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Am J Physiol Heart Circ Physiol 275: H1313-H1321, 1998;
0363-6135/98 $5.00
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Vol. 275, Issue 4, H1313-H1321, October 1998

Effect of cross-linked hemoglobin transfusion on endothelial-dependent dilation in cat pial arterioles

Yoshio Asano1, Raymond C. Koehler1, John A. Ulatowski1, Richard J. Traystman1, and Enrico Bucci2

1 Department of Anesthesiology/Critical Care Medicine, The Johns Hopkins University School of Medicine, Baltimore 21287; and 2 Department of Biological Chemistry, The University of Maryland at Baltimore School of Medicine, Baltimore, Maryland 21201

We determined whether addition of hemoglobin to the plasma would inhibit endothelial-dependent dilation in brain where tight endothelial junctions limit hemoglobin extravasation. Pial arteriolar diameter was measured by intravital microscopy through closed cranial windows in anesthetized cats either without transfusion (hematocrit = 32%) or after exchange transfusion with an albumin or sebacyl-cross-linked human hemoglobin solution (hematocrit = 18%). Dilation of small, medium, and large arterioles to acetylcholine and ADP was not significantly altered by hemoglobin transfusion. The dilatory responses were inhibited by the nitric oxide synthase inhibitor NG-nitro-L-arginine, although significant dilation to 30 µM acetylcholine persisted in small arterioles in the control and albumin-transfused group but not in the hemoglobin-transfused group. The dilatory response to the nitric oxide donor 3-morpholinosydnonimine was unaffected by albumin or hemoglobin transfusion, but the response to nitroprusside was reduced by one-third after hemoglobin transfusion. When cross-linked hemoglobin was superfused through the cranial window, the acetylcholine response became inhibited at a hemoglobin concentration of 0.1 µM and was completely blocked at 10 µM. Because this concentration is substantially less than the 500 µM hemoglobin concentration in plasma after transfusion when there was no inhibition of the acetylcholine response, hemoglobin permeation of the blood-brain barrier was considered negligible. We conclude that exchange of red cell-based hemoglobin with plasma-based hemoglobin does not produce a more effective sink for endothelial-derived nitric oxide evoked by agonist receptor-mediated activation. Furthermore, decreased hematocrit does not affect agonist-evoked endothelial-dependent dilation.

acetylcholine; adenosine 5'-diphosphate; anemia; cerebral blood vessels; nitric oxide


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