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

• Published in: Scientific reports Vol. 8; no. 1; pp. 16246 - 11
• Main Authors: Obata, Koji, Takeshita, Daisuke, Morita, Hironobu, Takaki, Miyako
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 02.11.2018; Nature Publishing Group
• Subjects: 13/95; 692/4019/2776; 692/4019/592; 82/29; Adenosine triphosphatase; Animals; Blood pressure; Blood Pressure - physiology; Body Temperature - physiology; Ca2+-transporting ATPase; Calcium (reticular); Calcium metabolism; Cardiac muscle; Contraction; Cross Circulation; Diastole - physiology; Energy Metabolism - physiology; Heart; Humanities and Social Sciences; Hyperthermia; Inotropism; Isolated Heart Preparation; Male; Metabolism; multidisciplinary; Muscle contraction; Myocardial Contraction - physiology; Myocardium - metabolism; Myosin; Myosin ATPase; Oxygen consumption; Oxygen Consumption - physiology; Phospholamban; Phosphorylation; Rats; Rats, Wistar; Sarcoplasmic reticulum; Science; Science (multidisciplinary); Temperature effects; Ventricle; Ventricular Function, Left - physiology; End-systolic Pressure-volume Relationship (ESPVR); Cardiac Irritability; Negative Inotropic Action; Mechanoenergetics; Increased Myosin ATPase Activity
• ISSN: 2045-2322; 2045-2322
• DOI: 10.1038/s41598-018-34666-3

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.