Transients in myocardial O-2 consumption after abrupt changes in perfusion pressure in goats

Previously we reported that glibenclamide decelerates the rate of coronary flow regulation by a factor of four [Am. J. Physiol. 266 (Heart Circ. Physiol. 35): H1715-H1721, 1994]. The dynamic oxygen content differences were analyzed in the present study. The left main coronary artery of the anesthetized, open-chest goat was perfused at constant pressure (P-p) P-p(t), arterial flow [Q(a)(t)], and the arteriovenous oxygen content difference [a-vO(2)(t)] were averaged per beat. The a-vO(2) signal was corrected for mixing processes in the capillaries and transport time from capillaries to the venous measuring site [a-vO*(2)(t)]. A change in P-p of 20 mmHg induced a 2 temporary change in MVo(2), referred to as the dynamic Gregg effect. With an increase in P-p, the maximal change of myocardial oxygen consumption [MVo(2)(t) = Q(a)(t). a-vO*(2)(t)] was 15.0 +/- 3.6% (means +/- SE) during control and 31.3 +/- 2.3% with glibenclamide. With a decrease in P-p these changes were 16.3 +/- 2.9 and 21.0 +/- 1.1%. During control, the half-time for the rate of return of the MVo(2) response was 4.2 +/- 0.8 s for an increase and 4.0 +/- 1.0 s for a decrease in P-p. With glibenclamide these values were 16.9 +/- 2.2 and 22.6 +/- 2.0 s. This study confirms that during steady state the P-p-induced MVo(2) (steady-state Gregg effect) is diminished by autoregulation. However, it is concluded that during transients following abrupt changes in P-p, large changes in MVo(2) occur depending on the rate of regulation (dynamic Gregg effect).