Role of Mechanical Ventilation During Ischemia on the Development of Reperfusion Injury of the Lung † 1746

Reperfusion injury is an important factor in the pathogenesis of necrotizing enterocolitis and hypoxic ischemic encephalopathy. Similar etiology has also been implicated in the development of lung injury seen in bronchopulmonary dysplasia. We used an isolated perfused rat lung model to study the effect of continuous mechanical ventilation during ischemia on the development of reperfusion injury. Sixteen Sprague-Dawely rats (wt 300-350 grams) were divided four groups, one control and three experimental groups. Lung preparations underwent 15 minutes of equilibration followed by 75 minutes of ischemia and 30 minutes of reperfusion (perfused with modified Krebs-Henseliet solution). Reperfusion injury was quantified by continuously monitoring the change in wet weight of the lung and by measuring the permeability to ¹²⁵I labeled albumin at the end of reperfusion. Control lung preparations were continuously ventilated (20% O₂) and perfused for 105 minutes. The experimental groups were ventilated with 20% O₂ prior to ischemia and during reperfusion. These groups differed only in the ventilatory gas mixture used during ischemia. Group I, ventilated with 20%O₂; Group II, ventilated with 100% N₂; Group III, remained collapsed and unventilated. Results: Values are expressed as mean±SE, * denotes statistical significance (p<0.01). Lung preperations in Groups I and II remained isogravimeric and the albumin PS product was similar to control. Lung preparations in Group III (collapsed and unventilated) demonstrated injury as evidenced by a 1.5 fold increase in wet weight and 3 fold increase in albumin PS product. Conclusions: 1) Reperfusion injury causes an increase in vascular permeability, resulting in an increase in the wet weight of the lung. 2) Reperfusion injury occurs only when the lung is both ischemic and unventilated. 3) Continuous mechanical ventilation (irrespective of the gas mixture used) during ischemia protects against reperfusion injury. We speculate that this protection is as a result of maintaining alveolar stability during ischemia. Table

Table 1 No caption available.