開心術後肺虚血再濯流障害に対する一酸化窒素(NO)吸入療法の確立

方法：14只麻醉杂种犬机械通气。在通过左肺门夹闭造成左肺缺血90分钟后，通过左肺门的松开和对侧肺门的夹闭实现同侧肺再灌注150分钟，使得所有的灌注和通气仅由左肺支持。7只犬在再灌注期间吸入30 ppm NO（组1）。另7只犬在无NO的情况下通气（组2）。分析实验结束时血流动力学参数、血气、左心房血超氧化物歧化酶（SOD）活性、过氧化脂质含量以及左肺湿/干比。结果;再灌注后即刻，组1的肺动脉收缩压显著降低（27.6± 4.5）mmHg对（44.3± 6.3）mmHg（P <0.05）。在第1组中还观察到肺血管阻力和右心室舒张末期压的显著改善。再灌注15分钟后，第2组SOD活性下降至缺血前的41%。另一方面，在组1中，在再灌注期间未观察到任何显著降低。左肺湿/干比在第1组显著降低（4.72± 0.36vs5.47 ± 0.52，p <0.05）。

Method; Fourteen anesthetized mongrel dogs were mechanically ventilated. After 90 min. of the left lung ischemia by the left hilum clamping, the same side lung reperfusion for 150 min. was achieved by declamping of the left hilum and clamping of the opposite side hilum so that all the perfusion and ventilation was supported only by the left lung. Seven dogs inhaled 30ppm NO during reperfusion (Group 1). The other seven dogs were ventilated without NO (Group 2). Hemodynamic parameters, blood gas, superoxide dismutase(SOD)activity and lipid peroxide content in the left atrial blood and the left lung wet/dry ratio at the end of the experiment were analysed.Results; Immediately after reperfusion, systolic pulmonary arterial pressure was significantly lower in Group 1(27.6±4.5mmHg vs 44.3±6.3mmHg,p<0.05).This significant reduction of The pulmonary blood pressure continued throughout reperfusion. Significant improvement was also observed in Group 1 on pulmonary vascular resistance and right ventricular enddiastolic pressure. SOD activity 15 min. after reperfusion in Group 2 droped to 41% of pre-ischemic value. On the other hand, in Group 1, any significant decrease was not observed during reperfusion. Left lung wet / dry ratio was significantly lower in Group 1(4.72±0.36 vs 5.47±0.52,p<0.05).