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Mechanical efficiency, thermodynamic efficiency and the cardiac Fenn effect
J Mol
S-()&6
Cell
Cardiol
24 (Supplement
I) (1992)
MECHANICAL EFFICIENCY, THERMODYNAMIC
EFFICIENCY AND THE CARDIAC FENN EFFECT
Cohn Gibbs, Sean Holroyd. Department of Physiology, Monash University, Clayton, Vie. 3168, Australia. It has been shown for both amphibian and mammalian cardiac tissue that the afterload against which a papillary muscle contracts determines the energy expenditure per beat. This means that there is a Fenn effect in the heart. Nonetheless a molecular or crossbridge explanation of the Fenn effect is still not available. The reasons why the profile of the energy:load relationship varies so much with the physiological conditions has continued to fascinate physiologists. In all the cardiac energetic data, maximum energy expenditure occurs in an isometric contraction. It has recently been suggested that the high series compliance of cardiac muscle is a major determinant of the energy:load profile. Our laboratory has obtained evidence from two different types of analyses that suggest another reason namely that there is little or no additional energy produced, aside from the external work, when cardiac muscle shortens. In one method muscle are allowed to shorten through various fiied distances from various muscle lengths at velocities near their maximum shortening velocity. Once the shortening is complete the muscles develop stress at their new length and the heat production in such a contraction is compared to the energy output predicted by control heat:stress curves. In the other method the external work and its recovery heat counterpart are subtracted from the total enthalpy in an isotonic contraction. The energy residue can be compared with that expected from the heat:stress relationship. We believe that the absence of shortening heat has a major effect on the energy:load profile and increases the mechanical efficiency. Recent myothermic estimates of the myocardial recoveqzinitial energy ratio allow estimation of mechanical and thermodynamic efficiency over the initial cycle of contraction.
S-08-7
INFLUENCE AND HUMAN Ch.Holubarsch,
OF CARDIOTONIC AGENTS ON MYOCARDIUM GHasenfuss, N.R.Alpert, H.Just
MYOCARDIAL
ENERGETICS
IN ANIMAL
Department of Cardiology, Medizinische Universitatsklinik Freihurg, FRG, Department of Physiology and Biophysics, The University of Vermont College of Medicine, Burlington, USA We investigated myocardial energetics in patients with idiopathic dilated cardiomyopathy in vivo as well as in isolated guinea-pig papillary muscles in vitro by analyzing the relationship between energy demand and svstolic stress-time internal (STI). In uatients. sodium nitronrusside decreased myocardial oxygen consumption per beit in proportion io reduction in STI. In contrast, xamoterol, isoproterenol, and enoximone increased mvocardial oxygen consumption relative to STI. Therefore, positive inotropic interventions that are brought about by increasing cyclic AMP levels seem to increase myocardial energy demand To further elucidate such an cyclic AMP dependent effect on myocardial energetics, papillary muscles from guinea pigs were treated with isoproterenol (ISO) and enoximone f E). Both interventions sienificantlv increased tension-indenendent heat which is associated with calcium turnover (+ 16-% and + 40X, respectively) and decreased contraction economy of the contractile proteins (- 55 % and - 25 %, respectivelv). In contrast, only small increases in tension-independent heat and no alterations of contraction economy were -observed under conditions of 11 mM calcium, ouabain, and the calcium sensitizer UDCG-115. This data indicates that stimulation of the cyclic AMP pathway increases myocardial energy demands, whereas inhibition of the sodium-potassium pump or sensitization of the regulatory proteins are more economical pharmacological principles.
S484OXYGEN Hiroyuki Saeki*,
COSTS OF MECRANICAL ENERGY AND CONTRACTILITY Suga, Yoichi Goto*, Katsuya Hata*, Toshiyuki Takehiko Nishioka*, Miyako Takaki, Taketoshi
OF
THE HEART Takasago*, Namba, Haruo
Akio Ito.
