吸入一氧化氮对犬肺血栓栓塞症再灌注后血气及血流动力学的影响

目的 建立血栓栓塞1周的犬肺栓塞(PTE)模型,观察吸入20 ppm一氧化氮(NO)对取栓再灌注后血气及血流动力学的影响并探讨其可能的机制.方法 对该PTE犬模型行取栓术,观察再灌注0、2、4、6 h后生命体征、血气变化,通过漂浮导管监测肺血流动力学的变化,再灌注6 h后肺泡灌洗液(BALF)中的白蛋白含量(g/L)、肺组织湿干重比值(W/D)、肺泡腔多核中性粒细胞(PMN)数.结果再灌注2 h后与再灌注前比较(下同)平均肺动脉压(MPAP)升高[(3.20±0.53)kPa对(2.27±0.67)kPa,F=63,P=0.02],再灌注6 h后,心率增快最明显[(175±8)次/min对(155±5)次/min,F=38.72,P=0.01],氧合指数下降(41.70±8.04对54.71±3.78,F=48.36,P=0.03);再灌注后2 h,吸入NO组与再灌注组(下同)比较MPAP降低((2.53±0.40)kPa对(3.20±0.53)kPa,F=55,P=0.04],4 h,氧合指数有升高趋势(49.17±7.37对39.71±7.31,F=2.36,P=0.11),再灌注后2、4、6 h,吸入NO组肺血管阻力较再灌注组也有减小趋势(F=1.49,P=0.26),6 h后吸入NO组肺泡腔PMN数低于再灌注组[(19±6)个/10 HPF对(31±11)个/10 HPF,F=98,P=0.01]. 结论 血栓栓塞1周的PTE犬模型再灌注后导致了肺再灌注损伤,再灌注不同时间点对肺组织损伤程度不一.吸入20 ppm NO可降低PTE再灌注损伤导致的升高的肺动脉压,减少PMN向肺组织的迁移而减轻再灌注损伤,可能减轻肺微血管渗漏.

Effects of an inhaled nitric oxide on blood gas and hemodynamic parameters after reperfusion in canine model mimicking chronic thromboembolism

Objective To establish a canine model with pulmonary thromboembolism(PTE) of selective lobar pulmonary artery embolization mimicking chronic thromboembolism, to assess the effects of an inhaled nitric oxide (NO) 20 ppm on vital signs, blood gas, hemodynamic parameters and neutrophils in the alveolar of the canine model. Methods Twenty canines were divided into four groups: group 1: sham group (n=5); group 2; ischemic lung group (PTE group without embolectomy, n=5); group 3; reperfusion lung group (PTE group with embolectomy, n=5); group 4: reperfusion lung group with inhaled NO (PTE group inhaled 20 ppm NO after embolectomy, n=5). And central venous pressure (CVP), mean pulmonary arterial pressure (MPAP), pulmonary arterial wedge pressure (PAWP) and carbon monoxide (CO) were recorded, pulmonary vascular resistance (PVR) was also calculated. Vital signs, blood gases were measured before embolectomy and at 2, 4, 6 hours after the operation. Albumin in bronchoalveolar lavage fluid (BALF) was measured by chromatometry of Coomassie brilliant blue. Lung wet to dry weight ratio(W/D) was also measured. Lung tissue pathology and alveolar PMN in the left lower lobar were observed by optical microscopy. Results MPAP increased significantly at 2 hours after reperfusion [(3. 20±0.53)kPa vs. (2. 27±0. 67)kPa,F=63,P=0.02]; At 6 hours after reperfusion as compared with baseline,HR increased significantly [(175±8) beats/min vs. (155±5) beats/min, F=38.72, P=0.01],PaO_2/FiO_2 also decreased significantly (41.70±8.04 vs. 54.71±3.78,F=48.36,P=0.03). MPAP decreased significantly in group 4 as compared with group 3 at 2 hours after reperfusion [(2.53±0.4)kPa vs. (3. 20±0. 53)kPa,F=55,P=0.04]. At 4 hours after reperfusion,PaO_2/FiO_2 raised in group 4,but there was no significant difference as compared with group 3 (49.17±7.37 vs. 39.71±7.31, F=2.36, P=0. 11). The quantities of alveolar PMN infiltration in group 4 decreased significantly as compared with group 3 (19±6/10 HPF vs. 31±11/10 HPF, F=98, P=0.01).Conclusions Lung ischemia-reperfusion injury can be induced by embolectomy from lower pulmonary artery in the PTE model embolized for one week. An inhaled NO 20 ppm can decrease the elevated pulmonary artery pressure induced by ischemia-reperfusion injury and may alleviate the injury by reducing the PMN immigration into the alveoli.