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1 Departments of Cardiovascular Dynamics and Medicine, National Cardiovascular Center, 5 Fujishirodai, Suita, Osaka, 565-8565; and 2 Department of Physiology II, Okayama University Medical School, 2 Shikatacho, Okayama, 700-8558 Japan
Heart temperature affects left
ventricular (LV) function and myocardial metabolism. However, how and
whether increasing heart temperature affects LV mechanoenergetics
remain unclear. We designed the present study to investigate effects of
increased temperature by 5°C from 36°C on LV contractility and
energetics. We analyzed the LV contractility index
(Emax) and the relation between the myocardial oxygen consumption (M
O2) and
the pressure-volume area (PVA; a measure of LV total mechanical energy)
in isovolumically contracting isolated canine hearts during
normothermia (NT) and hyperthermia (HT). HT reduced
Emax by 38% (P < 0.01) and
shortened time to Emax by 20%
(P < 0.05). HT, however, altered neither the slope nor
the unloaded M
O2 of the
M
O2-PVA relation. HT increased the
oxygen cost of contractility (the incremental ratio of unloaded M
O2 to Emax) by
49%. When Ca2+ infusion restored the reduced LV
contractility during HT to the NT baseline level, the unloaded
M
O2 in HT exceeded the NT value by 36%.
We conclude that HT-induced negative inotropism accompanies an increase
in the oxygen cost of contractility.
temperature; pressure-volume area; myocardial oxygen consumption
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