Abstract
Background: Acute respiratory distress syndrome (ARDS) is a severe inflammatory condition. Our earlier studies have characterized oleic acid (OA)-induced rat model of ARDS which was exacerbated by indomethacin (prostaglandin [PG] synthesis inhibitor).

Aim and Objectives: The role of PGs in ARDS is ill defined as the results of earlier studies are conflicting. This study was undertaken to determine the effect of PGE1 analog (misoprostol) in indomethacin-induced exacerbation of ARDS in rats.

Materials and Methods: The rats were anesthetized with urethane. Tracheal and jugular vein cannulation was done to keep the respiratory tract patent and deliver drugs, respectively. Respiratory excursions were recorded with the help of force displacement transducer. Cannulated carotid artery was connected to pressure transducer for recording of blood pressure. Electrocardiographic potentials were recorded by needle electrodes. Animals were divided into four groups. In Group I, OA (75 μl) was used to induce ARDS in rats. In Group II, OA was injected in indomethacinpretreated rats. In Group III (control group), animals were treated with ethanol. In Group IV, OA was administered after indomethacin + misoprostol pretreatment. Misoprostol treatment was repeated after OA injection at 20 min interval. Cardiorespiratory parameters (respiratory frequency, heart rate, mean arterial pressure, and pulmonary water content) were determined, and histological examination of the lung was done in all groups.

Results: Indomethacin pretreatment drastically advanced the OA-induced ARDS. Misoprostol protected against the deterioration as indicated by improvement in all the parameters and increase in survival time.

Conclusion: Results of this study indicate that PGs have protective role in ARDS.

Key words: Acute Respiratory Distress Syndrome; Prostaglandins; Oleic Acid; Prostaglandin E1 Analog