Hypothermic storage with University of Wisconsin solution preserves endothelial and vascular smooth-muscle function

The effect of University of Wisconsin (UW) solution on coronary endothelial function is debated. Although earlier studies demonstrated preservation of stimulated release of endothelial vasoactive factors, the effect of UW solution on basal nitric oxide release has not been investigated, and this was the purpose of the present study.

Isolated canine coronary arteries were evaluated immediately after being harvested (group 1) and after 24-hour hypothermic (4 degrees C) storage in either buffered physiological saline solution (group 2) or UW solution (group 3). Smooth-muscle vascular response to sodium nitroprusside (10(-9) to 10(-6) mol/L), KCl (5 to 50 mmol/L), and prostaglandin F2alpha (10(-9) to 10(-6) mol/L) was comparable among the groups, as was the endothelial response to acetylcholine (10(-9) to 10(-6) mol/L) and calcium ionophore A23187 (10(-9) to 10(-6) mol/L). Vessels in group 3 exhibited better preservation of basal release of nitric oxide, as measured by contraction to either N(G)-monomethyl L-arginine (10(-4) mol/L) or methylene blue (10(-5) mol/L), in comparison with control arteries exposed to saline solution (group 2). There was no difference in the basal production of nitric oxide between group 1 and group 3 vessels.

The present study demonstrated preservation of vascular smooth muscle and endothelium-dependent relaxations after prolonged hypothermic storage in UW solution. Furthermore, storage in this solution preserved basal release of nitric oxide.