Okuda M, Furuhashi K, Nakai Y, Muneyuki M
Department of Anaesthesiology, Mie University School of Medicine, Japan.
Scand J Clin Lab Invest. 1993 Oct;53(6):625-31.
Using isolated perfusion rat lung model, we studied the effect of continuous ventilation without perfusion and allopurinol on the development of ischaemia-reperfusion lung injury. Ischaemia was induced by stopping the perfusion. Normothermic ischaemia for 90 min without ventilation caused significant lung oedema. Continuous ventilation during ischaemia with 21% O2 decreased lung oedema significantly after 60 min of reperfusion. The same protection could be achieved by 100% N2 ventilation during 90 min of ischaemia, suggesting that xanthine oxidase (XO) is unlikely to cause the ischaemia-reperfusion lung injury. On the other hand allopurinol, XO inhibitor, equally inhibited lung oedema after 90 min of ischaemia and 60 min of reperfusion. These results indicate that mechanical movement of alveoli provides successful preservation of ischaemic lung, and allopurinol has some protective effect other than XO inhibition.
利用离体灌注大鼠肺模型,我们研究了无灌注持续通气和别嘌呤醇对缺血再灌注肺损伤发展的影响。通过停止灌注诱导缺血。在无通气情况下进行90分钟的常温缺血导致显著的肺水肿。在缺血期间用21%氧气持续通气,在再灌注60分钟后显著减轻了肺水肿。在90分钟缺血期间用100%氮气通气也能达到同样的保护效果,这表明黄嘌呤氧化酶(XO)不太可能导致缺血再灌注肺损伤。另一方面,XO抑制剂别嘌呤醇在缺血90分钟和再灌注60分钟后同样抑制了肺水肿。这些结果表明,肺泡的机械运动成功地保护了缺血肺,并且别嘌呤醇除了抑制XO外还有一些保护作用。