TRANSIENTS IN MYOCARDIAL O-2 CONSUMPTION AFTER ABRUPT CHANGES IN PERFUSION-PRESSURE IN GOATS

Previously we reported that glibenclamide decelerates the rate of coro nary flow regulation by a factor of four [Am. J. Physiol. 266 (Heart C irc. Physiol. 35): H1715-H1721, 1994]. The dynamic oxygen content diff erences were analyzed in the present study. The left main coronary art ery of the anesthetized, open-chest goat was perfused at constant pres sure (P-p) P-p(t), arterial flow [Q(a)(t)], and the arteriovenous oxyg en content difference [a-vO(2)(t)] were averaged per beat. The a-vO(2) signal was corrected for mixing processes in the capillaries and tran sport 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), r eferred to as the dynamic Gregg effect. With an increase in P-p, the m aximal 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 increas e and 4.0 +/- 1.0 s for a decrease in P-p. With glibenclamide these va lues were 16.9 +/- 2.2 and 22.6 +/- 2.0 s. This study confirms that du ring steady state the P-p-induced MVo(2) (steady-state Gregg effect) i s diminished by autoregulation. However, it is concluded that during t ransients following abrupt changes in P-p, large changes in MVo(2) occ ur depending on the rate of regulation (dynamic Gregg effect).