Atelectasis during ischemia is associated with reperfusion injury (see accompanying abstract # 700337h). We hypothesized that this is either due to decreased surfactant production or its inactivation. In the present study we used an isolated perfused rat lung model to study the effect of pretreatment with surfactant on the development of reperfusion injury. 20 Sprague-Dawely rats (wt 300-350g) were divided into five groups (n=4), control and four experimental groups. Lung preparations underwent 15 minutes of equilibration followed by 75 minutes of ischemia and 30 minutes of reperfsion (perfused with modified Krebs-Hanseliet solution). The change in wet weight of the lung and the pulmonary artery pressure were continuously monitored. The permeability to125 I labeled albumin was measured at the end of reperfusion. The control lung preparations were continuously ventilated with 20% O2 and perfused for 105 minutes.The experimental groups were ventilated with 20% O2 prior to ischemia and during reperfusion. During ischemia they were treated as follows: Group I, ventilated with 20%O2; Group II, remained collapsed and unventilated; Group III, same as Group II but were pretreated with 4 ml/kg of surfactant intra-tracheally; Group IV, same as Group II but were pretreated with 4 ml/kg normal saline intra-tracheally. Results: Values are expressed as mean±SE,* denotes statistical significance at p<0.01. Surfactant treated lung preparations (Group III), remained isogravimetric, the albumin PS product and the peakΔP(peak rise in pulmonary artery pressure upon reperfusion) were similar to control. While saline treated lung preparations (Group IV) showed a four fold increase in both the wet weight and peakΔP, and fourteen fold increase in vascular permeability. Conclusions: 1) Reperfusion injury causes an increase in vascular permeability, resulting in increase in wet weight of the lung. 2)Pretreatment with surfactant protects against reperfusion injury. Table

Table 1 No caption available.
Full size table