for 30 min followed by 60 min reperfusion. HR, CO, CVP, MPAP and PAWP were recorded immediately before the second anesthesia, immediately before ischemia, at 5 and 30 min of ischemia, immediately before reperfusion and at 5, 10, 15, 30 and 60 min of reperfusion （T1-10） . CI, PVR and PVRI were calculated. The change degree of CI, CVP, MPAP, PAWP and PVRI relative to those levels at T1 were also calculated at T2-10Blood samples were obtained from pulmonary artery at T2 , T4 and T9 to measure the concentrations of NO, ET,TXA2 and PGI2 in plasma and the ratios of NO/ET and PGI2/TXA2 were also calculated. Results CI, CVP and PVRI, PAWP and MPAP were significantly decreased during ischemia in both groups and the decreased degree was significantly lower in model group than in control group （ P 〈 0.05 or 0.01 ）. CVP, PAWP, MPAP and PVRI were significantly increased during reperfusion and the decreased degree of PAWP and PVRI were significantly higher in model group than in control group （P 〈 0.05 or 0.01 ）. The plasma NO concentration and＇ NO/ET ratio during reperfusion, and plasma TXA2 concentration and PGI2/TXA2 ratio during ischemia were significantly lower in model group than in control group （ P 〈 0.01 ）. Conclusion The pulmonary artery pressure increases during liver I/R in portal hypertension canines, and it may be relates to the decrease in pulmonary circulation NO level and the imbalance of NO and ET.