Cerebral O2 transport with hematocrit reduced by cross-linked hemoglobin transfusion

John A. Ulatowski, Enrico Bucci, Toshiaki Nishikawa, Anna Razynska, Michael A. Williams, Reiko Takeshima, Richard J. Traystman, Raymond C. Koehler

Research output: Contribution to journalArticlepeer-review

Abstract

The purpose of this study was to dissociate effects of reduced viscosity from those of low arterial O2 content (Ca(O2)) on cerebral blood flow (CBF) during anemia. Three groups (n = 8) of pentobarbital sodium-anesthetized cats were studied: 1) a time-control group with a hematocrit of 32 ± 1% (SE), 2) an anemia group that underwent an isovolumic exchange transfusion with albumin in a salt solution to decrease hematocrit to 18 ± 1%, and 3) a group transfused with cell-free, tetramerically stabilized hemoglobin to decrease hematocrit equivalently to that in the albumin-transfused group. Ca(O2) (in ml/dl) in the hemoglobin-transfused group (11.8 ± 0.3) and the control group (15.0 ± 0.6) was greater than that in the albumin group (8.7 ± 0.3). CBF (in ml · min-1 · 100 g-1) in the hemoglobin group (45 ± 3) and control group (36 ± 4) was less than that in the albumin group (60 ± 3). Consequently, cerebral O2 transport (Ca(O2) x CBF) was similar in the hemoglobin, control, and albumin groups (5.3 ± 0.3, 5.3 ± 0.4, and 5.2 ± 0.2 ml · min-1 · 100 g-1, respectively). After infusion of N(ω)- nitro-L-arginine methyl ester (L-NAME) to inhibit nitric oxide (NO) synthase, CBF in the hemoglobin group remained lower than that in the albumin group, suggesting that NO scavenging by hemoglobin did not solely account for the lower CBF. In contrast, the neurohypophysis (posterior pituitary) exhibited substantial decreases in blood flow that were not augmented by L-NAME administration after hemoglobin transfusion and that were similar in magnitude to L-NAME alone. Thus NO scavenging by cell-free hemoglobin may be more prominent in high-flow, protein-permeable regions enriched with NO synthase. These results support the hypothesis that O2 transport to cerebrum is well regulated when Ca(O2) is manipulated independently of hematocrit and viscosity.

Original languageEnglish (US)
Pages (from-to)H466-H475
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume270
Issue number2 39-2
DOIs
StatePublished - 1996

Keywords

  • anemia
  • blood
  • cats
  • cerebral blood flow
  • nitric oxide

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

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