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Effect of myocardial ischemia on protein synthesis in the heart
J Mel
p52
Cell
Cardiol
21 (Supplement
IV) (1989)
INOTROPIC RESPONSE OF THE RAT HEART IN VW0 DURING DEVELOPMENT AND REGRESSION OF TRDODOTHYRONINE-INDUCED HYPERTROPHY. SLortet, H.-G.Zimmer Physiological Institute, University of Munich, Federal Republic of Germany - Physiologie Cellulaire Cardiaque, Universid J. Fourier, Grenoble, France. The inotropic response of rat hearts to an increase in plasma calcium (i.v. infusion, 2mmol/kg/h) was studied in viva I4 days after triiodothyronine (T3) treatment and 14 days after discontinuation of 7’3 treatment. A Millar ultraminiature catheter pressure transducer (model PR-249) was used to measure left ventricular systolic pressure (LVSP) and LVdP/dt,,,. The hyperthyroid state was characterized by cardiac hypertrophy (heart weighmy weight ratio was elevated from 2.85 f 0.02 (n=18) to 4.48 +_ 0.08 (n=14)). All hemcdynarnic parameters were enhanced: heart rate (HR) from 336 f 11 (n=20) to 524 ? 8 (n=13) beats/min, LVSP from 145 + 3 (n=20) to 167 + 6 (n=13) mmHg and LVdP/dt,,,,, from 8601 * 316 (n=20) to 17843 f 1614 (n=12) mmHg/s. Infusion of calcium had a marked effect on LVdP/dtm,, which was increased to 16167 f 617 (n=8) mmHg/s in controls and to 23429 k 778 (n=5) mmHg/s in T%reated rats. Fourteen days after T3 treatment had been stopped, the hearts were still hypertrophied (heart weight/body weight ratio: 3.28 +- 0.05, n=16), but HR. contractility and the inotropic response to calcium were similar to those of the control heart. From these results, it is concluded that there is a disproportionate regression of the T3-induced left ventricular hemodynarnic and morphologic alterations, and that the heart both during the development and regression of the T3-hypertrophy retains its responsiveness to an inotropic stimulus. Supported by PROCOPE, a german (DAAD) and french (ANRT) scientific Program (ref: 88123)
P53CONTRACTILE FUNCTION DISORDERS AND ENERGY SUPPLY IN SEVERAL EXPERIMENTAL CARDIOMYOPATHIES. V.1 .Kapelko*, M. I .Popovich, S. I .Kostin, V.A.Kobets, V.V.Severin, S.A.Robkova, V.S.Gudtnnak, M.A.Golikov, N.A.Novikova*, V.G.Sharov* and V.A.Saks*. Institute of Experimental Cardiology, USSR Cardiology Research Center*, ~loscow. and Moldavian Institute of Preventive and Clinical Medicine. Kishinev. USSR. High energy phosphate content and left ventricular (LV) ptnnp function of isolated rat hearts were determined in four series of chronic myocardial damage induced by autoinnnunization, treatment with adriamycin or mixture of pesticides for 3 months and spontaneous smallpox virus infection. Focal necroses, mild fibrosis, swallen mitochondria and combination of hypercontracted and overdistended sarcomeres were most typical ultrastructural alterations in all series. The ATP and especially phosphocreatine (PCrI content as well as the cardiac outout at standard load were substantially lower in all series. The common features of cardiac pump failure were mild hradycardia. increased LV diastolic pressure and stiffness. The ability to develop higher LV systolic pressure at increased resistance was less impaired than the ability to maintain stroke volume. These data suggest that the cardiac pump failure may he caused by limited LV filling due to elevated LV wall stiffness. The content of both ATP and PCr correlated positively with heart rate and negatively with LV diastolic stiffness thus showing close relations between energy supply and cardiac contractile function in various experimental cardiomyopathies.
OF MYOCARDIAL ISCHEMIA ON PROTEIN SYNTHESIS IN THE HEART. R. Maskoliunas. A.Liekis. Kaunas Medical Institute. Central Research Laboratory, 233007,Kaunas, Z.JanugkeviEiaus 4, Lithuanian SSR, USSR. The functional activitv of translational machinerv in rabbit heart has been studied on the m‘bdel of myocardial ischemia". The rate of pro-
P%EFFECT
tein
synthesis
ses.
