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The effect of cold storage of porcine pulmonary microvessels in University of Wisconsin (UW) and Euro-Collins (EC) solutions on the cellular electrophysiologic properties remains unknown.The pulmonary microarteries (PA, 381.6 ± 62.8 μm; n = 60) and microveins (PV, 360.8 ± 54.5 μm; n = 60) were incubated with Krebs (control), UW, or EC solution at 4°C for 4 hours in a myograph. The resting membrane potential and the endothelium-derived hyperpolarizing factor-mediated hyperpolarization to bradykinin (0.1 μmol/L) in the presence of inhibitors of nitric oxide and prostacyclin, Nω-nitro-l-arginine, hemoglobin, and indomethacin, in a single smooth muscle cell were directly measured.The resting membrane potential (−60.8 ± 1.3 mV in PA and −48.1 ± 0.7 mV in PV, n = 6) was depolarized after exposure to UW solution (to −18.4 ± 0.7 mV in PA and −13.6 ± 0.8 mV in PV; n = 8; p < 0.001). The amplitude of endothelium-derived hyperpolarizing factor-mediated hyperpolarization to bradykinin was also decreased (from 7.4 ± 0.7 mV to 2.6 ± 0.7 mV in PA and from 4.6 ± 0.5 mV to 0.9 ± 0.4 mV in PV; p < 0.001). In comparison, EC depolarized the membrane potential to a lesser extent (to −28.3 ± 0.9 mV in PA and to −21.3 ± 0.8 mV in PV; n = 8; p < 0.001) and almost abolished the hyperpolarization to bradykinin. After washout, hyperpolarization was partially restored (UW, 4.9 ± 0.7 mV in PA and 2.0 ± 0.3 mV in PV. p < 0.01; EC, 2.3 ± 0.5 mV in PA and 1.0 ± 0.3 mV in PV. p < 0.01).Cold storage of porcine PA and PV with UW or EC solution impairs the electrophysiologic properties (hyperpolarization) related to endothelium-smooth muscle interaction. The alteration is more profound with EC than UW solution and in veins than in arteries. The findings urge further studies on lung preservation solutions.