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

SUMMARY In order to measure pulsatile pressures in microvessels of the left ventricular myocar-dium, 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 myocar-dium and left ventricular afterload are the major determinants of systolic coronary venular pressure. Ore Res 49: 1302-1311, 1981 THE microcirculatory events during the cardiac cycle are governed mainly by systemic arterial pres-sure, changes in coronary resistance (due to vascu-lar compression by the myocardium as well as re-laxation of heart muscle), vascular cross-sectional area and capacity, and Theological properties of the blood (Gregg, 1962; Raff et al., 1972; Tillmanns et al., 1974). Until recently, only partial success has resulted from any attempts to separately identify and estimate the changes in the two variables which control hemodynamics of the coronary microcircu-lation, namely, extravascular support and activ