Pressure measurements in the terminal vascular bed of the epimyocardium of rats and cats.

Publisher Website
Google Scholar
Abstract
To measure pulsatile pressures in microvessels of the left ventricular myocardium, a method was developed that extends the use of the resistance servo-nulling technique to the beating mammalian heart. In 9 cats and 25 rats, the terminal vascular bed of the ventricular epimyocardium was studied by incident light in vivo microscopy, using a highly sensitive television camera tape system. Following i.v. administration of fluorescent dextrans, microvascular diameters and flow patterns could be observed continuously. Intraluminal pressures in the microvascular bed of the cat and rat heart were determined by micropuncture and a micropipet servo-nulling system. In contrast to larger coronary arterioles (diameters 150-300 .mu.m), smaller arterioles with diameters < 100 .mu.m showed a considerable pressure drop between ascending aorta and the site of pressure recording. In venules of the epimyocardium, the pressure curve exhibited a late systolic peak, occurring just before aortic valve closure. Maximal coronary arteriolar dilatation by dipyridamole (0.5 mg/kg body wt, i.v.) provoked only a slight increase in systolic coronary venular pressure (controls 25 .+-. 3 mm Hg, dipyridamole 27 .+-. 6 mm Hg). Positive inotropic intervention by i.v. infusion of dobutamine (6 .mu.g/kg per min) and the application of norepinephrine resulted in a marked rise of systolic coronary venular pressure. The contractile state of the myocardium and left ventricular afterload apparently are the major determinants of systolic coronary venular pressure.