title: Impaired autoregulation in an experimental model of chronic cerebral hypoperfusion in rats.
abstract: OBJECTIVE
  To verify the hypothesis that impaired autoregulation may contribute to cerebral swelling or hemorrhage after a sudden recovery of perfusion pressure, we studied the chronic effects of cerebral hypoperfusion on the autoregulatory responses of the pial arterioles in situ.
  
  
  METHODS
  Eight to 12 weeks after a carotid-jugular fistula was created in rats, experiments were performed under alpha-chloralose and urethane anesthesia. Regional cerebral blood flow (rCBF) was determined by the hydrogen clearance method, and carotid pressure was measured. Using a closed cranial window, we determined the autoregulatory responses of the arterioles (30 to 50 microns) to both hypertension induced by norepinephrine and sudden fistula closure at various mean arterial pressures (MAPs).
  
  
  RESULTS
  rCBF on the fistula side was reduced by 27%. Carotid pressure was significantly lower than normal but was immediately increased by fistula closure. The pial arterioles showed marked elongation and enlargement. During induced hypertension, the arterioles in the fistula group started to dilate at an MAP lower than that of the control group (130 versus 180 mm Hg, respectively). The arterioles constricted when the fistula was occluded at normal MAP. However, when the fistula was occluded at an MAP higher than 130 mm Hg, the vessels dilated.
  
  
  CONCLUSIONS
  It was demonstrated that (1) chronic hypoperfusion induced impairment of the upper limit of autoregulation and (2) sudden fistula closure under hypertensive conditions caused vasodilation of the arterioles. These findings suggest that rapid restoration of perfusion pressure is possibly followed by a pressure breakthrough phenomenon in a chronically hypoperfused cerebrovasculature.
authors.affiliation: Department of Neurosurgery, Kitasato University School of Medicine, Kanagawa, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Irikura
authors.forename: S
authors.initials: S
authors.lastname: Morii
authors.forename: Y
authors.initials: Y
authors.lastname: Miyasaka
authors.forename: M
authors.initials: M
authors.lastname: Yamada
authors.forename: K
authors.initials: K
authors.lastname: Tokiwa
authors.forename: K
authors.initials: K
authors.lastname: Yada
mesh_terms: D000818:Animals; D001164:Arteriovenous Fistula / Q000601:surgery; D002545:Brain Ischemia / Q000503:physiopathology*; D002339:Carotid Arteries / Q000503:physiopathology; D002560:Cerebrovascular Circulation / Q000502:physiology*; D002908:Chronic Disease; D004195:Disease Models, Animal; D006706:Homeostasis / Q000502:physiology*; D006935:Hypercapnia / Q000503:physiopathology; D006973:Hypertension / Q000503:physiopathology; D016857:Hypocapnia / Q000503:physiopathology; D007601:Jugular Veins / Q000503:physiopathology; D008297:Male; D008833:Microcirculation / Q000502:physiology; D010841:Pia Mater / Q000098:blood supply / Q000503:physiopathology; D011312:Pressure; D051381:Rats; D017207:Rats, Sprague-Dawley; D012039:Regional Blood Flow