title: Influence of severe hemodilution on brain function and brain oxidative metabolism in the cat.
abstract: OBJECTIVE
  It has been established that during constant pressure arterio-venous bypass perfusion, brain metabolism gradually deteriorates in parallel with the declining hematocrit. However, whether this is due to a disturbance of flow regulation or to the decline in the oxygen-carrying capacity of the blood has not been documented. Therefore, intact animals were submitted to severe hemodilution to determine the threshold for the beginning of functional and biochemical impairment of the brain.
  
  
  METHODS
  Six anesthetized and paralyzed adult mongrel cats were submitted to gradual isovolemic hemodilution by stepwise exchange of blood with Ringer lactate/dextran (1 : 1) solution. Exchange of 80 ml/kg body weight resulted in a final hematocrit level ranging from 6.1% to 11%.
  
  
  RESULTS
  Cerebral blood flow gradually increased during hemodilution, with a sharp rise to eight times the prehemodilution value when the hematocrit fell below 10%. The calculated oxygen delivery to the brain remained relatively unchanged. Hemodilution did not cause suppression of spontaneous ECoG or somatically evoked primary cortical potentials, even at the lowest hematocrit value of 6.1%. Brain tissue ATP and phosphocreatine content were largely maintained, although tissue lactate content was elevated (9.54 +/- 5.99 micromol/g).
  
  
  CONCLUSIONS
  The hemodynamically unimpaired healthy mammal is able to support a substantial degree of hemodilution without major functional or biochemical disturbance to the brain. The previously observed disturbances during prolonged bypass perfusion are, therefore, most probably due to the associated abnormalities of flow regulation.
authors.affiliation: Max-Planck Institute for Neurological Research, Department of Experimental Neurology, Koln, Germany.
authors.forename: R
authors.initials: R
authors.lastname: Bauer
authors.forename: T
authors.initials: T
authors.lastname: Iijima
authors.forename: K A
authors.initials: KA
authors.lastname: Hossmann
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001921:Brain / Q000378:metabolism* / Q000473:pathology; D002415:Cats; D002560:Cerebrovascular Circulation / Q000502:physiology*; D005071:Evoked Potentials; D006400:Hematocrit; D006438:Hemodilution / Q000009:adverse effects*; D006439:Hemodynamics; D006863:Hydrogen-Ion Concentration; D007773:Lactates / Q000378:metabolism; D016018:Least-Squares Analysis; D008297:Male; D018709:Statistics, Nonparametric
chemical_list: D007773:Lactates; D000255:Adenosine Triphosphate