Studies of the mechanism of the vasoconstrictor activity of stroma-free hemoglobin in the isolated perfused rat kidney and rabbit heart.

We have found that DBBF-Hb and Hb Ao have significantly less vasoconstrictor activity than unmodified Hb in the rabbit heart. In striking contrast to these findings, DBBF-Hb and unmodified Hb have comparable hemodynamic effects in the isolated kidney. We have demonstrated that lipophilic contamination of fraction V BSA causes vasoconstriction in the coronary vasculature and speculate that similar contaminants may contribute to the vasoconstrictor activity of SFH solutions. Finally, we have shown that renal vasoconstriction induced by DBBF-Hb is reversed by acetylcholine as well as nitroprusside. These studies suggest that renal vasoconstriction induced by DBBF-Hb is not related to inhibition of EDRF. These studies make it clear that SFH solutions have different effects on the heart and kidney vasculature. The use of both heart and kidney models should provide important information on the mechanisms by which SFH causes vasoconstriction in these two organs.