[Ultrastructural morphological changes of cortical microvessels following transient cerebral ischemia--a transmission...

Post-ischemic hypoperfusion may play a significant role in reperfusion injury. Since there is no established treatment for hypoperfusion, however we decided to explore the morphological cause of post-ischemic hypoperfusion. In this study we used transmission electron microscopy to investigate the capillaries in ischemic/reperfused neocortex induced by 2 hours of middle cerebral artery occlusion followed by either 3 or 24 hours of reperfusion in 14 cats. Post-ischemic hypoperfusion was confirmed by measuring regional blood flow through a cranial window just above the left ectosylvian gyrus, which has poor anastomosis. A greater number of endothelial microvilli and capillary endothelial cell swelling were detected in the ischemic/reperfused neocortex, when compared with contralateral control neocortex. Especially after 24-hour reperfusion, collapse of some capillaries was observed with severe perivascular glial swelling and adhesion of PMN leukocytes to the endothelium. These findings yielded the following statistically significant results. 1) The number of endothelial microvilli in the ischemic/reperfused neocortex (mean +/- SD/1 blood vessel = 6.58 +/- 4.32) was significantly greater than in the control neocortex (3.13 +/- 2.68, p = 0.0001). 2) The ratio of capillary inner diameter (ID) to outer diameter (OD) in the ischemic/reperfused neocortex (ID/OD%, mean +/- SD = 75.4 +/- 16.7) was significantly smaller than in the control neocortex (89.2 +/- 10.8, p = 0.0001), indicating endothelial cell swelling. We concluded that these ultrastructural changes might be the cause of the multifactorial development of post-ischemic hypoperfusion, and that especially the number of endothelial microvilli and the endothelial cell swelling ratio might serve as morphological indicators of therapeutic efficacy for reperfusion injury in experimental studies.