1. Volume 19, Issue 3, Pages 163-170 (June 2012)
Cardiac mechanoenergetics for understanding isoproterenol-induced rat heart failure 
Miyako Takaki 
Pathophysiology 
Volume 19, Issue 3, Pages (June 2012)
DOI: /j.pathophys
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2. Fig. 1
Key framework of ESPVR-VO2–PVA for assessment of left ventricular mechanoenergetics. Vertical bidirectional arrow: isovolumic contraction and relaxation at mLVV. ESPVR, end-systolic pressure–volume relation; EDPVR, end-diastolic pressure–volume relation; mLVV, midrange left ventricular volume; VO2, myocardial oxygen consumption per beat; PVA, systolic pressure–volume area; black star, PVAmLVV; E–C, excitation–contraction; V0: volume intercept of ESPVR. Detailed explanations are described in the text.
Pathophysiology  , DOI: ( /j.pathophys )
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3. Fig. 2
An example of the plotting data of PVA-independent VO2 and eEmaxmLVV during a Ca2+ inotropism run at mLVV. The data moved as indicated by the arrow during Ca2+-infusion. In this linear relation, the slope is calculated as 0.81×10−4μlO2mlmmHg−1beat−1g−2.
Pathophysiology  , DOI: ( /j.pathophys )
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4. Fig. 3
Possible mechanisms for ISO-induced hypertrophy from our results and literatures. Main role players are illustrated. ISO, isoproterenol; AR, adrenergic receptor; AT1, angiotensin1 receptor; NCX1, Na+–Ca2+ exchanger 1; PLM, phospholemman; NKA, Na+–K+ pump; NHE, Na+–H+ exchanger; SR, sarcoplamic reticulum; SERCA2, SR Ca2+ ATPase; PLB, phospholamban; PKA, protein kinase A; PPI-1, protein phosphatase inhibitor-1; PP1, protein phosphatase 1; MAPKs, mitogen-activated protein kinases; CaMK, calmodulin kinase; CN, calcineurin; PI3Kγ, phosphoinositide 3-kinase class IB; Akt, protein kinase B; ROS, reactive oxygen species; T-BARS, thiobarbituric acid reactive substances; IGF-1, insulin growth factor-1; HDAC1, histone deacetylase 1; AP-1, activator protein 1; Epac, a cAMP-regulated guanine nucleotide exchange factor; HSP47, heat shock protein 47.
Pathophysiology  , DOI: ( /j.pathophys )
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