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. 1999 Oct 1;520(Pt 1):271–280. doi: 10.1111/j.1469-7793.1999.00271.x

Table 1.

Regional myocardial arterial-venous oxygen difference and myocardial oxygen consumption at normal and increased perfusion pulse pressure

PP (mmHg) [Hb] (mg dl−1) A–VO2(ml O2 ml−1) MO2 (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; MO2, 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.