title: Effect of systemic hypotension on cerebral energy metabolism during chronic cerebral vasospasm in primates.
abstract: The influence of systemic hypotension on cerebral blood flow (CBF) and energy metabolism during chronic cerebral vasospasm after subarachnoid hemorrhage was studied in 15 monkeys. Changes in the phosphorus spectrum, as demonstrated by in vivo phosphorus-31 (31P) magnetic resonance (MR) spectroscopy, or in regional CBF were measured in the parietal cortex during graded hypotension. Sequential changes in the phosphorus spectrum were observed during moderate hypotension in the animals 7 days after the introduction of an autologous blood clot around the right middle cerebral artery (MCA). Angiograms revealed a reduction in vessel caliber by approximately 50% in the right MCA. The mean CBF in the spasm side decreased in parallel with a decrease in the mean arterial blood pressure (MABP) from 120 to 40 mm Hg, indicating the abolition of autoregulation. There were no significant differences in the mean percentage totals of inorganic phosphate (Pi), phosphocreatine (PCr), adenosine triphosphate (ATP), and pH between the hemispheres at baseline MABP before hypotension. The values of PCr, ATP, and pH decreased significantly (p < 0.05) and Pi increased significantly (p < 0.05) at an MABP of less than 60 mm Hg in the involved hemisphere. The ratio of PCr:Pi decreased in parallel with a decrease in MABP. The ATP showed a stepwise decrease during moderate hypotension (MABP 60 mm Hg) and was reduced significantly 20 minutes after the beginning of hypotension (p < 0.05). The results indicate that, during chronic vasospasm, changes in cerebral energy metabolism are coupled with changes in CBF in the state of impaired autoregulation. There exists a critical level for ischemia below which high-energy phosphorus metabolites become markedly depleted. It is suggested that 31P MR spectroscopy may be useful to evaluate the ischemic vulnerability of brain tissue in order to prevent delayed neurological deficit during cerebral vasospasm.
authors.affiliation: Department of Neurosurgery, Fukui Medical School, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Handa
authors.forename: T
authors.initials: T
authors.lastname: Kubota
authors.forename: A
authors.initials: A
authors.lastname: Tsuchida
authors.forename: M
authors.initials: M
authors.lastname: Kaneko
authors.forename: H
authors.initials: H
authors.lastname: Caner
authors.forename: H
authors.initials: H
authors.lastname: Kobayashi
authors.forename: T
authors.initials: T
authors.lastname: Kubota
mesh_terms: D000818:Animals; D001921:Brain / Q000378:metabolism* / Q000503:physiopathology; D002560:Cerebrovascular Circulation; D002908:Chronic Disease; D004734:Energy Metabolism; D005260:Female; D005947:Glucose / Q000378:metabolism; D007022:Hypotension / Q000378:metabolism* / Q000503:physiopathology; D002546:Ischemic Attack, Transient / Q000378:metabolism* / Q000503:physiopathology; D008252:Macaca fascicularis; D009682:Magnetic Resonance Spectroscopy; D010100:Oxygen / Q000378:metabolism; D010758:Phosphorus / Q000378:metabolism
chemical_list: D010758:Phosphorus; D005947:Glucose; D010100:Oxygen