TY - JOUR
T1 - Role of nitric oxide scavenging in peripheral vasoconstrictor response to β cross-linked hemoglobin
AU - Hemoglobin, Cross Linked
AU - Ulatowski, John A.
AU - Koehler, Raymond C.
AU - Nishikawa, Toshiaki
AU - Traystman, Richard J.
AU - Razynska, Anna
AU - Kwansa, Herman
AU - Urbaitis, Barbara
AU - Bucci, Enrico
N1 - Funding Information:
This work was supported by a grant from the National Institutes of Health (HL 48517). The authors wish to thank Yarvis Simmons for help in preparing the manuscript and Freddie Jackson, Matthew Fallau, and Stephan Bullock for excellent technical assistance.
PY - 1995/1/1
Y1 - 1995/1/1
N2 - Transfusion with many crosslinked hemoglobin solutions causes an increase 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 ordinarily seen with such inhibition. In pentobarbital anesthetized cats, we tested whether administration of the NO synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME), produced peripheral vasoconstriction after isovolemic exchange transfusion with hemoglobin to the same extent as occurs with L-NAME infusion in time controls and in controls matched for reduced hematocrit (17%) with albumin transfusion. Bovine hemoglobin was treated aerobically with bis-(3,5-dibromosalicyl) fumarate to produce β β-81 lysine crosslinks. Hemoglobin exchange transfusion increased mean arterial blood pressure and there was no further increase after L-NAME. In contrast, L-NAME increased pressure in the time controls and albumin controls. Hemoglobin transfusion decreased intestinal 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 separate group of cats, there was little further increase in arterial pressure 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.
AB - Transfusion with many crosslinked hemoglobin solutions causes an increase 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 ordinarily seen with such inhibition. In pentobarbital anesthetized cats, we tested whether administration of the NO synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME), produced peripheral vasoconstriction after isovolemic exchange transfusion with hemoglobin to the same extent as occurs with L-NAME infusion in time controls and in controls matched for reduced hematocrit (17%) with albumin transfusion. Bovine hemoglobin was treated aerobically with bis-(3,5-dibromosalicyl) fumarate to produce β β-81 lysine crosslinks. Hemoglobin exchange transfusion increased mean arterial blood pressure and there was no further increase after L-NAME. In contrast, L-NAME increased pressure in the time controls and albumin controls. Hemoglobin transfusion decreased intestinal 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 separate group of cats, there was little further increase in arterial pressure 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.
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U2 - 10.3109/10731199509117942
DO - 10.3109/10731199509117942
M3 - Article
C2 - 7493047
AN - SCOPUS:0029039011
SN - 1073-1199
VL - 23
SP - 263
EP - 269
JO - Artificial Cells, Blood Substitutes, and Biotechnology
JF - Artificial Cells, Blood Substitutes, and Biotechnology
IS - 3
ER -