Ontology highlight
ABSTRACT: Objective
Treatment of relapses in multiple sclerosis (MS) has not advanced beyond steroid use, which reduces acute loss of function, but has little effect on residual disability. Acute loss of function in an MS model (experimental autoimmune encephalomyelitis [EAE]) is partly due to central nervous system (CNS) hypoxia, and function can promptly improve upon breathing oxygen. Here, we investigate the cause of the hypoxia and whether it is due to a deficit in oxygen supply arising from impaired vascular perfusion. We also explore whether the CNS-selective vasodilating agent, nimodipine, may provide a therapy to restore function, and protect from demyelination in 2 MS models.Methods
A variety of methods have been used to measure basic cardiovascular physiology, spinal oxygen
SUBMITTER: Desai RA
PROVIDER: S-EPMC7737229 | biostudies-literature | 2020 Jul
REPOSITORIES: biostudies-literature