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。90分钟后。左肺缺血后夹闭左肺门，同侧肺再灌流150min。通过去夹左侧肺门，夹闭对侧肺门，使所有的灌流和呼吸仅由左肺支持。7只犬在再灌流期间吸入30ppm NO(第1组)。其余7只犬在无NO的情况下呼吸(第2组)。结果：再灌流即刻，第1组大鼠的肺动脉收缩压显著降低(27.6±4.5 mm Hgvs44.3±6.3 mm Hg，p&lt；0.05)，并持续至再灌流结束。第1组肺血管阻力和右室舒张压也有明显改善。超氧化物歧化酶活性15min。再灌流后，第2组降至缺血前的41%。另一方面，组1在再灌流期间没有观察到任何明显的下降。左肺湿/干比值显著低于对照组(4.72±0.36vs5.47±0.52，p&lt；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).