Local blood-brain barrier damage, cerebral edema, and cell injury during reperfusion after 2 hours of focal cerebral ischemia

Reperfusion injury is likely to involve a variety of processes. The proposition that such injury and such processes vary among brain areas was tested with a rat model of 2 h of middle cerebral artery occlusion plus reperfusion. Local cerebral blood flow (lCBF), blood-brain barrier (BBB) permeability, and edema flow were measured by quantitative autoradiography and laser scanning confocal microscopy (LSCM). Tissue injury was assessed by histopathology and electron microscopy. lCBF varied widely among brain areas during reperfusion and was very high in the caudate-putamen (hyperperfusion). As indicated by alpha -aminoisobutyric acid (AIB), the BBB was open throughout the preoptic area after Ih of reperfusion. A few small foci of AIB leakage were seen in the caudate-putamen at 4 h. Albumin was seen by LSCM to leak from postcapillary venules. Later the BBB opening expanded over the entire striatum and into the cortex. Tissue swelling began in the caudate-putamen, where lCBF was high, after 1.0 h of reperfusion. Tissue damage varied broadly among areas, differing in cell type, ultrastructure, and pattern (scattered versus widespread). This diversity in blood flow BBB permeability, edema, and tissue damage indicates the complexity of reperfusion injury.