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In order to measure pulsatile pressures in microvessels of the left ventricular myocardium, we developed a method that extends the use of the resistance servo-nulling technique to the beating mammalian heart. In 9 cats and 25 rate, we studied the terminal vascular bed of the ventricular epimyocardium by incident light in vivo microscopy, using a highly sensitive television camera tape system. Following intravenous administration of fluorescent dextrans, microvascular diameters and flow patterns could be observed continuously. Intrahuninal pressures in the microvascular bed of the cat and rat heart were determined by micropuncture and a micropipet servo-nulling sy stem. In contrast to larger coronary arterioles (diameters 160-300 pan), smaller arterioles with diameters <100 fim 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 weight, iv) provoked only a slight increase in systolic coronary venular pressure (controls 25 3 mm Hg, dipyridamole 27 6 mm Hg). On the other hand, positive inotropic intervention by intravenous infusion of dobutamine (6 /ig/kg per min), as well as the application of norepinepht-ine, resulted in a marked rise of systolic coronary venular pressure. These data suggest that the contractile state of the myocardium and left ventricular afterload are the major determinants of systolic coronary venular pressure.
Tillmanns et al. (Sun,) studied this question.