Pial microvascular hemodynamics in anemia

P. D. Hurn, R. J. Traystman, A. A. Shoukas, M. D. Jones

Research output: Contribution to journalArticlepeer-review

Abstract

Isovolemic hemodilution and subsequent anemia increase cerebral blood flow (CBF). We hypothesized that pial microvascular pressure also increases with hemodilution and that arteriolar diameter varies concurrently as a myogenic autoregulatory response. First- and second-order arterioles (31-92 μm, n = 29) and large venules (65-215 μm, n = 17) were studied in thiopental- anesthetized rats. Microvascular pressure was determined using the servo- null technique, and vessel diameters were obtained directly from a video monitoring system. We measured the increase in CBF (radiolabeled microspheres) that accompanies hemodilution in a separate group of animals (n = 20). Hematocrit was reduced to 16-36% with homologous plasma (hemodilution group, n = 13) or held constant with homologous whole blood (control group, n = 4). In control animals, arteriolar and venular diameter varied ±1-2 μm from baseline values, and microvascular pressure remained unchanged from baseline. In the hemodilution group, CBF increased, but there was no systematic pial vasodilation. Furthermore, intraluminal pressure did not increase in pial microvessels, suggesting that proximal vasodilation was negligible even at the lowest hematocrit studied. Vascular resistance fell proportionately in both large vessel and microvascular segments. We conclude that experimental anemia does not produce alterations in microvascular pressure in rats, and the hyperemia accompanying hemodilution is largely viscosity mediated.

Original languageEnglish (US)
Pages (from-to)H2131-H2135
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume264
Issue number6 33-6
DOIs
StatePublished - 1993

Keywords

  • anemia
  • cerebral blood flow
  • hemodilution
  • microcirculation

ASJC Scopus subject areas

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

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