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Arterial Blood Pressure Responses to Cell-free Hemoglobin Solutions and the Reaction with Nitric Oxide

Changes in mean arterial pressure were monitored in rats following 50% isovolemic exchange transfusion with solutions of chemically modified hemoglobins. Blood pressure responses fall into three categories: 1) an immediate and sustained increase, 2) an immediate yet transient increase, or 3) no sign...

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Bibliographic Details
Published in:The Journal of biological chemistry 1998-05, Vol.273 (20), p.12128-12134
Main Authors: Rohlfs, Ronald J., Bruner, Eric, Chiu, Albert, Gonzales, Armando, Gonzales, Maria L., Magde, Douglas, Magde, Michael D., Vandegriff, Kim D., Winslow, Robert M.
Format: Article
Language:English
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Summary:Changes in mean arterial pressure were monitored in rats following 50% isovolemic exchange transfusion with solutions of chemically modified hemoglobins. Blood pressure responses fall into three categories: 1) an immediate and sustained increase, 2) an immediate yet transient increase, or 3) no significant change either during or subsequent to exchange transfusion. The reactivities of these hemoglobins with nitric monoxide (⋅NO) were measured to test the hypothesis that different blood pressure responses to these solutions result from differences in ⋅NO scavenging reactions. All hemoglobins studied exhibited a value of 30 μm−1 s−1 for both⋅NO bimolecular association rate constants and the rate constants for ⋅NO-induced oxidation in vitro. Only the ⋅NO dissociation rate constants and, thus, the equilibrium dissociation constants varied. Values of equilibrium dissociation constants ranged from 2 to 14 pm and varied inversely with vasopressor response. Hemoglobin solutions that exhibited either transient or no significant increase in blood pressure showed tighter⋅NO binding affinities than hemoglobin solutions that exhibited sustained increases. These results suggest that blood pressure increases observed upon exchange transfusion with cell-free hemoglobin solutions can not be the result of ⋅NO scavenging reactions at the heme, but rather must be due to alternative physiologic mechanisms.
ISSN:0021-9258
1083-351X
DOI:10.1074/jbc.273.20.12128