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Positive and negative inotropic effects of left ventricular mechano‐energetics in hypothermic and hyperthermic rat hearts
Author(s) -
Obata Koji,
Morita Hironobu,
Takaki Miyako
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.732.9
Subject(s) - contractility , hypothermia , medicine , inotrope , cardiology , ventricular pressure , anesthesia , chemistry , blood pressure
We investigated the effects of cardiac hypothermia or hyperthermia, including capsaicin (a TRPV1 agonist) on LV myocardial mechano‐energetics using the excised, cross‐circulated rat heart model. We analyzed the left ventricular (LV) end‐systolic pressure‐volume relation (ESPVR) and the linear relation between the myocardial oxygen consumption per beat (VO 2 ) and systolic pressure‐volume area (PVA; a total mechanical energy per beat) in isovolumically contracting rat hearts during hypothermia (32°C), normothermia (37°C), and hyperthermia (42°C) under 300‐beats per minute (bpm) pacing. LV ESPVR shifted upward in cardiac hypothermia compared with that in cardiac normothermia, whereas it shifted downward in cardiac hyperthermic and capsaicin‐treated hearts. The hypothemic, normothermic and hyperthermic VO 2 ‐PVA relations were superimposable, however, each data point of VO 2 ‐PVA at each LV volume at 32°C shifted right‐upward from that at 42°C on the VO 2 ‐PVA relation line. In capsaicin treated‐hearts, the slope of VO 2 ‐PVA relation was not also significantly different. However, the VO 2 intercept was decreased in capsaicin treated‐hearts differently from that in hyperthermic‐hearts. Decreasing cardiac temperature increased the excitation‐contraction (E‐C) coupling VO 2 for Ca 2+ handling, and decreased the basal metabolism and oxygen cost of LV contractility. The results indicate that cardiac temperature plays an important role on control ling cardiac mechano‐energetics. In addition, capsaicin decreased the LV contractility like hyperthermia due to the down‐regulation of the calcium handling in E‐C coupling. We conclude that the thermic intervention modulated cardiac inotropism by changing Ca 2+ handling and cross‐bridge cycling in rat hearts.