It
in
cell-free
protein
synthesizing
system
from
myocardium decreases significantly under different times of chemia. The rate of the average polypeptide chain synthesis has
been
observed
that
the
decrease
of
protein
synthesis
rabbit total
isdecreadoes
not depend on the cell energy supply. The most observable alterations exhibit polyribosome preparations. The content of free ribosomes diminishes in case of myocardial ischemia from 92% to 59a, whereas the content of membrane-bound ribosomes sreatlv increases (from 8% to 41%). The part of polyribosomes in The toial ribosome‘preparations decreases to 83% and in the free ribosome preparations to 87% of the initial value, respectively. The content of polyribosomes in the membrane-bound ribosome preparations remains unchanged. These data suggest that observed structural alterations of polyribosome preparations are most likely responsible for the impaired protein synthesis. 3.27
p52
Cell
Cardiol
21 (Supplement
IV) (1989)
INOTROPIC RESPONSE OF THE RAT HEART IN VW0 DURING DEVELOPMENT AND REGRESSION OF TRDODOTHYRONINE-INDUCED HYPERTROPHY. SLortet, H.-G.Zimmer Physiological Institute, University of Munich, Federal Republic of Germany - Physiologie Cellulaire Cardiaque, Universid J. Fourier, Grenoble, France. The inotropic response of rat hearts to an increase in plasma calcium (i.v. infusion, 2mmol/kg/h) was studied in viva I4 days after triiodothyronine (T3) treatment and 14 days after discontinuation of 7’3 treatment. A Millar ultraminiature catheter pressure transducer (model PR-249) was used to measure left ventricular systolic pressure (LVSP) and LVdP/dt,,,. The hyperthyroid state was characterized by cardiac hypertrophy (heart weighmy weight ratio was elevated from 2.85 f 0.02 (n=18) to 4.48 +_ 0.08 (n=14)). All hemcdynarnic parameters were enhanced: heart rate (HR) from 336 f 11 (n=20) to 524 ? 8 (n=13) beats/min, LVSP from 145 + 3 (n=20) to 167 + 6 (n=13) mmHg and LVdP/dt,,,,, from 8601 * 316 (n=20) to 17843 f 1614 (n=12) mmHg/s. Infusion of calcium had a marked effect on LVdP/dtm,, which was increased to 16167 f 617 (n=8) mmHg/s in controls and to 23429 k 778 (n=5) mmHg/s in T%reated rats. Fourteen days after T3 treatment had been stopped, the hearts were still hypertrophied (heart weight/body weight ratio: 3.28 +- 0.05, n=16), but HR. contractility and the inotropic response to calcium were similar to those of the control heart. From these results, it is concluded that there is a disproportionate regression of the T3-induced left ventricular hemodynarnic and morphologic alterations, and that the heart both during the development and regression of the T3-hypertrophy retains its responsiveness to an inotropic stimulus. Supported by PROCOPE, a german (DAAD) and french (ANRT) scientific Program (ref: 88123)
P53CONTRACTILE FUNCTION DISORDERS AND ENERGY SUPPLY IN SEVERAL EXPERIMENTAL CARDIOMYOPATHIES. V.1 .Kapelko*, M. I .Popovich, S. I .Kostin, V.A.Kobets, V.V.Severin, S.A.Robkova, V.S.Gudtnnak, M.A.Golikov, N.A.Novikova*, V.G.Sharov* and V.A.Saks*. Institute of Experimental Cardiology, USSR Cardiology Research Center*, ~loscow. and Moldavian Institute of Preventive and Clinical Medicine. Kishinev. USSR. High energy phosphate content and left ventricular (LV) ptnnp function of isolated rat hearts were determined in four series of chronic myocardial damage induced by autoinnnunization, treatment with adriamycin or mixture of pesticides for 3 months and spontaneous smallpox virus infection. Focal necroses, mild fibrosis, swallen mitochondria and combination of hypercontracted and overdistended sarcomeres were most typical ultrastructural alterations in all series. The ATP and especially phosphocreatine (PCrI content as well as the cardiac outout at standard load were substantially lower in all series. The common features of cardiac pump failure were mild hradycardia. increased LV diastolic pressure and stiffness. The ability to develop higher LV systolic pressure at increased resistance was less impaired than the ability to maintain stroke volume. These data suggest that the cardiac pump failure may he caused by limited LV filling due to elevated LV wall stiffness. The content of both ATP and PCr correlated positively with heart rate and negatively with LV diastolic stiffness thus showing close relations between energy supply and cardiac contractile function in various experimental cardiomyopathies.
OF MYOCARDIAL ISCHEMIA ON PROTEIN SYNTHESIS IN THE HEART. R. Maskoliunas. A.Liekis. Kaunas Medical Institute. Central Research Laboratory, 233007,Kaunas, Z.JanugkeviEiaus 4, Lithuanian SSR, USSR. The functional activitv of translational machinerv in rabbit heart has been studied on the m‘bdel of myocardial ischemia". The rate of pro-
P%EFFECT
tein
synthesis
ses.
It
in
cell-free
protein
synthesizing
system
from
myocardium decreases significantly under different times of chemia. The rate of the average polypeptide chain synthesis has
been
observed
that
the
decrease
of
protein
synthesis
rabbit total
isdecreadoes
not depend on the cell energy supply. The most observable alterations exhibit polyribosome preparations. The content of free ribosomes diminishes in case of myocardial ischemia from 92% to 59a, whereas the content of membrane-bound ribosomes sreatlv increases (from 8% to 41%). The part of polyribosomes in The toial ribosome‘preparations decreases to 83% and in the free ribosome preparations to 87% of the initial value, respectively. The content of polyribosomes in the membrane-bound ribosome preparations remains unchanged. These data suggest that observed structural alterations of polyribosome preparations are most likely responsible for the impaired protein synthesis. 3.27