Storage in sodium chloride does not impair arterial prostacyclin release

Heparinised sodium chloride solution is often used for the storage of veins and to prevent clotting in the arterial tree during vascular surgery. Sodium chloride deranges the morphology of endothelial cells and has therefore been interpreted as "toxic" to the endothelial cell. Perfused human saphenous veins and rabbit aortas show the same pattern of prostanoid release even though veins have a lower release than arteries. Excised rabbit aortas were stored in either (a) 0.9% sodium chloride or (b) 0.9% sodium chloride with heparin 5 I.U. ml-1 prior to being mounted in a perfusion model. The vessels were perfused ex vivo for 5 x 15 min with either Hanks' balanced salt solution (HBSS), calcium- and magnesium-free HBSS or 0.9% sodium chloride. For the last period, arachidonic acid (AA) 4 micrograms ml-1 was added. The release of prostacyclin, measured as the stable degradation product 6-keto-PGF1 alpha by radioimmunoassay, was not altered by storage in sodium chloride, or 0.9% sodium chloride plus heparin when compared with control segments. Perfusion with 0.9% sodium chloride did, however, significantly (p greater than 0.05) decrease the prostacyclin production when AA was added. This is most likely to be due to the low pH of the sodium chloride solution. It is concluded that short-term storage of rabbit aorta in sodium chloride plus heparin or 0.9% sodium chloride does not impair the prostacyclin cascade from the vessel wall, which might be of importance when choosing storage medium for reversed veins and veins used for coronary bypass surgery.