BACKGROUND: Because blood flow modulates endothelial prostacyclin production, the extent of this production in autologous vein grafts implanted in poor distal runoff limbs needed to be examined. METHODS: Endothelial prostacyclin production in canine autologous vein grafts was measured in poor distal runoff limbs (poor runoff group) and compared with findings in normal runoff limbs (control group). Vein grafts were perfused in a closed circuit at 3 days and 1, 2, 3, and 4 weeks after implantation; after perfusion for the first 30 minutes in a steady flow (basal prostacyclin production), the grafts were exposed to arachidonic acid (stimulated prostacyclin production) for the following 30 minutes. Prostacyclin, as the metabolite 6-keto-PGF1 alpha, was radioimmunoassayed. RESULTS: Basal and stimulated prostacyclin production increased in both groups during a period of time after implantation. At 2 weeks when endothelialization was complete, prostacyclin production in the poor runoff group was impaired, compared with the findings in the control group, and this difference increased with time. At 4 weeks the stimulated prostacyclin production was 18.91 +/- 4.03 ng/cm2 in the control group and 11.60 +/- 1.67 ng/cm2 in the poor runoff group (p < 0.05). CONCLUSIONS: We propose that the impaired capacity of the vein graft to produce prostacyclin in a poor distal runoff may lead to loss of graft patency in reconstructed arteries.
BACKGROUND: Because blood flow modulates endothelial prostacyclin production, the extent of this production in autologous vein grafts implanted in poor distal runoff limbs needed to be examined. METHODS: Endothelial prostacyclin production in canine autologous vein grafts was measured in poor distal runoff limbs (poor runoff group) and compared with findings in normal runoff limbs (control group). Vein grafts were perfused in a closed circuit at 3 days and 1, 2, 3, and 4 weeks after implantation; after perfusion for the first 30 minutes in a steady flow (basal prostacyclin production), the grafts were exposed to arachidonic acid (stimulated prostacyclin production) for the following 30 minutes. Prostacyclin, as the metabolite 6-keto-PGF1 alpha, was radioimmunoassayed. RESULTS: Basal and stimulated prostacyclin production increased in both groups during a period of time after implantation. At 2 weeks when endothelialization was complete, prostacyclin production in the poor runoff group was impaired, compared with the findings in the control group, and this difference increased with time. At 4 weeks the stimulated prostacyclin production was 18.91 +/- 4.03 ng/cm2 in the control group and 11.60 +/- 1.67 ng/cm2 in the poor runoff group (p < 0.05). CONCLUSIONS: We propose that the impaired capacity of the vein graft to produce prostacyclin in a poor distal runoff may lead to loss of graft patency in reconstructed arteries.