Kiyooka Takahiko, Oshima Yu, Fujinaka Waso, Iribe Gentaro, Mohri Satoshi, Shimizu Juichiro
Division of Cardiology, Tokai University Oiso Hospital, 21-1 Gakkyo, Oisomachi, Nakagun, Kanagawa 259-0198, Japan.
Tokai J Exp Clin Med. 2014 Mar 20;39(1):51-8.
Although tachycardia is well known to increase cardiac oxygen consumption (Vo2) per min, the relationship between Vo2 for excitation-contraction (E-C) coupling per beat and heart rate change over its full working range still remains controversial.
To elucidate this relationship, we varied heart rate over a reasonably wide range (60-180 beat/min) and studied the relationship between left ventricular (LV) Emax (load-independent contractility index), PVA (pressure-volume area)-independent Vo2, and basal metabolic Vo2 in nine excised, cross-circulated canine hearts.
PVA-independent Vo2 per min significantly increased linearly with increasing heart rate while Emax remained unchanged. Basal metabolic Vo2 per min was measured under KCl arrest. E-C coupling Vo2 per min obtained by subtracting the constant basal metabolic Vo2 from the PVA-independent Vo2 also significantly increased linearly with increasing heart rate. However, PVA-independent Vo2 per beat significantly decreased with increasing heart rate. In contrast, E-C coupling Vo2 per beat, as well as that normalized to Emax, slightly but significantly increased with increasing heart rate.
The E-C coupling energy for myocardial Ca2+ handling increases with heart rate despite constant contractility in the left ventricle of the excised cross-circulated canine heart.
