Is vasospasm related to platelet deposition? Relationship in a porcine preparation of arterial injury in vivo.

Publisher Website
Google Scholar
Abstract
Although aggregating platelets can release potent vasoactive substances in vitro, the importance of platelets in mediating naturally occurring or provoked spasm in vivo is not clear. To investigate the possible role of platelets in arteiral spasm following arterial injury induced by angioplasty, quantitative platelet deposition of the dilated arterial segment and the degree of vasoconstriction (average percent diameter narrowing just proximal and distal to the dilated segment) produced during angioplasty of the common carotid arteries were studied in 42 heparinized normal pigs that were killed immediately after the angioplasty procedure. Angiographic films of the carotid arteries were taken before and after the dilatation to assess the vasoconstriction. Vasoconstriction was greater (40% vs 19%, p < .002) when platelet deposition (.times. 106/cm2) was in excess of 10, and the severity of vasoconstriction in vivo had a close positive exponential correlation (r = .77, p < .001) with the extent of platelet deposition in 24 untreated pigs. Platelet deposition and vasoconstriction were greater with severe atrial wall injury than with mild injury (58.8 versus 6.9, p < .0001; 37% vs. 21%, p < .001, respectively). After severe injury in 18 pigs pretreated with 1 mg/kg/day aspirin, platelet deposition decreased (from 58.8 to 19.6, p < .02) and vasocontriction decreased (from 37% to 21%, p < .003) relative to control. After mild injury, platelet deposition and vasoconstriction were mild and unchanged by aspirin. Thus, local vasoconstriction is influenced by the degree of platelet deposition. This is the first reported correlation in vivo between quantitative platelet deposition and localized vasoconstriction at the site of the arterial injury and the reduction of vasoconstriction by platelet inhibitor therapy.