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 erythrocytes. 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 acetylcho-line through the donor artery. RESULTS: Supervision 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, i 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 erythrocytes. 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 five five second interval for transfer of EDRF from donor to detector. Changes in isometric tension was monitored in both the donor and the detector preparations. EDRF, as determined by sustained relaxations during the contractions to phenylephrine, was induced by infusing acetylcho-line through the donor artery. RESULTS: Supervision with normal and sickle erythrocytes caused impairment of the endothelium-dependent relaxations in both detector and donor tissues. through the transfer line, sickle cells were less potent than normal erythrocytes in inhibiting relaxation in the detector tissu es. In contrast, i