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 PGF1α (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.
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine