EFFECT OF TRANSIENT FOCAL ISCHEMIA ON BLOOD-BRAIN-BARRIER PERMEABILITY IN THE RAT - CORRELATION TO CELL INJURY

Prolonged ischemia is known to damage the blood-brain barrier, causing an increase in vascular permeability to proteins. We studied the time course of extravasation of endogenous albumin in rats after I and 2 h of middle cerebral artery (MCA) occlusion followed by 6, 12, and 24 h of recirculation. In a separate group of rats that had undergone 1 h of MCA occlusion and 6 h of recirculation, influx of [C-14]aminoisobut yric acid (AIB) from blood to brain was also measured. After I h of oc clusion followed by 6 h of recirculation, neuronal damage was evident in caudoputamen, but there were no signs of blood-brain barrier leakag e to either AIB or albumin, At 12 h. the caudoputamen contained extrav asated albumin, and a; 24 h extravasation was extended to the somatose nsory cortex. Animals subjected to 2 h of MCA occlusion showed albumin extravasation in caudoputamen already al. 6 h of recirculation, and a t 12 and 24 It albumin was abundant in the major part of the right hem isphere, This study suggests that damage to neurons precedes leakage o f the blood-brain barrier. Even a relatively short period of ischemia such as 1 h will result in markedly increased vascular permeability. H owever, a longer transient ischemic insult disrupts the blood-brain ba rrier earlier than a shorter one.