STROMA-FREE HEMOGLOBIN INCREASES BLOOD-PRESSURE AND GFR IN THE HYPOTENSIVE RAT - ROLE OF NITRIC-OXIDE

The shortterm systemic and renal hemodynamic effects of two stroma-fre e hemoglobin (SFH) solutions, one unmodified and the other modified by cross-linking, were examined in anesthetized rats after hemorrhagic h ypotension. Both forms of SFH increased mean arterial pressure (MAP) a nd glomerular filtration rate (GFR) to baseline (prehemorrhage) values . The increase in MAP induced by unmodified SFH was greater than the i ncrease in MAP caused by an albumin solution isoncotic to the unmodife d SFH solution. Similarly, the increase in MAP caused by the modified SFH was also substantially greater than that induced by an albumin sol ution of comparable oncotic pressure to the modified SFH solution. Bot h unmodified and modified SFH increased GFR. As with MAP, the increase in GFR induced by both SFH solutions was greater than that associated with the oncotically matched albumin solutions. In separate experimen ts, the effects of nitric oxide (NO) inhibition with N-omega-nitro-L-a rginine methyl ester (L-NAME) on MAP after hemorrhagic hypotension and subsequent infusion of unmodified SFH or albumin were also examined. In the albumin-infused rats, L-NAME increased MAP. In marked contrast, NO inhibition with L-NAME had no further effect on MAP when infused a fter SFH. We conclude that both unmodified and modified SFH solutions acutely improve MAP and GFR by the combined effects of intravascular v olume expansion resulting from the colloid effect of the protein and b y inactivation of NO.