title: Cerebral hematocrit decreases with hemodynamic compromise in carotid artery occlusion: a PET study.
abstract: OBJECTIVE
  This study investigated whether in patients with internal carotid artery occlusion the regional cerebral hematocrit correlates with cerebral hemodynamics or metabolic state and, if so, how the regional cerebral hematocrit changes in the hemodynamically compromised region.
  
  
  METHODS
  We used positron emission tomography to study seven patients with unilateral internal carotid artery occlusion and no cortical infarction in the chronic stage. The distributions of red blood cell and plasma volumes were assessed using oxygen-15-labeled carbon monoxide and copper-62-labeled human serum albumin-dithiosemicarbazone tracers, respectively. The calculated hematocrit value was compared with the hemodynamic and metabolic parameters measured with the oxygen-15 steady-state technique.
  
  
  RESULTS
  In the cerebral cortex, the value of the cerebral hematocrit varied but was correlated with the hemodynamic and metabolic status. Stepwise regression analysis revealed that the large vessel hematocrit, the cerebral metabolic rate of oxygen, and the cerebral blood flow or the oxygen extraction fraction accounted for a significant proportion of variance of the cerebral hematocrit. The oxygen extraction fraction and the cerebral metabolic rate of oxygen negatively correlated with the cerebral hematocrit, whereas the cerebral blood flow correlated positively: patients with reduced blood supply relative to metabolic demand (decreased blood flow with increased oxygen extraction fraction) showed low hematocrit values.
  
  
  CONCLUSIONS
  In carotid artery occlusion in the chronic stage, regional cerebral hematocrit may vary according to cerebral hemodynamics and metabolic status. Regional cerebral hematocrit may decrease with hemodynamic compromise unless oxygen metabolism concomitantly decreases.
authors.affiliation: Department of Neurology, Faculty of Medicine, Kyoto University, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Yamauchi
authors.forename: H
authors.initials: H
authors.lastname: Fukuyama
authors.forename: Y
authors.initials: Y
authors.lastname: Nagahama
authors.forename: Y
authors.initials: Y
authors.lastname: Katsumi
authors.forename: H
authors.initials: H
authors.lastname: Okazawa
mesh_terms: D000368:Aged; D001921:Brain / Q000000981:diagnostic imaging / Q000378:metabolism* / Q000503:physiopathology; D002545:Brain Ischemia / Q000097:blood* / Q000000981:diagnostic imaging / Q000503:physiopathology; D002248:Carbon Monoxide; D002340:Carotid Artery Diseases / Q000097:blood* / Q000000981:diagnostic imaging / Q000503:physiopathology; D002343:Carotid Artery, Internal / Q000000981:diagnostic imaging / Q000503:physiopathology; D002540:Cerebral Cortex / Q000000981:diagnostic imaging / Q000378:metabolism / Q000503:physiopathology; D002544:Cerebral Infarction / Q000097:blood / Q000000981:diagnostic imaging / Q000503:physiopathology; D002560:Cerebrovascular Circulation / Q000502:physiology; D002908:Chronic Disease; D003301:Copper Radioisotopes; D005260:Female; D006400:Hematocrit; D006439:Hemodynamics; D006801:Humans; D008297:Male; D008875:Middle Aged; D010101:Oxygen Consumption / Q000502:physiology; D010104:Oxygen Radioisotopes; D010953:Plasma Volume; D019275:Radiopharmaceuticals; D012044:Regression Analysis; D012709:Serum Albumin; D013882:Thiosemicarbazones; D014055:Tomography, Emission-Computed
chemical_list: D003301:Copper Radioisotopes; D010104:Oxygen Radioisotopes; D019275:Radiopharmaceuticals; D012709:Serum Albumin; D013882:Thiosemicarbazones; C015848:dithiosemicarbazone; D002248:Carbon Monoxide