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Hemodilution causes size-dependent constriction of pial arterioles in the cat
M L Hudak1, M D Jones, A S Popel
1Department of Pediatrics (Eudowood Neonatal Pulmonary Division, Johns Hopkins Medical Institutions, Baltimore, Maryland 21205.
Insights
Anemia causes cerebral vasoconstriction, not vasodilation, as hematocrit decreases. Pial arterioles constricted initially, with greater effect in smaller vessels, contrary to prior hypotheses.
Area of Science:
- Neuroscience
- Physiology
- Cardiovascular Research
Background:
- Cerebral blood flow (CBF) increases as hematocrit (Hct) decreases.
- Previous theories suggested decreased O2 content and blood viscosity independently cause CBF rise.
- Hypothesis: Anemia-induced decreased O2 content causes cerebral vasodilation.
Purpose of the Study:
- To test the hypothesis that anemia causes cerebral vasodilation.
- To investigate the relationship between hematocrit levels and pial arteriole diameter.
Main Methods:
- Used a closed cranial window in 7 cats.
- Measured pial arteriole diameters (35-305 microns) during serial isovolemic hemodilution.
- Lowered Hct by 44% (from 31±4% to 17±3%) and measured CBF using microspheres.
Main Results:
- Hemodilution increased CBF but did not alter mean arterial blood pressure or blood gases.
- Contrary to hypothesis, pial arterioles constricted as Hct decreased.
- Maximum vasoconstriction occurred at 65-70% of initial Hct; constriction lessened at lower Hcts but remained above baseline.
Conclusions:
- Anemia is accompanied by cerebral vasoconstriction, not vasodilation.
- Initial constriction may be myogenic or due to vasodilator washout.
- Further hemodilution may induce metabolic vasodilation, overriding initial constriction.
Abstract:
Cerebral blood flow (CBF) rises as hematocrit (Hct) falls. We previously attributed this rise in CBF to two independent factors of equal importance, decreased arterial O2 content and decreased blood viscosity. We hypothesized that decreased arterial O2 content would dilate cerebral arterioles and that the magnitude of the vasodilation would depend on the magnitude of the passive fall in vascular resistance attributable to decreased viscosity. The present study was designed to test the hypothesis that anemia is accompanied by cerebral vasodilation. Using a closed cranial window, we measured the diameters of 42 pial arterioles (35-305 microns) in 7 cats as serial isovolemic hemodilution lowered Hct by 44% from 31 +/- 4 to 17 +/- 3%. Hemodilution increased CBF (microsphere technique) but did not change mean arterial blood pressure or arterial blood gases. Anticipated vasodilation did not occur; instead, pial arterioles constricted as Hct fell. Maximum vasoconstriction was observed when Hct reached 65-70% of the initial value. Vasoconstriction lessened as Hct was lowered further, but arteriolar diameters at the lowest Hcts remained less than base-line levels. Constriction was greater in small (less than 100 microns) than in large (greater than or equal to 100 microns) arterioles. The initial constriction of pial arterioles may represent myogenic vasoconstriction in response to flow-induced vasodilation of more proximal portions of the cerebrovascular bed and/or to washout of an endogenous vasodilator. Arteriolar relaxation with more profound hemodilution may reflect superimposed metabolic vasodilation.