title: Impaired response of perforating arteries to hypercapnia in chronic hyperglycemia.
abstract: Diabetes mellitus increases the risk of cerebrovascular disease, the effects of hypercapnia on CBF (cerebral blood flow) and cerebrovascular reactivity during diabetes are still inconsistent. Here, we have established a new microangiographic technique using synchrotron radiation (SPring-8, Japan), which enabled us to visualize rat cerebral vessels with high spatial resolution in real time. The goal of the study presented here was to identify the effects of chronic hyperglycemia on hypercapnia-induced vascular responses (endothelium-dependent vasodilatation) and nitric oxide (NO) donor- induced vascular responses (endothelium-independent) of perforating arteries and of the deeply located large cerebral arteries. We found a significant vasodilatation of rat perforating arteries after hypercapnia with a maximum diameter of approximately 140% of baseline in normal Wistar rats. Chronic hyperglycemia impaired vasodilatation of perforating arteries in genetically diabetic GK rats. SNP (sodium nitroprusside) caused a similar vasodilatation of perforating vessels in normal and chronic hyperglycemia, indicating that endothelium-dependent vasodilatation of perforating arteries may be specifically impaired in chronic hyperglycemia. Possible impairment of endothelium-dependent vasodilatation in perforating vessels during chronic hyperglycemia may cause decreased vascular reserve capacity of perforating artery, resulting in the increased ischemic insults and cerebrovascular diseases in diabetes.
authors.affiliation: Division of Internal and Geriatric Medicine, Kobe University Graduate School of Medicine, Japan.
authors.forename: Ximena-Sayuri
authors.initials: XS
authors.lastname: Oizumi
authors.forename: Taichi
authors.initials: T
authors.lastname: Akisaki
authors.forename: Yoshiyuki
authors.initials: Y
authors.lastname: Kouta
authors.forename: Xiu Z
authors.initials: XZ
authors.lastname: Song
authors.forename: Toshihiro
authors.initials: T
authors.lastname: Takata
authors.forename: Takeshi
authors.initials: T
authors.lastname: Kondoh
authors.forename: Keiji
authors.initials: K
authors.lastname: Umetani
authors.forename: Masatsugu
authors.initials: M
authors.lastname: Hirano
authors.forename: Katsuhito
authors.initials: K
authors.lastname: Yamasaki
authors.forename: Eiji
authors.initials: E
authors.lastname: Kohmura
authors.forename: Koichi
authors.initials: K
authors.lastname: Yokono
authors.forename: Takashi
authors.initials: T
authors.lastname: Sakurai
mesh_terms: D000818:Animals; D001921:Brain / Q000098:blood supply; D002245:Carbon Dioxide / Q000008:administration & dosage; D002536:Cerebral Arteries / Q000503:physiopathology*; D003925:Diabetic Angiopathies / Q000503:physiopathology; D004730:Endothelium, Vascular / Q000503:physiopathology; D006935:Hypercapnia / Q000503:physiopathology*; D006943:Hyperglycemia / Q000503:physiopathology*; D008297:Male; D020030:Nitric Oxide Donors / Q000494:pharmacology; D009599:Nitroprusside / Q000494:pharmacology; D051381:Rats; D011921:Rats, Inbred WKY; D014664:Vasodilation / Q000187:drug effects
chemical_list: D020030:Nitric Oxide Donors; D002245:Carbon Dioxide; D009599:Nitroprusside