title: Significance of resting and stimulated cerebral blood flow for predicting the risk of hemodynamic cerebral ischemia in a model of chronic hemodynamic insufficiency.
abstract: OBJECTIVE
  It has been postulated that patients with a compromised cerebrovascular reserve capacity (RC), defined as cerebral blood flow (CBF) response to acetazolamide (ACZ) (by percent), are at higher risk for ischemic stroke. The value of CBF and RC for predicting the risk of hemodynamically induced impairment of cerebral function is examined.
  
  
  METHODS
  Both common carotid arteries were occluded in 22 Wistar-Kyoto rats. Thirty-one days later, mean arterial blood pressure was reduced to 40 mm Hg for 30 minutes. Laser Doppler scanning of CBF at resting conditions and after intraperitoneal administration of ACZ (0.1 mg/g body weight) was performed 30 minutes and 28 days after occlusion as well as before and during hypotension. Memory and motor functions were examined before and after CBF measurements.
  
  
  RESULTS
  After occlusion, CBF dropped significantly and ACZ did not increase CBF. Four weeks later, resting CBF had significantly improved but remained impaired, as did RC, showing a distinct interindividual variability. Hypotension reduced CBF by 57 +/- 4% (P < 0.001) and significantly impaired memory and motor functions. CBF during hypotension correlated with resting CBF before hypotension (r = 0.495, P = 0.027) and with CBF before (r = 0.392, P = 0.048) and after (r = 0.476, P = 0.034) ACZ, as determined 4 weeks after occlusion. There was no correlation with RC (r = 0.091, P = 0.702). Neurological tests performed 1 day after hypotension correlated with CBF during hypotension (memory function, P = 0.03; motor function, P = 0.02) but not with RC.
  
  
  CONCLUSIONS
  In this model of chronic hemodynamic insufficiency, the risk of impairment to global cerebral function was predicted by resting CBF and CBF after ACZ but not by RC determined with ACZ.
authors.affiliation: Institute for Neurosurgical Pathophysiology, Johannes Gutenberg University, Mainz, Germany.
authors.forename: S
authors.initials: S
authors.lastname: Kroppenstedt
authors.forename: P
authors.initials: P
authors.lastname: Ulrich
authors.forename: A
authors.initials: A
authors.lastname: Heimann
authors.forename: O
authors.initials: O
authors.lastname: Kempski
mesh_terms: D000086:Acetazolamide; D000818:Animals; D001783:Blood Flow Velocity / Q000187:drug effects / Q000502:physiology; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D001921:Brain / Q000098:blood supply*; D002545:Brain Ischemia / Q000503:physiopathology*; D004195:Disease Models, Animal; D006439:Hemodynamics / Q000502:physiology*; D006801:Humans; D008297:Male; D018782:Maze Learning / Q000502:physiology; D011939:Mental Recall / Q000502:physiology; D009043:Motor Activity / Q000502:physiology; D051381:Rats; D011921:Rats, Inbred WKY; D012153:Retention, Psychology / Q000502:physiology; D020521:Stroke / Q000503:physiopathology*
chemical_list: D000086:Acetazolamide