Background: Moderate and severe hypothermia with cardiopulmonary bypass during aortic surgery can cause some complications such as endothelial cell dysfunction or coagulation disorders. This study found out the difference of vascular reactivity by phenylephrine in moderate and severe hypothermia. Methods: Preserved aortic endothelium by excised rat thoracic aorta was sectioned, and then down the temperature rapidly to $25^{circ}C$ by 15 minutes at $38^{circ}C$ and then the vascular tension was measured. The vascular tension was also measured in rewarming at $25^{circ}C$ for temperatures up to $38^{circ}C$. To investigate the mechanism of the changes in vascular tension on hypothermia, NG-nitro-L-arginine methyl esther (L-NAME) and indomethacin administered 30 minutes before the phenylephrine administration. And to find out the hypothermic effect can persist after rewarming, endothelium intact vessel and endothelium denuded vessel exposed to hypothermia. The bradykinin dose-response curve was obtained for ascertainment whether endothelium-dependent hyperpolarization factor involves decreasing the phenylnephrine vascular reactivity on hypothermia. Results: Fifteen minutes of the moderate hypothermia blocked the maximum contractile response of phenylephrine about 95%. The vasorelaxation induced by hypothermia was significantly reduced with L-NAME and indomethacin administration together. There was a significant decreasing in phenylephrine susceptibility and maximum contractility after 2 hours rewarming from moderate and severe hypothermia in the endothelium intact vessel compared with contrast group. Conclusion: The vasoplegic syndrome after cardiac surgery might be caused by hypothermia when considering the vascular reactivity to phenylephrine was decreased in the endothelium-dependent mechanism.