We investigated the effect of hypoxia-reoxygenation (H-R) on the contractility and non-nitric oxide (NO)-non-PGI2 (NNONPG)-mediated relaxation and the effect of UW, a heart preservation solution, during hypothermic preservation in porcine coronary microarteries (diameter 200 to 450 μm). The arteries (n=6) were subjected to 1, 2, or 4 hr- hypoxia (PO2<5 mmHg) and reoxygenation (30 min) in Krebs at 37°C (Group I) and Krebs or UW for 4 hr-H-R at 4°C (Group II). The contractility was unchanged after 1 hr but significantly reduced after 2 or 4 hr H-R (Group I). In Group II, higher doses of U46619 were required to induce similar contraction after H-R (Krebs: -7.46±0.25 vs. -8 logM, p=0.004; in UW: -6.95±0.27 vs. -8 logM, p<0.001) with more changes in UW (p=0.007). The NNONPG-mediated relaxation to bradykinin (-10~-6.5 logM) in U46619-precontraction was established when endothelium-derived NO and PGI2 were inhibited with indomethacin (7 μM), NG-nitro-L-arginine (300 μM), and oxyhemoglobin (20 μM). The maximal NNONPG-mediated relaxation was significantly reduced (p<0.05) after H-R in either Krebs (55.6±13.6% vs. 82.9±5.9%) or UW (61.9±7.4% vs. 83.7±3.1%). We conclude that in the coronary microarteries normothermic H-R impaired contractility after 1 hr; under hypothermic H-R for 4 hr, the reduction of the contractility was more severe in UW than in Krebs; and the NNONPG-mediated relaxation reduced after 4-hr hypothermic H-R that was not protected by UW. (Supported by RGC 4383/03M, CUHK Direct Grant 2041164, 4450169, 4450171)