Original Article

Ability of sickle cells to scavenge endothelium-derived nitric oxide is reduced.



AIM: To assess the ability of sickle cells to interfere with the release or
transfer of endothelium-derived relaxing factor (EDRF) in comparison to normal
METHODS: A perfusion-superfusion bioassay system was used a canine carotid artery
with endothelium (donor of EDRF) and a ring of the same vessel without
endothelium (detector) were separated by tubing resulting in a five second
interval for transfer of EDRF from donor to detector. Changes in isometric
tension were monitored in both the donor and the detector preparations. Release
of EDRF, as determined by sustained relaxations during the contractions to
phenylephrine, was induced by infusing acetylcholine through the donor artery.
RESULTS: Superfusion with normal and sickle erythrocytes caused impairment of the
endothelium-dependent relaxations in both detector and donor tissues. When
infused through the transfer line, sickle cells were less potent than normal
erythrocytes in inhibiting relaxation in the detector tissues. In contrast,
infusion of either normal erythrocytes or sickle cell through the donor artery
caused similar degrees of inhibition in donor and detector arteries. Hemolysates
from both types of erythrocytes were equieffective at either site of infusion.
CONCLUSION: These results indicate that sickle cells are intrinsically less
potent scavengers of EDRF than normal erythrocytes. However, exposure to the
endothelium enhances the ability of sickle cells to inhibit lumenal release of
endothelium-derived relaxing factor.

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