Cortical hypoperfusion after global forebrain ischemia in rats is not caused by microvascular leukocyte plugging.

作者：Ulrich Dirnagl, Koki Niwa, Gabriele Johanna Sixt, Arno Villringer · 发表于：Stroke · 年份：1994 · DOI：10.1161/01.str.25.5.1028 · 被引用次数：70 · 研究领域：Neurological Disease Mechanisms and Treatments、Neuroinflammation and Neurodegeneration Mechanisms、Neonatal and fetal brain pathology

BACKGROUND AND PURPOSE: We tested the hypothesis that cerebral hypoperfusion after experimental global cerebral ischemia is caused by plugging of the microcirculation with activated leukocytes using in vivo microscopic observation of the behavior of leukocytes in the cortical microcirculation during the transition from postischemic hyperperfusion to hypoperfusion. METHODS: Anesthetized and ventilated rats (n = 24) were equipped with a closed cranial window. Physiological variables and cortical regional cerebral blood flow (laser-Doppler flowmetry) were measured continuously. Leukocytes were labeled intravitally with rhodamine 6G and visualized in the microcirculation of the brain surface and outer layers of the cortex with confocal laser scanning microscopy from preischemia to 4 hours after reperfusion that followed 10 minutes of global cerebral ischemia (rCBF < 10% of control). RESULTS: In controls (n = 8), there were no signs of leukocyte activation over the 4-hour observation period. In ischemic rats (n = 16), during the transition from hyperperfusion to hypoperfusion there was no change in the behavior of leukocytes. Most notably, no capillary pluggers were seen. In the postischemic period only a slight increase of the number of leukocytes rolling along or sticking to the venular endothelium was seen, and very few capillaries were plugged by leukocytes. Extravasation of leukocytes into the brain tissue was observed in 8 rats beginning 2 hours after ischemia with a variabl...