TY - JOUR
T1 - Plasma viscosity and cerebral blood flow
AU - Tomiyama, Yoshinobu
AU - Brian, Johnny E.
AU - Todd, Michael M.
PY - 2000
Y1 - 2000
N2 - We hypothesized that the response of cerebral blood flow (CBF) to changing viscosity would be dependent on 'baseline' CBF, with a greater influence of viscosity during high-flow conditions. Plasma viscosity was adjusted to 1.0 or 3.0 cP in rats by exchange transfusion with red blood cells diluted in lactated Ringer solution or with dextran. Cortical CBF was measured by H2 clearance. Two groups of animals remained normoxic and normocarbic and served as controls. Other groups were made anemic, hypercapnic, or hypoxic to increase CBF. Under baseline conditions before intervention, CBF did not differ between groups and averaged 49.4 ± 10.2 ml·100 g-1·min-1 (±SD). In control animals, changing plasma viscosity to 1.0 or 3.0 cP resulted in CBF of 55.9 ± 8.6 and 42.5 ± 12.7 ml·100 g-1·min-1, respectively (not significant). During hemodilution, hypercapnia, and hypoxia with a plasma viscosity of 1.0 cP, CBF varied from 98 to 115 ml·100 g-1·min-1. When plasma viscosity was 3.0 cP during hemodilution, hypercapnia, and hypoxia, CBF ranged from 56 to 58 ml·100 g-1·min-1 and was significantly reduced in each case (P < 0.05). These results support the hypothesis that viscosity has a greater role in regulation of CBF when CBF is increased. In addition, because CBF more closely followed changes in plasma viscosity (rather than whole blood viscosity), we believe that plasma viscosity may be the more important factor in controlling CBF.
AB - We hypothesized that the response of cerebral blood flow (CBF) to changing viscosity would be dependent on 'baseline' CBF, with a greater influence of viscosity during high-flow conditions. Plasma viscosity was adjusted to 1.0 or 3.0 cP in rats by exchange transfusion with red blood cells diluted in lactated Ringer solution or with dextran. Cortical CBF was measured by H2 clearance. Two groups of animals remained normoxic and normocarbic and served as controls. Other groups were made anemic, hypercapnic, or hypoxic to increase CBF. Under baseline conditions before intervention, CBF did not differ between groups and averaged 49.4 ± 10.2 ml·100 g-1·min-1 (±SD). In control animals, changing plasma viscosity to 1.0 or 3.0 cP resulted in CBF of 55.9 ± 8.6 and 42.5 ± 12.7 ml·100 g-1·min-1, respectively (not significant). During hemodilution, hypercapnia, and hypoxia with a plasma viscosity of 1.0 cP, CBF varied from 98 to 115 ml·100 g-1·min-1. When plasma viscosity was 3.0 cP during hemodilution, hypercapnia, and hypoxia, CBF ranged from 56 to 58 ml·100 g-1·min-1 and was significantly reduced in each case (P < 0.05). These results support the hypothesis that viscosity has a greater role in regulation of CBF when CBF is increased. In addition, because CBF more closely followed changes in plasma viscosity (rather than whole blood viscosity), we believe that plasma viscosity may be the more important factor in controlling CBF.
KW - Brain
KW - Hemodilution
KW - Hypercapnia
KW - Hypoxia
KW - Oxygen
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U2 - 10.1152/ajpheart.2000.279.4.h1949
DO - 10.1152/ajpheart.2000.279.4.h1949
M3 - Article
C2 - 11009484
AN - SCOPUS:0033724821
SN - 0363-6143
VL - 279
SP - H1949-H1954
JO - American Journal of Physiology - Cell Physiology
JF - American Journal of Physiology - Cell Physiology
IS - 4 48-4
ER -