Aortic constriction in canine left ventricles shifted the end-systolic pressure-volume relationship upward (P<0.001), but this contractility increase was not driven by coronary perfusion pressure.
Does the concomitant increase in coronary arterial pressure with increased afterload contribute to the afterload-induced increase in contractile force in the intact canine left ventricle?
Coronary perfusion pressure does not influence left ventricular contractile function unless coronary flow changes, indicating that increased coronary arterial pressure does not mediate afterload-induced increases in contractile force.
p-value: p=<0.001
BACKGROUND: Increased left ventricular (LV) contractile force or oxygen consumption has been documented with increased coronary arterial pressure (CAP) and flow (Gregg phenomenon). We investigated whether the increase in contractile force with increased LV afterload might be mediated by the concomitant increase in CAP when coronary autoregulation is intact. METHODS AND RESULTS: The LV of 6 autonomically blocked open-chest dogs was perfused through the left main coronary artery by a cannula with a side gate to the aortic root. With the gate open, CAP increased from 77+/-20 to 93+/-20 mm Hg (P<0.05) with aortic constriction (AC). With the gate closed, CAP was maintained at a constant level of 100 mm Hg. A small reduction in the slope of the preload recruitable stroke work (PRSW) relationship was observed with AC, but this response was not altered by the coronary perfusion gate position. The end-systolic pressure-volume (ESPV) relationship shifted upward significantly with AC (P<0.001), but this shift was not greater with open-gate perfusion than with closed-gate perfusion. Furthermore, with coronary autoregulation intact, wide changes in CAP (between 60 and 180 mm Hg, n=5) did not alter either the PRSW or ESPV relationship. In contrast, when autoregulation was abolished with intracoronary adenosine (n=6), both indexes of contractility increased progressively with increased CAP. CONCLUSIONS: The concomitant increase in CAP with increased afterload in the intact canine LV does not contribute to the afterload-induced increase in contractile force. Coronary perfusion pressure per se does not influence LV contractile function. Coronary perfusion pressure influences contractility only when coronary flow changes.
Karunanithi et al. (Tue,) conducted a other in Normal cardiac physiology (canine model) (n=6). Aortic constriction with open vs. closed coronary perfusion gate vs. Closed-gate perfusion (constant coronary arterial pressure) was evaluated on Left ventricular contractile force (preload recruitable stroke work and end-systolic pressure-volume relationship) (p=<0.001). Aortic constriction in canine left ventricles shifted the end-systolic pressure-volume relationship upward (P<0.001), but this contractility increase was not driven by coronary perfusion pressure.