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J Thorac Cardiovasc Surg 1997;114:332-338
© 1997 Mosby, Inc.

CARDIAC AND PULMONARY REPLACEMENT

INFLUENCE OF OXYGEN IN INFLATION GAS DURING LUNG ISCHEMIA ON ISCHEMIA-REPERFUSION INJURY

Received for publication August 23, 1996; revisions requested Dec. 23, 1996; revisions received April 22, 1997; accepted for publication April 22, 1997. Address for reprints: Atsushi Watanabe, MD, The Second Department of Surgery, Sapporo Medical University School of Medicine and Hospital, South 1, West 16, Chuo-ku, Sapporo 060, Japan.

Abstract

Objectives: Previous studies have reported that hyperinflation during lung ischemia improves pulmonary function after reperfusion. However, it has not been clarified whether hyperinflation itself or oxygen in inflation gas causes good pulmonary function. The aim of this study is to evaluate the effect of oxygen in pulmonary inflation gas during lung ischemia on ischemia-reperfusion injury. Methods: Twenty-one mongrel dogs were randomly divided into three groups: the lung during a 90-minute period of warm ischemia was inflated to 30 cm H₂O with 100% oxygen in group A and 100% nitrogen in group B; it was not inflated in group C. Pulmonary function and hemodynamics were measured before ischemia and 1,2, and 3 hours after reperfusion. Total protein and phosphorous of phospholipid in bronchoalveolar lavage fluid were measured 210 minutes after reperfusion. Results: No significant differences in pulmonary function and hemodynamics were noted between group A and group B, but these two groups had significantly better pulmonary function and hemodynamics than group C. No significant differences were detected in the concentrations of total protein and phosphorus of phospholipids in bronchoalveolar lavage fluid and in adenine nucleotide levels of lung tissue after reperfusion among the three groups. Conclusions: The results indicate that pulmonary inflation during warm ischemia improves pulmonary function and hemodynamics after reperfusion in this model. The effect is caused by inflation itself and is not due to oxygen as a metabolic substrate during warm ischemia.

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