Mechanisms for vasoconstriction and decreased blood flow following intravenous administration of cell-free native

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Modeling Neonatal Intraventricular Hemorrhage Through Intraventricular Injection of Hemoglobin
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Hae W Kim, A Gerson Greenburg

    Advances in Experimental Medicine and Biology
    |April 6, 2006
    PubMed

    Acellular free hemoglobin-based oxygen carriers (HBOC) are being developed as red cell substitutes. However, following intravenous administration of some HBOC, decreased systemic blood flow and decreased functional capillary density have been observed. In isolated blood vessels, hemoglobin (Hb) in solution free of erythrocyte membranes has been shown to elicit vascular contraction. Therefore, the decreased blood flow and functional capillary density may be due to inherent vasoactive property of native Hb. There are two plausible mechanisms for the Hb-mediated vasoconstriction: nitrosylation of heme-irons and S-nitrosation of reactive beta-chain cysteines (Cys93beta). In this study, we investigated whether Hb Cys93beta thiols play a role in Hb-mediated vascular contraction using functional bioassays with isolated rat thoracic aorta. To better define the roles of globin thiols and heme-iron, Hbs modified at the heme-iron and/or Cys93beta sites were prepared and their vasoactivities tested. In addition, vasoactivities of natural heme proteins with heme and/or cysteine sites unavailable for NO reaction were also examined.

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