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We investigated the effects of altering cardiac temperature on left ventricular (LV) myocardial mechanical work and energetics using the excised, cross-circulated rat heart model. We analyzed the LV end-systolic pressure–volume relationship (ESPVR) and linear relationship between myocardial oxygen consumption per beat (VO 2 ) and systolic pressure–volume area (PVA; total mechanical energy per beat) in isovolumically contracting rat hearts during hypo- (32 °C), normo- (37 °C), and hyperthermia (42 °C) under a 300-beats per minute pacing. LV ESPVR shifted downward with increasing cardiac temperature. The VO 2 –PVA relationship was superimposable in these different thermal conditions; however, each data point of VO 2 –PVA shifted left-downward during increasing cardiac temperature on the superimposable VO 2 –PVA relationship line. VO 2  for Ca 2+  handling in excitation–contraction coupling decreased, which was associated with increasing cardiac temperature, during which sarcoplasmic reticulum Ca 2+ -ATPase (SERCA) activity was suppressed, due to phospholamban phosphorylation inhibition, and instead, O 2  consumption for basal metabolism was increased. The O 2  cost of LV contractility for Ca 2+  also increased with increasing cardiac temperature. Logistic time constants evaluating LV relaxation time were significantly shortened with increasing cardiac temperature related to the acceleration of the detachment in cross-bridge (CB) cycling, indicating increased myosin ATPase activity. The results suggested that increasing cardiac temperature induced a negative inotropic action related to SERCA activity suppression in Ca 2+  handling and increased myosin ATPase activity in CB cycling. We concluded that thermal intervention could modulate cardiac inotropism by changing CB cycling, Ca 2+  handling, and basal metabolism in rat hearts.

Left ventricular mechanoenergetics in excised, cross-circulated rat hearts under hypo-, normo-, and hyperthermic conditions