Microangiographic investigation of the effects of radiographic contrast media and hyperkalaemia on coronary artery calibre in the rabbit.

Abstract

A microangiographic technique, using novel methods of contact X-ray microscopy, was developed and used to study the effects of ionic (Urografin 370) and non-ionic (Omnipaque 350) radiographic contrast media, and hyperkalaemia (exposure to 15, 30 and 60 mM-K+ solutions) on coronary artery calibre and total coronary vascular resistance in isolated, Langendorff-perfused rabbit hearts. Repeated injection of both types of contrast media produced similar haemodynamic effects and some reduction in coronary diameter, but greater variation in arterial calibre was observed with Urografin (P less than 0.001). Perfusion with hyperkalaemic solutions produced a dose-related increase in total coronary vascular resistance (P less than 0.001), but this was associated with a complex pattern of changes in large-vessel calibre. The direction and magnitude of the responses to hyperkalaemia varied depending on the site within the artery studied; in general hyperkalaemia produced a dose-related vasoconstriction which was greater distally than proximally. Thus, with 15 mM-K+ vasoconstriction occurred in the left anterior descending artery (4.3% proximally; 15.6% distally) which increased to 40.7 and 52.1% (proximally and distally, respectively) with 30 mM-K+. With 60 mM-K+ further diffuse and segmental vasoconstriction occurred in 4/5 and 1/5 hearts respectively (mean values 31.5 and 56.7% at the proximal and distal sites). During perfusion with 15 mM-K+, net vasodilatation (17% at both the proximal and distal sites) was noted in the left ventricular branch of the circumflex artery, but with 30 mM-K+ vasoconstriction (18.3% proximally and 38.0% distally) occurred. Thus, while hyperkalaemia consistently increased coronary vascular resistance, these changes were associated with marked variation in the extent and distribution of in situ constriction and dilatation within the coronary circulation.