ROLE OF NITRIC-OXIDE SCAVENGING IN PERIPHERAL VASOCONSTRICTOR RESPONSE TO BETA-BETA CROSS-LINKED HEMOGLOBIN

Transfusion with many crosslinked hemoglobin solutions causes an incre ase in arterial pressure that may be mediated by scavenging of nitric oxide (NO). If so, we postulated that inhibiting synthesis of NO after hemoglobin transfusion would fail to cause vasoconstriction ordinaril y seen with such inhibition. In pentobarbital anesthetized cats, we te sted whether administration of the NO synthase inhibitor, N-G-nitro-L- arginine methyl ester (L-NAME), produced peripheral vasoconstriction a fter isovolemic exchange transfusion with hemoglobin to the same exten t as occurs with L-NAME infusion in time controls and in controls matc hed for reduced hematocrit (17%) with albumin transfusion. Bovine hemo globin was treated aerobically with bis-(3,5-dibromosalicyl) fumarate to produce beta beta-81 lysine crosslinks. Hemoglobin exchange transfu sion increased mean arterial blood pressure and there was no further i ncrease after L-NAME. In contrast, L-NAME increased pressure in the ti me controls and albumin controls. Hemoglobin transfusion decreased int estinal and renal blood flow, and there was no further decrease after L-NAME. In contrast, L-NAME decreased intestinal and renal blood flow in time controls and albumin controls. With L-NAME pretreatment in a s eparate group of cats, there was little further increase in arterial p ressure or visceral vasoconstriction after hemoglobin transfusion. We conclude that the increase in arterial blood pressure after isovolemic crosslinked hemoglobin transfusion is best explained by scavenging of NO in intestinal and renal vascular beds.