Table 1.
PP (mmHg) | [Hb] (mg dl−1) | A–VO2(ml O2 ml−1) | MV̇O2 (ml O2 min−1) | |
---|---|---|---|---|
Control (n = 16) | 40 | 11.5 ± 2.1 | 6.1 ± 0.5 | 7.6 ± 0.5 |
100 | 11.6 ± 1.9 | 5.8 ± 0.6 | 7.6 ± 0.7 | |
Adenosine (n = 7) | 40: pre-drug | 12.4 ± 1.2 | 6.4 ± 0.7 | 8.1 ± 1.0 |
40: post-drug | 11.9 ± 1.1 | 3.0 ± 0.5† | 10.3 ± 1.8* | |
100: post-drug | 11.3 ± 1.0 | 2.7 ± 0.4 | 10.45 ± 1.7 | |
Bradykinin (n = 6) | 40: pre-drug | 12.1 ± 0.9 | 6.3 ± 0.5 | 7.5 ± 0.5 |
40: post-drug | 11.3 ± 1.1 | 4.1 ± 0.7† | 9.9 ± 1.7 | |
100: post-drug | 11.4 ± 1.1 | 4.1 ± 0.55 | 9.8 ± 1.7 | |
Verapamil (n = 5) | 40: pre-drug | 11.6 ± 1.1 | 6.1 ± 0.5 | 8.0 ± 0.7 |
40: post-drug | 11.2 ± 1.2 | 2.1 ± 0.3† | 5.5 ± 1.6† | |
100: post-drug | 11.4 ± 1.0 | 2.6 ± 1.0 | 5.7 ± 1.4 |
PP, coronary perfusion pulse pressure; [Hb], haemoglobin concentration; A-V O2, arterial-venous oxygen difference; MV̇O2, myocardial oxygen consumption.
P = 0.06
P < 0.05 vs. pre-drug. Data are provided for the control condition and with adenosine, bradykinin or verapamil infusion. There was no significant change in regional oxygen consumption with increased pulse pressure under any of the conditions.