title: Influence of exercise training on ischemic brain injury in type 1 diabetic rats.
abstract: While exercise training (ExT) appears to influence cerebrovascular function during type 1 diabetes (T1D), it is not clear whether this beneficial effect extends to protecting the brain from ischemia-induced brain injury. Thus our goal was to examine whether modest ExT could influence transient focal ischemia-induced brain injury along with nitric oxide synthase (NOS)-dependent dilation of cerebral (pial) arterioles during T1D. Sprague-Dawley rats were divided into four groups: nondiabetic sedentary, nondiabetic ExT, diabetic (streptozotocin; 50 mg/kg ip) sedentary, and diabetic ExT. In the first series of studies, we measured infarct volume in all groups of rats following right MCA occlusion for 2 h, followed by 24 h of reperfusion. In a second series of studies, a craniotomy was performed over the parietal cortex, and we measured responses of pial arterioles to an endothelial NOS (eNOS)-dependent, a neuronal NOS (nNOS)-dependent, and a NOS-independent agonist in all groups of rats. We found that sedentary diabetic rats had significantly larger total, cortical, and subcortical infarct volumes following ischemia-reperfusion than sedentary nondiabetic, nondiabetic ExT, and diabetic ExT rats. Infarct volumes were similar in sedentary nondiabetic, ExT nondiabetic, and ExT diabetic rats. In contrast, ExT did not alter infarct size in nondiabetic compared with sedentary nondiabetic rats. In addition, ExT diabetic rats had impaired eNOS- and nNOS-dependent, but not NOS-independent, vasodilation that was restored by ExT. Thus ExT of T1D rats lessened ischemic brain injury following middle cerebral artery occlusion and restored impaired eNOS- and nNOS-dependent vascular function. Since the incidence of ischemic stroke is increased during T1D, we suggest that our finding are significant in that modest ExT may be a viable preventative therapeutic approach to lessen ischemia-induced brain injury that may occur in T1D subjects.
authors.affiliation: Department of Cellular Biology and Anatomy and the Center of Excellence in Cardiovascular Diseases and Sciences, Louisiana State University Health Science Center-Shreveport, Shreveport, LA, USA.
authors.forename: Denise M
authors.initials: DM
authors.lastname: Arrick
authors.forename: Hong
authors.initials: H
authors.lastname: Sun
authors.forename: William G
authors.initials: WG
authors.lastname: Mayhan
mesh_terms: D000818:Animals; D001160:Arterioles / Q000378:metabolism / Q000503:physiopathology; D001930:Brain Injuries / Q000378:metabolism / Q000503:physiopathology*; D002540:Cerebral Cortex / Q000098:blood supply* / Q000378:metabolism / Q000503:physiopathology; D002560:Cerebrovascular Circulation / Q000502:physiology; D003922:Diabetes Mellitus, Type 1 / Q000378:metabolism / Q000503:physiopathology*; D008297:Male; D020768:Middle Cerebral Artery / Q000378:metabolism / Q000503:physiopathology; D052248:Nitric Oxide Synthase Type I / Q000378:metabolism; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism; D010805:Physical Conditioning, Animal; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000378:metabolism / Q000503:physiopathology*; D014664:Vasodilation / Q000502:physiology
chemical_list: D052248:Nitric Oxide Synthase Type I; D052250:Nitric Oxide Synthase Type III