Cerebrovascular response to decreased hematocrit: effect of cell-free hemoglobin, plasma viscosity, and CO2.
The effect of transfusing a nonextravasating, zero-link polymer of cell-free hemoglobin on pial arteriolar diameter, cerebral blood flow (CBF), and O2 transport (CBF x arterial O2 content) was compared with that of transfusing an albumin solution at equivalent reductions in hematocrit (approximately 19%) in anesthetized cats. The influence of viscosity was assessed by coinfusion of a high-viscosity solution of polyvinylpyrrolidone (PVP), which increased plasma viscosity two- to threefold. Exchange transfusion of a 5% albumin solution resulted in pial arteriolar dilation, increased CBF, and unchanged O2 transport, whereas there were no significant changes over time in a control group. Exchange transfusion of a 12% polymeric hemoglobin solution resulted in pial arteriolar constriction and unchanged CBF and O2 transport. Coinfusion of PVP with albumin produced pial arteriolar dilation that was similar to that obtained with transfusion of albumin alone. In contrast, coinfusion of PVP with hemoglobin converted the constrictor response to a dilator response that prevented a decrease in CBF. Pial arteriolar dilation to hypercapnia was unimpaired in groups transfused with albumin or hemoglobin alone but was attenuated in the largest vessels in albumin and hemoglobin groups coinfused with PVP. Unexpectedly, hypocapnic vasoconstriction was blunted in all groups after transfusion of albumin or hemoglobin alone or with PVP. We conclude that 1) the increase in arteriolar diameter after albumin transfusion represents a compensatory response that prevents decreased O2 transport at reduced O2-carrying capacity, 2) the decrease in diameter associated with near-normal O2-carrying capacity after cell-free polymeric hemoglobin transfusion represents a compensatory mechanism that prevents increased O2 transport at reduced blood viscosity, 3) pial arterioles are capable of dilating to an increase in plasma viscosity when hemoglobin is present in the plasma, 4) decreasing hematocrit does not impair pial arteriolar dilation to hypercapnia unless plasma viscosity is increased, and 5) pial arteriolar constriction to hypocapnia is impaired at reduced hematocrit independently of O2-carrying capacity.
Rebel
Annette
A
Department of Anesthesiology and Critical Care Medicine, The Johns Hopkins Medical Institutions, 600 N. Wolfe St., Baltimore, MD 21205, USA.
Ulatowski
John A
JA
Kwansa
Herman
H
Bucci
Enrico
E
Koehler
Raymond C
RC
D000418:Albumins / Q000494:pharmacology; D000818:Animals; D001160:Arterioles / Q000187:drug effects / Q000502:physiology; D001809:Blood Viscosity / Q000187:drug effects; D002245:Carbon Dioxide / Q000494:pharmacology*; D002415:Cats; D002560:Cerebrovascular Circulation / Q000187:drug effects* / Q000502:physiology*; D005078:Exchange Transfusion, Whole Blood; D006400:Hematocrit; D006438:Hemodilution; D006454:Hemoglobins / Q000494:pharmacology*; D006801:Humans; D006935:Hypercapnia / Q000503:physiopathology; D016857:Hypocapnia / Q000503:physiopathology; D008297:Male; D010841:Pia Mater / Q000098:blood supply; D010952:Plasma Substitutes / Q000494:pharmacology; D011205:Povidone / Q000494:pharmacology; D014661:Vasoconstriction; D014664:Vasodilation
D000418:Albumins; D006454:Hemoglobins; D010952:Plasma Substitutes; D002245:Carbon Dioxide; D011205:Povidone