No abstract

Pulmonary surfactant facilitates breathing by reducing the surface tension at the air/liquid interface. We examined the effect of experimental lung transplantation on the phospholipid pool sizes of alveolar surfactant large and small aggregates, the composition of the large aggregates, the surface tension-reducing ability of lipid extract surfactant, and the leakage of serum proteins into the lung. A double-lung block from the donor animal was stored for 2 or 12 h after perfusion with either Euro-Collins solution or University of Wisconsin solution. The right donor lung was lavaged immediately after the storage period to determine the effects of storage on pulmonary surfactant. The left donor lung was transplanted. The recipient animal, containing its own native right lung and the transplanted left lung, was reperfused for 6 h. After the reperfusion period, the transplanted left lung and the native right lung were lavaged. After an ischemic time of 12 h, impaired gas exchange was observed in the transplanted lung as well as the native lung during the 6 h of reperfusion. This impaired gas exchange was associated with several significant changes in pulmonary surfactant: (1) total serum protein in the lung lavage was increased, (2) the small to large surfactant aggregate ratio was increased, (3) sphingomyelin content was increased and phosphatidylglycerol content was decreased in large aggregates, and (4) the surfactant-associated protein A content was decreased in large aggregates. No significant differences were observed between the results obtained with Euro-Collins and University of Wisconsin solutions.(ABSTRACT TRUNCATED AT 250 WORDS)

Changes in the surfactant system have been observed in patients with acute respiratory distress syndrome (ARDS). These alterations in surfactant are thought to contribute to lung dysfunction in this disease. In this report we describe the changes in surfactant subfractions in bronchoalveolar wash obtained from five patients with established ARDS compared with five non-ARDS patients. Our results show that, in addition to the changes in surfactant composition and yield reported previously, the ratio of small to large surfactant aggregates is significantly increased in patients with ARDS compared with non-ARDS patients (0.48 +/- 0.09 versus 0.20 +/- 0.05 respectively [p < 0.05]). This increased ratio was associated with a decreased level of SP-A in the large aggregate fraction. We suggest that this increased ratio represents a marker for surfactant alterations in ARDS that is independent of lavage technique and can be measured in a very small surfactant sample.

Sepsis is the most common factor leading to the acute respiratory distress syndrome (ARDS) and is associated with the highest mortality rate. It has been suggested that the pulmonary surfactant system is altered and contributes to the lung dysfunction associated with ARDS. The objective of this study was to characterize the lung injury, specifically the endogenous surfactant system in septic adult rats. Sepsis was induced in male Sprague-Dawley rats by cecal ligation and perforation and resulted in significant increases in heart rates, respiratory rates, and lactate levels along with positive blood cultures in septic animals compared with a sham control group. Two distinct septic groups were developed, a septic group and a sepsis with lung injury (septic+LI) group. The septic group had no significant differences in oxygenation compared with the sham group, whereas the septic+LI group had significantly lower PaO2 and higher A-a gradient values compared to both the sham and septic groups. The total surfactant pool size was significantly lower in the septic+LI group compared with the sham group. The small surfactant aggregate to large surfactant aggregate ratio was significantly lower in the septic group and was further reduced in the septic+LI group. There were also significantly higher levels of surfactant protein A (SP-A) in both septic and septic+LI groups compared to the sham group. These results demonstrated that the endogenous surfactant system was altered in systemic sepsis without lung dysfunction and is further altered when a lung injury is present.