Coronary pressure-function and steady-state pressure-flow relations during autoregulation in the unanesthetized dog.

The present study was intended to define the interrelation among endocardial flow, endocardial function, and coronary arterial pressure during spontaneous autoregulation in the left ventricle of chronically instrumented unanesthetized dogs. Steady-state sonomicrometric measurements of regional function and epicardial coronary artery pressure were used to determine the lower pressure limit of endocardial autoregulation while global indexes of myocardial demand remained constant. Transmural wall thickening in the circumflex bed remained unchanged (+/- 5% of control values) until coronary pressure fell below 39 +/- 5.6 (SD) mm Hg. Endocardial segment shortening was similarly constant until coronary pressure fell below 42 +/- 7.4 mm Hg. There was no significant change in endocardial flow as coronary pressure was reduced over the autoregulatory plateau from 84 to 49 mm Hg (1.05-0.99 ml/min/g, p = NS). Below the critical pressure limits, small additional reductions in pressure were associated with marked reductions in both endocardial flow and function. The coronary pressure-function relation was linear as well as steep in this range for both wall thickening (r = 0.94 +/- 0.05) and segment shortening (r = 0.96 +/- 0.03). Although the relation between endocardial flow and function showed more variability than pressure-function relations at low pressures, wall thickening reductions and endocardial flow reductions related on a nearly one-to-one basis. The present study establishes that the coronary pressure-function relation can be used to define the lower limit of endocardial autoregulation. It also indicates that the lower pressure limit of endocardial autoregulation is considerably less than in anesthetized animals (40 vs. 70 mm Hg) and that steady-state flow above this limit is controlled more tightly. Although these differences may relate to systemic hemodynamics, it seems likely that general anesthesia and/or acute surgical instrumentation alter coronary autoregulation under at least some experimental circumstances.