Cellular electrophysiological and mechanical effects of celsior solution on endothelial function in resistance...

We investigated a relatively new organ preservation (Celsior) solution regarding its effect on the endothelium-derived hyperpolarizing factor (EDHF)-mediated function with comparison to St. Thomas Hospital (ST) solution.

The EDHF-mediated relaxation was induced by bradykinin (BK, -10 to -6.5 logM) in the presence of inhibitors of nitric oxide and prostacyclin in porcine small resistance coronary arteries, before and after incubation in ST (Group Ia, n=11), Celsior (Group Ib, n=13), or Krebs (Group Ic, control, n=12) at 4 degrees C for 4 hr. The EDHF-mediated hyperpolarization of the membrane potential of smooth muscle cells was measured by microelectrode with simultaneous relaxation after cold storage in ST (IIa, n=7), Celsior (IIb, n=6), or Krebs (IIc, control, n=6), or followed by washout with Krebs (ST: IIIa, n=6, Celsior: IIIb, n=6).

The EDHF-mediated relaxation was significantly decreased in Group Ia (56.4+/-7.2% vs. 71.2+/-5.3%, P<0.05) and Ib (44.8+/-4.9% vs. 74.7+/-3.3%, P<0.05) but not in Ic. The sensitivity to BK was also significantly decreased (Ia: -7.51+/-0.14 vs. -7.76+/-0.12 log M, P<0.05; Ib: -7.36+/-0.09 vs. -7.60+/-0.09 logM, P<0.05). The resting membrane potential was depolarized in IIa (-44.3+/-1.9 mV, n=7, P<0.05) and IIb (-33.0+/-2.2 mV, n=6, P<0.05) compared with IIc (-57.1+/-1.5 mV, n=6). The EDHF-mediated hyperpolarization decreased significantly in IIa and IIb (3.4+/-0.3 and 3.0+/-0.2 vs. 6.3+/-0.5 mV, P<0.05) and partially restored in IIIa (5.0+/-0.2 vs. 3.4+/-0.3 mV, P<0.05) and IIIb (4.1+/-0.3 vs. 3.0+/-0.2 mV, P<0.05).

Storage with Celsior and ST solutions reduces the EDHF-mediated endothelial function (hyperpolarization and associated relaxation) in porcine small resistance coronary arteries.