The Effect of Sodium Nitrite on Acute Hemolysis in a Canine Model

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The primary goal of this study was to determine the therapeutic value of intravenous sodium nitrite in a canine model of acute intravascular hemolysis. Nitric oxide (NO) is a vasodilator which is constantly produced by the vascular endothelium. The amount of NO available in the circulation is, in part, regulated by the binding of NO to hemoglobin. Hemoglobin is normally contained within the red blood cell and reacts with nitric oxide at a relatively slow rate. However, the destruction of red blood cells within the circulation (intravascular hemolysis) causes the release of hemoglobin (cell-free hemoglobin) from the red blood cell into the circulation. The cell-free hemoglobin released into the circulation during hemolysis binds to NO at a much faster rate than hemoglobin within the red blood cell. This rapid binding of NO by cell-free hemoglobin disrupts the normal balance of NO within the circulation and leads to a decrease in the amount of NO available. This decrease in the amount of available NO leads to vasoconstriction and subsequently to decreased blood flow and organ injury. Intravenous sodium nitrite can bind to cell-free hemoglobin and may prevent the cell-free hemoglobin from binding to NO. If the nitrite can prevent the cell-free hemoglobin from binding NO, it may prevent the vasoconstriction and organ injury that occurs during hemolysis. This study tested the ability of nitrite to prevent cell-free hemoglobin binding of NO during hemolysis. This study using intravenous sodium nitrite is a follow-up to a study which found efficacy in using nitric oxide gas to block vasoconstriction and minimize organ damage caused during intravascular hemolysis. We found that nitrite is similar to in effect but not as powerful as our finding with nitric oxide. This study has been completed and the results are presently being analyzed. A manuscript is expected to be completed in the next 3-4 months.