Abstract
The effect of tranilast, an anti-releasing drug for slow reacting substance (SRS) on incomplete ischemia produced by a bilateral common carotid artery occlusion/recirculation model in the spontaneous hypertensive rat (SHR-SR) was investigated. Na+-K+ adenosinetriphosphatase (ATPase) activity in brain microvessels and brain parenchyma were measured separately. Na+-K+ ATPase activity in the microvessels was not influenced by tranilast treatment. Brain parenchymal Na+-K+ ATPase activity decreased progressively after recirculation. At 3 hours after recirculation, parenchymal Na+-K+ ATPase activity returned to the control level when treated by tranilast, and progressive decrease was observed in SHR-SR without tranilast treatment. Data suggest that the SRS produced in the brain parenchyma during ischemic insult was very important for production of brain edema. Tranilast might be very useful for the treatment of ischemic brain edema.
