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Hemoglobin mediated vasoactivity in isolated vascular rings
1Department of Surgery, Miriam Hospital, Providence, RI, USA.
Summary
Human stroma-free hemoglobin (SFH) causes vasoconstriction in isolated blood vessels, potentially by interacting with nitric oxide. This effect is reversible with vasodilators, suggesting pharmacologic modulation of hemoglobin-based oxygen carriers is possible.
Area of Science:
- Pharmacology
- Cardiovascular Physiology
- Biochemistry
Background:
- Hemoglobin-based oxygen carriers (HBOCs) are investigated as blood substitutes.
- Understanding HBOC vasoactivity is crucial for their clinical application.
- Previous studies suggest potential vasoconstrictive effects of HBOCs.
Purpose of the Study:
- To define the vasoactivity of hemoglobin-based oxygen carriers (HBOCs).
- To investigate the mechanism of HBOC-induced vasoconstriction.
- To explore potential pharmacologic modulation of HBOC vasoactivity.
Main Methods:
- Isolated rat pulmonary artery and aortic ring preparations were used.
- Isometric tension was recorded in response to norepinephrine, human stroma-free hemoglobin (SFH), and methemoglobin.
- Vessels preconstricted with SFH were treated with vasodilators (sodium nitroprusside, glyceryl trinitrate, isoproteranol).
Main Results:
- Human stroma-free hemoglobin (SFH) caused a dose-dependent increase in vascular tension.
- Methemoglobin did not significantly affect vascular tension.
- SFH-induced vasoconstriction was significantly reversed by sodium nitroprusside, glyceryl trinitrate, and isoproteranol.
Conclusions:
- SFH at micromolar concentrations induces significant vasoconstriction in isolated vessels.
- The mechanism appears to involve interaction with endothelium-derived nitric oxide.
- Pharmacologic modulation of SFH vasoactivity is feasible using vasodilators and beta-receptor agonists.