Vessel wall arachidonate metabolism after angioplasty: Possible mediators of postangioplasty vasospasm

The mechanism of postangioplasty vasospasm is uncertain. It was postulated that a reduction in vasodilator prostaglandin I₂ (PGI₂) or prostaglandin E₂ (PGE₂) or an increase in vasoconstrictor hydroperoxy acids might contribute to spasm of a dilated artery. Twelve mongrel dogs were anesthetized, intubated, and mechanically ventilated. Heart rate and aortic pressures were continuously monitored and arterial blood gases maintained within physiologic limits. A single carotid artery was dilated in each animal (4 atm × 1 minute × 3) using nonex-pandable polyethylene balloon catheters with inflated balloon diameters 50 to 100% larger than the internal arterial lumen. The opposite carotid artery served as a control. In 4 animals, aspirin (10 mg/kg, intravenously) was injected 30 minutes before dilation. Sixty minutes after dilation, animals were heparinized and the carotid arteries carefully removed. The in vitro conversion of carbon-14(¹⁴C) -arachidonic acid (AA) to 6-keto PGF_1α (PGI₂), PGE₂, and 12L-hydroxy-5,8,10,14-eicosatetraenoic acid (HETE) was determined using thin-layer radiochromatography. Angioplasty caused a 70% decrease in vessel wall PGI₂ production and a 44% decrease in PGE₂ production (n = 4, p < 0.05). Reductions in in vitro conversion of ¹⁴C-AA to PGI₂ and PGE₂ induced by angioplasty were comparable to that produced by cyclooxygenase inhibition with aspirin. Angioplasty, in addition, caused a 104% increase in vessel wall HETE production (n = 4, p < 0.05). Therefore, angioplasty results in a local derangement of AA metabolism characterized by decreases in vasodilator prostaglandins and increases in vasoconstrictor hydroperoxy acids. These local changes may contribute, in part, to sudden arterial occlusion after angioplasty.