Percutaneous transluminal coronary angioplasty (PTCA) has gained widespread acceptance as a therapeutic option in the treatment of selected patients with coronary artery disease. The morphologic sequelae of balloon angioplasty (BA) have been well described and include plaque fracture, endothelial denudation with platelet deposition, and medial/adventitial stretching. Despite its widespread use and well-defined morphologic correlates, little is known about the vasomotor consequences of BA-induced arterial injury and their role in abrupt occlusion and restenosis. The objective of the proposed research is to delineate the effects of BA-induced vessel injury on the vasomotor behavior of human coronary and peripheral arteries. A series of experiments have been designed to examine: 1) the effects of BA on vasoconstrictor responses to pharmacologic agents; 2) BA-induced alterations in endothelial-dependent and endothelial-independent vasorelaxation; and 3) the role of atherosclerosis in altering the vasomoter effects of BA. Segmental changes in arterial vasomotion following BA will be assessed using a recently developed technique, utilizing high frequency 2-D long axis ultrasonic imaging of vessels, suspended and perfused in a specially designed flow chamber/muscle bath. Quantitation of changes in segmental vessel diameter will be determined by computerized edge detection analysis of digitized ultrasonic vessel images. Motility data will be correlated with vessel histology (including scanning EM) and smooth muscle cyclic GMP determinations (by radioimmunoassay technique). This integration of motility, morphologic and cyclic nucleotide data should provide important insight into the mechanism(s) of altered vasoreactivity which has been clinically observed following BA. Ultimately, a better understanding of the vasomotor response to BA-induced injury may be of relevance in the refined application of PTCA.
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