Suzuki T, Fukuda T, Inoue Y, Aki A, Cho Y
Department of Cardiovascular Surgery, Tokyo Metropolitan Children's Hospital, Japan.
Nihon Kyobu Geka Gakkai Zasshi. 1997 Jan;45(1):31-6.
The oxygen free radicals and the interaction between neutrophils and endothelium have been implicated in the pathogenesis of lung injury associated with cardiopulmonary bypass (CPB), and in the setting of total CPB, the ischemia-reperfusion injury has been suspected as the mechanism of lung injury. To prevent this reperfusion induced lung injury, we performed continuous pulmonary perfusion during total CPB. We studied 26 infants less than 1 year of age who underwent patch closure of ventricular septal defect. Intermittent mechanical ventilation (5/min) and continuous perfusion of pulmonary artery (30 ml/kg/min) were performed during total CPB in 7 infants (Group P). Whereas 19 infants underwent ordinary CPB (Group N). PaO2/FiO2 ratio was employed for the predictor of lung injury and was calculated before and after CPB. PaO2/FiO2 ratio decreased from 3 to 12 hours after CPB and then increased by 24 hours after CPB in both groups. The lowest PaO2/FiO2 ratio measured at 12 hours after CPB correlated with age and body weight at operation (Spearman's correlation coefficient, 0.59; p = 0.01 and 0.61; p = 0.009, respectively) and strongly correlated with preoperative Rp/Rs ratio (-0.73; p = 0.003). PaO2/FiO2 ratio, however, did not correlate with duration of CPB and aortic cross clamping, preoperative Pp/Ps and Qp/Qs ratio in group N. PaO2/FiO2 ratio of group P at 3, 6, and 12 hours after CPB were higher than those of group N, although there were no significant difference When analysis was made on the infants with high pulmonary vascular resistance (preoperative Rp/Rs ratio > or = 0.1), PaO2/FiO2 ratio of group P (n = 6) at 3, 6 and 12 hours after CPB were higher than those of group N (n = 11), and the difference was statistically significant at 12 hours after CPB (291.1 +/- 15.5 versus 199.6 +/- 27.0, p = 0.027. These results implicate that young age, low body weight and especially high pulmonary vascular resistance were incremental risk factor of lung injury after CPB and, furthermore, ischemia reperfusion injury can be the initiating factor of lung injury. The results also suggest that continuous pulmonary perfusion during total CPB is an effective mean to prevent lung injury particularly for the infants with high pulmonary vascular resistance.
氧自由基以及中性粒细胞与内皮细胞之间的相互作用被认为与体外循环（CPB）相关的肺损伤发病机制有关，在全CPB情况下，缺血再灌注损伤被怀疑是肺损伤的机制。为预防这种再灌注诱导的肺损伤，我们在全CPB期间进行了持续肺灌注。我们研究了26例年龄小于1岁、接受室间隔缺损修补术的婴儿。7例婴儿（P组）在全CPB期间进行了间歇机械通气（5次/分钟）和肺动脉持续灌注（30毫升/千克/分钟）。而19例婴儿接受了普通CPB（N组）。采用PaO2/FiO2比值作为肺损伤的预测指标，并在CPB前后进行计算。两组在CPB后3至12小时PaO2/FiO2比值下降，然后在CPB后24小时升高。CPB后12小时测得的最低PaO2/FiO2比值与手术时的年龄和体重相关（Spearman相关系数分别为0.59；p = 0.01和0.61；p = 0.009），并与术前Rp/Rs比值密切相关（-0.73；p = 0.003）。然而，N组中PaO2/FiO2比值与CPB持续时间、主动脉阻断时间、术前Pp/Ps和Qp/Qs比值无关。CPB后3、6和12小时P组的PaO2/FiO2比值高于N组，尽管无显著差异。当对肺血管阻力高（术前Rp/Rs比值≥0.1）的婴儿进行分析时，CPB后3、6和12小时P组（n = 6）的PaO2/FiO2比值高于N组（n = 11），且在CPB后12小时差异有统计学意义（291.1±15.5对199.6±27.0，p = 0.027）。这些结果表明，年龄小、体重低，尤其是肺血管阻力高是CPB后肺损伤的增加危险因素，此外，缺血再灌注损伤可能是肺损伤的起始因素。结果还提示，全CPB期间持续肺灌注是预防肺损伤的有效手段，尤其对于肺血管阻力高的婴儿。