2nd Dept of Physiol, Okayama Univ Medical School, Okayama 700, and *National Cardiovascular Center, Suita, Osaka 565, JAPAN We briefly review recent advances of cardiac mechanoenergetics in terms of cardiac oxygen consumption (VO ), total mechanical energy (TME) and contractility index (Emax) in our la b s. Left ventricular (LV) TME was quantified by the systolic pressure-volume (P-V) area (PVA) bounded by the end-systolic and end-diastolic P-V relations and the systolic P-V trajectory in a P-V diagram. LV Emax is the slope of the end-systolic PV relation. Experiments in excised cross-circulated dog hearts at a given Emax yielded an empirical equation: VOa = aPVA + b, where a is the oxygen cost of mechanical energy, aPVA is the PVA-dependent VO and b is the PVA-indeoendent VO,. Varied Emax bv inotroDic aments aT a aiven enddiastolic and stroks volumes yielded-a new V&2-PVA-relation as-a function of Emax: V09 = aPVA + cEmax + d, where cEmax + d = b and c is the oxygen cost of Em&. We have found that the oxygen costs of TME and Emax-&an characterize changes in cardiac mechanoenergetics caused by various physiological and pathological inotropic interventions. s.30
S-()&6
Cell
Cardiol
24 (Supplement
I) (1992)
MECHANICAL EFFICIENCY, THERMODYNAMIC
EFFICIENCY AND THE CARDIAC FENN EFFECT
Cohn Gibbs, Sean Holroyd. Department of Physiology, Monash University, Clayton, Vie. 3168, Australia. It has been shown for both amphibian and mammalian cardiac tissue that the afterload against which a papillary muscle contracts determines the energy expenditure per beat. This means that there is a Fenn effect in the heart. Nonetheless a molecular or crossbridge explanation of the Fenn effect is still not available. The reasons why the profile of the energy:load relationship varies so much with the physiological conditions has continued to fascinate physiologists. In all the cardiac energetic data, maximum energy expenditure occurs in an isometric contraction. It has recently been suggested that the high series compliance of cardiac muscle is a major determinant of the energy:load profile. Our laboratory has obtained evidence from two different types of analyses that suggest another reason namely that there is little or no additional energy produced, aside from the external work, when cardiac muscle shortens. In one method muscle are allowed to shorten through various fiied distances from various muscle lengths at velocities near their maximum shortening velocity. Once the shortening is complete the muscles develop stress at their new length and the heat production in such a contraction is compared to the energy output predicted by control heat:stress curves. In the other method the external work and its recovery heat counterpart are subtracted from the total enthalpy in an isotonic contraction. The energy residue can be compared with that expected from the heat:stress relationship. We believe that the absence of shortening heat has a major effect on the energy:load profile and increases the mechanical efficiency. Recent myothermic estimates of the myocardial recoveqzinitial energy ratio allow estimation of mechanical and thermodynamic efficiency over the initial cycle of contraction.
S-08-7
INFLUENCE AND HUMAN Ch.Holubarsch,
OF CARDIOTONIC AGENTS ON MYOCARDIUM GHasenfuss, N.R.Alpert, H.Just
MYOCARDIAL
ENERGETICS
IN ANIMAL
Department of Cardiology, Medizinische Universitatsklinik Freihurg, FRG, Department of Physiology and Biophysics, The University of Vermont College of Medicine, Burlington, USA We investigated myocardial energetics in patients with idiopathic dilated cardiomyopathy in vivo as well as in isolated guinea-pig papillary muscles in vitro by analyzing the relationship between energy demand and svstolic stress-time internal (STI). In uatients. sodium nitronrusside decreased myocardial oxygen consumption per beit in proportion io reduction in STI. In contrast, xamoterol, isoproterenol, and enoximone increased mvocardial oxygen consumption relative to STI. Therefore, positive inotropic interventions that are brought about by increasing cyclic AMP levels seem to increase myocardial energy demand To further elucidate such an cyclic AMP dependent effect on myocardial energetics, papillary muscles from guinea pigs were treated with isoproterenol (ISO) and enoximone f E). Both interventions sienificantlv increased tension-indenendent heat which is associated with calcium turnover (+ 16-% and + 40X, respectively) and decreased contraction economy of the contractile proteins (- 55 % and - 25 %, respectivelv). In contrast, only small increases in tension-independent heat and no alterations of contraction economy were -observed under conditions of 11 mM calcium, ouabain, and the calcium sensitizer UDCG-115. This data indicates that stimulation of the cyclic AMP pathway increases myocardial energy demands, whereas inhibition of the sodium-potassium pump or sensitization of the regulatory proteins are more economical pharmacological principles.
S484OXYGEN Hiroyuki Saeki*,
COSTS OF MECRANICAL ENERGY AND CONTRACTILITY Suga, Yoichi Goto*, Katsuya Hata*, Toshiyuki Takehiko Nishioka*, Miyako Takaki, Taketoshi
OF
THE HEART Takasago*, Namba, Haruo
Akio Ito.
2nd Dept of Physiol, Okayama Univ Medical School, Okayama 700, and *National Cardiovascular Center, Suita, Osaka 565, JAPAN We briefly review recent advances of cardiac mechanoenergetics in terms of cardiac oxygen consumption (VO ), total mechanical energy (TME) and contractility index (Emax) in our la b s. Left ventricular (LV) TME was quantified by the systolic pressure-volume (P-V) area (PVA) bounded by the end-systolic and end-diastolic P-V relations and the systolic P-V trajectory in a P-V diagram. LV Emax is the slope of the end-systolic PV relation. Experiments in excised cross-circulated dog hearts at a given Emax yielded an empirical equation: VOa = aPVA + b, where a is the oxygen cost of mechanical energy, aPVA is the PVA-dependent VO and b is the PVA-indeoendent VO,. Varied Emax bv inotroDic aments aT a aiven enddiastolic and stroks volumes yielded-a new V&2-PVA-relation as-a function of Emax: V09 = aPVA + cEmax + d, where cEmax + d = b and c is the oxygen cost of Em&. We have found that the oxygen costs of TME and Emax-&an characterize changes in cardiac mechanoenergetics caused by various physiological and pathological inotropic interventions. s.30