title: Cerebral blood flow and vasodilatory capacity in anemia secondary to chronic renal failure.
abstract: BACKGROUND
  Our previous study reported that cerebral oxygen extraction fraction (OEF) increased in hemodialysis patients with anemia. The increased OEF suggests that the cerebral vasodilatory capacity might be impaired in these patients. To clarify this issue, we measured the CO2 response in patients with anemia secondary to chronic renal failure (CRF) using positron emission tomography (PET).
  
  
  METHODS
  Ten anemic patients with CRF (6 females and 4 males) and 6 age-matched normal controls were studied. The underlying diseases of CRF were glomerulonephritis in 8 patients, systemic lupus erythematosus (SLE) in one patient, and hypertension in one patient; in this cohort, 5 patients were on hemodialysis treatment and the remaining 5 patients were in a pre-hemodialysis state. The cerebral blood flow (CBF) was measured by the O-15 H2O bolus injection method with each patient in a resting state and during 5% CO2 inhalation. The CO2 response was estimated as the percentage change of CBF per 1 mm Hg change of PaCO2.
  
  
  RESULTS
  The CO2 response was significantly attenuated in anemic patients with CRF in comparison to the normal controls, and it inversely correlated with the severity of anemia. There was no significant difference in the CO2 response between the hemodialysis and pre-hemodialysis patients. The CO2 response significantly correlated with CBF and the cerebral metabolic rate for oxygen (CMRO2) at rest, however, it did not correlate with OEF and cerebral blood volume (CBV).
  
  
  CONCLUSIONS
  The present study revealed the existence of a reduced cerebral vasodilatory capacity in anemic patients with CRF, suggesting that chronic hypoxic brain damage might play a role in the impaired cerebrovascular response to CO2.
authors.affiliation: Departments of Clinical Radiology and Second Internal Medicine, Graduate School of Medical Sciences,Kyushu University, Fukuoka, Japan. kuwabara@dr.hosp.kyushu-u.ac.jp
authors.forename: Yasuo
authors.initials: Y
authors.lastname: Kuwabara
authors.forename: Masayuki
authors.initials: M
authors.lastname: Sasaki
authors.forename: Hideki
authors.initials: H
authors.lastname: Hirakata
authors.forename: Hirofumi
authors.initials: H
authors.lastname: Koga
authors.forename: Makoto
authors.initials: M
authors.lastname: Nakagawa
authors.forename: Tao
authors.initials: T
authors.lastname: Chen
authors.forename: Koichiro
authors.initials: K
authors.lastname: Kaneko
authors.forename: Kouji
authors.initials: K
authors.lastname: Masuda
authors.forename: Masatoshi
authors.initials: M
authors.lastname: Fujishima
mesh_terms: D000328:Adult; D000368:Aged; D000740:Anemia / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology*; D001921:Brain / Q000378:metabolism; D002245:Carbon Dioxide / Q000378:metabolism; D002560:Cerebrovascular Circulation / Q000502:physiology*; D005260:Female; D006801:Humans; D006935:Hypercapnia / Q000378:metabolism / Q000503:physiopathology; D002534:Hypoxia, Brain / Q000378:metabolism / Q000503:physiopathology; D007676:Kidney Failure, Chronic / Q000150:complications / Q000503:physiopathology* / Q000628:therapy; D008297:Male; D008875:Middle Aged; D010100:Oxygen / Q000378:metabolism; D006435:Renal Dialysis; D014664:Vasodilation / Q000502:physiology*
chemical_list: D002245:Carbon Dioxide; D010100:Oxygen