Effect Oxygen in Inflation Gas for Warm Ischemia-reperfusion Injury in the Lung of a Mongrel Dog

황견에서 폐장의 산소가 온열 허혈후 재관류 시폐손상에 미치는 영향

  • 성숙환 (서울대학교병원 흉부과) ;
  • 김현조 (서울대학병원 흉보외과) ;
  • 김영태 (서울대학교 병원 흉부외과)
  • Published : 2000.02.01

Abstract

Background: Hyperinflation during lung ischemia has been known to improve pulmonary functions after reperfusion which may be exerted through a pulmonary vasodilation and avoidance of atelectasis by an increased surfactant release and been known whether the improvement of pulmonary function was the effect of hyperinflation itself or the oxygen content in inflation gas. Therefore we attempted to clarify the effect of hyperinflation with oxygen in pulmonary inflation gas during warm ischemia on pulmonary function after reperfusion to solve the problem of ischemia-reperfusion injury after lung transplantation. Material and Method: sixteen mongrel dogs were randomly divided into two groups: the left lung was inflated to 30-35 cm H2O with 100% oxygen in oxygen group and 100% nitrogen in nitrogen group. The inflated left lung was maintained with warm ischemia for 100 minutes. Arterial and mixed venous blood gas analysis and hemodynamics were measured before ischemia and 30, 60, 120, 180 and 240 minutes afer reperfusion. Lung biopsy was taken for the measurement of lung water content after the end of reperfusion. Result: In oxygen group arterial oxygen tension the difference of arterial and mixed venous oxygen tension and the difference of alveolar-arterial oxygen tension at 30-minute after reperfusion were not significantly different from those before ischemia and were stable during the 40hour reperfusion. However in nitrogen group these values were significantly deteriorated at 30-minute after reperfusion. there was no significant difference between two groups in hemodynamic data peak airway pressure and lung water content. Conclusion : The results indicated that the oxygenation one of the most important pulmonary functions was improved by pulmonary inflation with 100% oxygen during warm ischemia but the hemodynamics were not. Oxygen as a metabolic substrate during warm ischenia was believed to make the pulmonary tissues to maintain aerobic metabolism and to prevent ischemic damage of alveoli and pulmonary capillary.

Keywords

References

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