Previous studies have demonstrated that vein storage in normal saline leads to significant mechanical morphological, and biochemical aberrations. However, little information is available regarding the functional damage that occurs. The purpose of this study was to evaluate the effect of saline storage on venous smooth muscle and endothelial function. Segments of ten external jugular veins from male New Zealand White rabbits were placed nondistended in either modified Krebs solution at 37 °C (Krebs-stored, KS) or heparinized normal saline at room temperature (saline-stored, SS) for 1 h. Segments 4 mm in length were then simultaneously studied in vitro under isometric tension. There was no difference in maximum tension or sensitivity to either bradykinin or histamine. Acetylcholine-induced relaxation in KS segments was not significantly different from relaxation in a historical cohort of nonstored segments (nonstored 87.4 ± 1.0% vs. KS 84.5 ± 2.0%; p = NS). However, there were significant attenuations in SS segment endothelium-dependent relaxation in response to both acetylcholine (KS 84.5 ± 2.0% vs. SS 76.4 ± 2.7%, p < 0.02) and aden-osine diphosphate (KS 47.9 ± 2.9% vs. SS 40.6 ± 3.7%, p < 0.002). Relaxant responses to sodium nitroprusside (endothelium-independent) were not significantly different in the two groups (KS 94.6 ± 1.6% vs. SS 95.7 ± 2.2%; p = NS). Electron microscopic evaluation of SS segments revealed endothelial cell disruption with cellular edema and loss of intact junctions. These results demonstrate that rabbit external jugular vein storage in normal saline at room temperature for 1 h (1) is associated with significant morphologic damage, (2) impairs endothelial-dependent relaxation, and (3) appears to have no effect on smooth muscle cell function. Additionally, KS-stored (37 °C) veins exhibit a level of endothelium-dependent relaxation that is equivalent to nonstored controls.</jats:p