Balloon dilatation of porcine pulmonary arteries decreases endothelium-dependent relaxations and increases vasoconstriction to aggregating platelets.

Abstract

Balloon dilatation of muscular coronary arteries disrupts endothelium and smooth muscle and allows platelet aggregation and adherence and cell proliferation, which can lead to restenosis. Balloon dilatation of the more distensible pulmonary artery is commonly performed, but the extent of damage to endothelium and its effect on the release of endothelium-derived nitric oxide (EDNO) and prostacyclin has not been studied. We dilated distal pulmonary arteries of intact ex vivo porcine lungs (n = 20; balloon-dilated [BD] group) using similar-sized adjacent vessels as controls with (E+group) and without (E- group) endothelium. Isolated rings were studied in vitro. Aggregating platelets caused constrictions of quiescent rings from the BD (27.4 +/- 8% of constriction to 80 mmol/L KCl) and E- groups (24 +/- 5%), which were inhibited by pyrilamine, a histamine blocker (11 +/- 4%; P < .05), and an intact endothelium (8 +/- 5%; P < .05). Constrictions to histamine and KCl were similar in the BD and E- groups. In rings with increased tone, platelets caused endothelium-dependent relaxations in the E+ group (70 +/- 6% relaxation), which were significantly (P < .05) inhibited in the BD group (20 +/- 7%), by L-nitro-arginine (EDNO blocker, 17 +/- 7%) and in the E- group (21 +/- 9%). Balloon dilatation markedly reduced endothelium-dependent relaxations to 5-hydroxytryptamine, thrombin, acetylcholine, and the calcium ionophore A23187, but relaxations to sodium nitroprusside were unaffected. Despite the distensibility of the pulmonary artery, balloon dilatation significantly damages the pulmonary endothelium, decreases EDNO production, impairs vasodilation, and favors platelet-induced vasoconstriction.