Effects of Thapsigargin and KCl on the O2Use of the Excised Blood-perfused Rat Heart

Hata, Yoshiki; Sakamoto, Tsukasa; Hosogi, Shingo; Ohe, Tohru; Suga, Hiroyuki; Takaki, Miyako

doi:10.1006/jmcc.1998.0766

Cited by 29 publications

(118 citation statements)

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“…If pacing rate is decreased, myocardial O 2 consumption per minute will decrease. As shown previously (6,7,32,33), the V O2-PVA relation was linear in the rat LV. Its slope represents the oxygen cost of PVA, the efficiency of chemical to mechanical energy transduction (29).…”

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confidence: 73%

“…V0 was then finally determined as the volume-axis intercept of the best-fit endsystolic pressure (ESP)-volume relationship (ESPVR) in each vol-run. We obtained the best-fit ESPVR and end-diastolic pressure-volume relationship (EDPVR) from five to six different pressure (P)-volume (V) data with the two different exponential functions by means of the least-squares method (Delta-Graph; DeltaPoint, Monterey, CA) on a personal computer (6,7,32,33). Correlation coefficients of the best-fit ESPVRs and EDPVRs were higher than 0.91.…”

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confidence: 99%

“…The heartlung section was isolated from the left common carotid artery, descending aorta, inferior vena cava, and pulmonary trunk in this order. The beating heart was excised without interruption of coronary perfusion and supported by cross circulation with the metabolic supporter rat as previously reported in detail (6,7). The excised heart was maintained at 37°C.…”

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confidence: 99%

“…The RV was kept collapsed by continuous hydrostatic drainage of the coronary venous return, so that the RV PVA and hence PVAdependent V O2 were assumed to be negligible (6,7,32,33). The RV component of PVA-independent V O2 was calculated by multiplying biventricular PVA-independent V O2 in each contractile state with the ratio of RV weight divided by the sum of RV and LV weights.…”

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confidence: 99%

“…The RV component of PVA-independent V O2 was calculated by multiplying biventricular PVA-independent V O2 in each contractile state with the ratio of RV weight divided by the sum of RV and LV weights. The RV PVA-independent V O2 (6,7,32,33) was subtracted from the total V O2 to yield LV V O2. The LV, including the septum, and the RV were weighed for normalizing LVV.…”

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confidence: 99%

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Left ventricular function of isoproterenol-induced hypertrophied rat hearts perfused with blood: mechanical work and energetics

Nakajima-Takenaka

Zhang

Okihara

et al. 2009

American Journal of Physiology-Heart and Circulatory Physiology

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Ϫ1 ⅐ day Ϫ1 for 3 days (Iso3) or 7 days (Iso7)]-induced hypertrophied rat heart preparation under isovolumic contractionrelaxation. We evaluated pressure-time curves per beat, end-systolic pressure-volume and end-diastolic pressure-volume relations, and myocardial O 2 consumption per beat (V O2)-systolic pressure-volume area (PVA; a total mechanical energy per beat) linear relations at 240 beats/min, because Iso-induced hypertrophied hearts failed to completely relax at 300 beats/min. The LV relaxation rate at 240 beats/min in Iso-induced hypertrophied hearts was significantly slower than that in control hearts [saline 24 l/day for 3 and 7 days (Sa)] with unchanged contraction rate. The V O2-intercepts (composed of basal metabolism and Ca 2ϩ cycling energy consumption in excitationcontraction coupling) of V O2-PVA linear relations were unchanged associated with their unchanged slopes in Sa, Iso3, and Iso7 groups. The oxygen costs of LV contractility were also unchanged in all three groups. The amounts of expression of sarcoplasmic reticulum Ca 2ϩ -ATPase, phospholamban (PLB), phosphorylated-Ser 16 PLB, phospholemman, and Na ϩ -K ϩ -ATPase are significantly decreased in Iso3 and Iso7 groups, although the amount of expression of NCX1 is unchanged in all three groups. Furthermore, the marked collagen production (types I and III) was observed in Iso3 and Iso7 groups. These results suggested the possibility that lowering the heart rate was beneficial to improve mechanical work and energetics in isoproterenol-induced hypertrophied rat hearts, although LV relaxation rate was slower than in normal hearts. cardiac function; excitation-contraction coupling; systolic pressurevolume area; oxygen consumption CARDIAC HYPERTROPHY IS A MAJOR risk factor for the development of heart failure and sudden cardiac death. Therefore, to reduce mortality from cardiovascular diseases, elucidation of the mechanisms involved in cardiac hypertrophy is pivotal. It is recognized that activation of the sympathetic nervous system is associated with cardiac hypertrophy and heart failure in humans (4, 11). In addition, chronic treatment of hearts with an ␣,␤-stimulant, norepinephrine, or a ␤-stimulant, isoproterenol, induces cardiac hypertrophy accompanied with enhanced fibrosis among cardiac interstitial cells in experimental animal models (3,21,25,26). So far, various mechanisms for this remodeling have been proposed (25,26,10,36).We have recently reported that 3-day and 7-day subcutaneous infusions of isoproterenol to rats induced cardiac hypertrophy with unchanged left ventricular (LV) systolic and diastolic functions compared with normal hearts that was reversible to the control levels after the cessation of infusion (8,30). In in vivo ejecting heart model, the significant decrease of mechanical work due to the decrease of LV volume (LVV) was observed. Furthermore, these short-term models did not show any marked differences in the LV mechanical work capability compared with that induced by a 2-wk isoproterenol infusion (30). The expression l...

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confidence: 99%

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confidence: 99%

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confidence: 99%

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confidence: 99%

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Left ventricular function of isoproterenol-induced hypertrophied rat hearts perfused with blood: mechanical work and energetics

Nakajima-Takenaka

Zhang

Okihara

et al. 2009

American Journal of Physiology-Heart and Circulatory Physiology

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Methods for the Preparation of an Excised, Cross-Circulated Rat Heart

Okihara

Takaki

2018

Methods in Molecular Biology

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The Emax-Pressure-Volume Area (PVA)-VO framework proposed by Dr. Suga for canine hearts has dramatically advanced the field of cardiac mechanical work and energetics, i.e., mechanoenergetics. He and his collaborators investigated mechanoenergetics in the left ventricle (LV) of excised, cross-circulated canine heart preparations. We instituted the excised cross-circulated rat whole heart preparations and found a curvilinear end-systolic pressure-volume relation (ESPVR) in the rat LV, in contrast to the linear ESPVR in canine, rabbit, and human LVs. Although Emax, the slope of the linear ESPVR, could be used as an index of LV contractility, it was not applicable for evaluating LV contractility in the rat LV. Thus, we proposed a new index of contractility, equivalent Emax (eEmax) in the rat LV. We also found a linear VO-PVA relationship in the rat LV. Here, we introduce the methods for the preparation of excised, cross-circulated rat whole hearts and the eEmax-PVA-VO framework in the rat LV. Using this method, we can obtain accurate LV volume and myocardial O consumption in real time for estimating cardiac mechanoenergetics, which is very challenging in in vivo experiments.

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