CHARACTERIZATION OF THE MICROVASCULAR GLYCOCALYX IN NORMAL AND INJURED SPINAL-CORD IN THE RAT

Citation
Lj. Noble et al., CHARACTERIZATION OF THE MICROVASCULAR GLYCOCALYX IN NORMAL AND INJURED SPINAL-CORD IN THE RAT, Journal of comparative neurology, 376(4), 1996, pp. 542-556
Citations number
41
Categorie Soggetti
Neurosciences
ISSN journal
00219967
Volume
376
Issue
4
Year of publication
1996
Pages
542 - 556
Database
ISI
SICI code
0021-9967(1996)376:4<542:COTMGI>2.0.ZU;2-K
Abstract
The glycocalyx of microvasculature in normal and injured spinal cord w as characterized by using cationized ferritin to define anionic sites and the lectins concanavalin agglutinin (Con A) and Ricinus communis a gglutinin I (RCA) to delineate carbohydrate moities. Binding of cation ized ferritin was evaluated at the ultrastructural level in control an imals and at 3 hours after spinal cord injury. Horseradish peroxidase (HRP) was administered intravenously before euthanasia. In control spi nal cord, there was continuous even binding of cationized ferritin alo ng the luminal front of microvasculature and no evidence of barrier pe rmeability to HRP. After spinal cord injury, there was a reduction in binding of cationized ferritin in those regions of spinal cord that ex hibited barrier breakdown to HRP. Lectin binding in the spinal cord wa s evaluated at 3 hours and 3 days postinjury. At the light microscopic level, there appeared to be increased binding of Con A and RCA in mic rovessels by 3 days postinjury as compared with the control spinal cor d. At the ultrastructural level, a significant increase in RCA binding was noted along luminal fronts in the injured spinal cord. This incre ased binding coincided with a significant elaboration of the endotheli al glycocalyx. These findings demonstrate that the charge, structure, and carbohydrate composition of the endothelial glycocalyx in microves sels in the spinal cord may be dramatically altered after spinal cord injury. Furthermore, there is an association between the loss of charg e and disruption of the barrier, suggesting that anionic sites may con tribute to maintenance of the blood-spinal cord barrier. (C) 1996 Wile y-Liss, Inc.