Linear O2 Use-Pressure-Volume Area Relation from Curved End-Systolic Pressure-Volume Relation of the Blood-Perfused Rat Left Ventricle.

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

doi:10.2170/jjphysiol.48.197

Cited by 37 publications

(155 citation statements)

References 9 publications

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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).…”

supporting

confidence: 83%

“…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.…”

mentioning

confidence: 99%

“…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%

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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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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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“…However, the cardiac mechanoenergetics studies have not yet been well conducted. We have established a method to analyze specifically the LV mechanical work and energetics in an excised, blood-perfused whole heart preparation with a cross-circulation method (7,14,17,19,20,24) and analyzed LV mechanoenergetics in a PO heart failure model.In the present study, we focused on the investigation of the mechanical work and energetics in a VO heart failure model with an arteriovenous (AV) shunt in rats. …”

mentioning

confidence: 99%

“…All rats were heparinized (1,000 units intravascular). The beating donor heart was excised without an interruption of coronary perfusion and supported by cross circulation with the other metabolic supporter rat as previously reported in detail (7,14,17,19,24). The coronary arterial oxygenated blood of the donor heart was supplied from the common carotid arteries of the supporter rat using arterial cross-circulation tubing and a cannula inserted into the brachiocephalic artery of the donor heart.…”

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confidence: 99%

Mechanical work and energetic analysis of eccentric cardiac remodeling in a volume overload heart failure in rats

Takewa

Chemaly²,

Takaki³

et al. 2009

American Journal of Physiology-Heart and Circulatory Physiology

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Eccentric cardiac remodeling seen in dilated cardiomyopathy or regurgitant valvular disease is a well-known process of heart failure progression, but its mechanoenergetic profile has not been yet established. We made a volume overload (VO) heart failure model in rats and for the first time investigated left ventricular (LV) mechanical work and energetics in cross-circulated whole heart preparations. Laparotomy was performed in 14 Wistar male rats, and abdominal aortic-inferior vena caval shunt was created in seven rats (VO group). Another seven rats underwent a sham operation without functional shunt (Sham group). LV dimensions changes were followed with weekly transthoracic echocardiography. Three months after surgery, we measured LV pressure and volume and myocardial O2 consumption in isolated heart cross circulation. LV internal dimensions in both systolic and diastolic phases were significantly increased in the VO group versus the Sham group (P Ͻ 0.05). LV pressure was markedly decreased in the VO group versus in the Sham group (P Ͻ 0.05). LV end-systolic pressurevolume relation shifted downward, and myocardial O2 consumption related to Ca 2ϩ handling significantly decreased. The contractile response to Ca 2ϩ infusion was attenuated. Nevertheless, the increase in Ca 2ϩ handling-related O2 consumption per unit change in LV contractility in the VO group was significantly higher than that in the Sham group (P Ͻ 0.05). The levels of sarco(endo)plasmic reticulum Ca 2ϩ -ATPase 2a protein were reduced in the VO group (P Ͻ 0.01). In conclusion, VO failing rat hearts had a character of marked contractile dysfunction accompanied with less efficient energy utilization in the Ca 2ϩ handling processes. These results suggest that restoring Ca 2ϩ handling in excitation-contraction coupling would improve the contractility of the myocardium after eccentric cardiac remodeling. eccentric left ventricular hypertrophy; myocardial oxygen consumption; Ca 2ϩ handling; sarco(endo)plasmic reticulum Ca 2ϩ -ATPase 2a; cross circulation; aortocaval shunt HEART FAILURE IS A MAJOR CAUSE of mortality and morbidity. It is due to various diseases such as hypertension, ischemic heart disease, valvular heart disease, congenital heart disease, cardiomyopathy, myocarditis, and others. The heart is subject to excessive and/or long-term overload, which induces myocardial hypertrophy. Hypertrophy initially compensates cardiac function but finally leads to heart failure. The process of hypertrophy and heart failure progression is divided into two mechanisms, depending on the type of overload: pressure overloading (PO) and volume overloading (VO). PO induces concentric hypertrophy to normalize wall stress from the increase in pressure placed on cardiomyocytes. Concentric remodeling of the left ventricle (LV) is characterized by an increase in ventricular wall thickness due to vertical growing of cardiomyocytes, which is caused by the parallel addition of sarcomeres (8).Conversely, VO promotes eccentric hypertrophy to compensate for excess blood volum...

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Mysterious Beauty of Beating Heart: Cardiac mechano-energetico-informatics

Suga¹

Sliding Filament Mechanism in Muscle Contraction

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Linear O2 Use-Pressure-Volume Area Relation from Curved End-Systolic Pressure-Volume Relation of the Blood-Perfused Rat Left Ventricle.

Cited by 37 publications

References 9 publications

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

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

Mechanical work and energetic analysis of eccentric cardiac remodeling in a volume overload heart failure in rats

Mysterious Beauty of Beating Heart: Cardiac mechano-energetico-informatics

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