Domenech R J, Macho P, Barros F
Department of Pathophysiology, Faculty of Medicine, University of Chile, Santiago.
Cardiovasc Res. 1990 Oct;24(10):851-6. doi: 10.1093/cvr/24.10.851.
The aim was to test the hypothesis of a vascular waterfall in the epicardial veins due to compression by the left ventricular (LV) pressure. If this were so, the epicardial venous pressure should be a direct function of the LV pressure.
Canine arrested hearts were used, without autoregulation and perfused with the Langendorff technique. Coronary flow and outflow pressure were measured in the great cardiac vein, which was the only outflow of the system. The pressure in an epicardial vein was also measured. The measurements were done with LV pressures varying from zero to 40 mm Hg. The outflow pressure was progressively increased until a steady decrease in flow occurred. This pressure was considered the critical outflow pressure.
19 mongrel dogs, 18-25 kg, were used. The animals were anaesthetised and the hearts perfused in the Langendorff manner with homologous blood.
The epicardial venous pressure before outflow pressure was increased was higher than LV pressure (even at zero LV pressure), and increased linearly with the increase in LV pressure (epicardial venous pressure = 0.74 LV pressure +6.18; r = 0.93). The increase in outflow pressure did not modify flow until it reached a value (critical outflow pressure) similar to epicardial venous pressure. Critical outflow pressure was linearly related to LV pressure (critical outflow pressure = 0.65 LV pressure +5.13, r = 0.87).
The results support the hypothesis of a waterfall circulation in the epicardial veins during diastole, the magnitude of which is a function of the LV pressure.
