Release of nitric oxide by intact human and canine pericardium

Pericardial mesothelial cells and vascular endothelial cells have a common embryological origin. We examined human and canine pericardial production of vasoactive factors with superfusion bioassay after fashioning pericardial conduits. Both canine and human pericardial effluent relaxed precontracted de-endothelialized coronary artery segments under basal conditions (2±4% and 4±5%, n=25, 9; P<0.05, respectively). Calcium ionophore A23187 stimulated factor production in canine (27±21%, n=26, P<0.001 vs. basal) and human pericardium (21±17%, n=9, P<0.05). Indomethacin inhibited basal and stimulated release in both canine (basal 0±1 vs. 2±4%, n=7, P<0.01; stimulated 2±4% vs. 27±21%, n=7, P<0.001), and human pericardium (basal 0±0 vs. 4±5%, n=5, P<0.05; stimulated 0±0% vs. 21±17%, n=5, P<0.05). N^G-Arg also inhibited both the basal and stimulated release of relaxing factors by the canine pericardium (basal 1±1 vs. 2±4%, n=7, P<0.05, stimulated -2±5% vs. 27±21%, n=7, P<0.001). In the human pericardium, N^G-Arg inhibited the basal release and decreased stimulated release of relaxing factors (basal -2±3 vs. 4±5%, n=5, P<0.05; stimulated 14±8% vs. 21±17%, n=5, P=0.3). This study demonstrates that intact pericardium releases nitric oxide and may have important implications for its use as a material for surgical implantation.