期刊
JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY
卷 75, 期 7, 页码 673-688出版社
OXFORD UNIV PRESS INC
DOI: 10.1093/jnen/nlw040
关键词
Astrocytes; Autophagosomes; Blood-spinal cord barrier (BSCB); Middle cerebral artery occlusion (MCAO); Stroke; Subacute and chronic diaschisis; Tract demyelination
资金
- Center for Excellence and Brain Repair, Department of Neurosurgery and Brain Repair at the University of South Florida
We previously demonstrated blood-brain harrier impairment in remote contralateral brain areas in rats at 7 and 30 days alter transient middle cerebral artery occlusion (tMCAO), indicating ischemic diaschisis. Here, we focused on effects of subacute and chronic focal cerebral ischemia on the blood-spinal cord barrier (BSCB). We observed BSCB damage on both sides of the cervical spinal cord in rats at 7 and 30 days post-tMCAO. Major BSCB ultrastructural changes in spinal cord gray and white matter included vacuolated endothelial cells containing autophagosomes, pericyte degeneration with enlarged mitochondria, astrocyte end-feet degeneration and perivascular edema; damaged motor neurons, swollen axons with unraveled myelin in ascending and descending tracts and astrogliosis were also observed. Evans Blue dye extravasation was maximal at 7 days. There was immunofluorescence evidence of reduction of microvascular expression of tight junction occludin, upregulation of Beclin-1 and LC3B immunoreactivities at 7 days and a reduction of the latter at 30 days post-ischemia. These novel pathological alterations on the cervical spinal cord microvasculature in rats after tMCAO suggest pervasive and long-lasting BSCB damage after focal cerebral ischemia, and that spinal cord ischemic diaschisis should be considered in the pathophysiology and therapeutic approaches in patients with ischemic cerebral infarction.
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