Myocardial function in different models of cardiac hypertrophy. An attempt at correlating mechanical, biochemical, and morphological parameters

Jacob, R.; Ebrecht, G.; Kämmereit, A; Medugorac, I.; Wendt-Gallitelli, M. F.

doi:10.1007/978-3-642-85299-2_11

Cited by 4 publications

(8 citation statements)

References 5 publications

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“…In addition to the previously reported structural and functional alterations of the hypertrophied myocardium (6,10,13,14), substantial alterations in the transmembrane electrical properties of the hypertrophied myocardial cell can be identified based on the present results: with unchanged resting potential and action potential amplitude the duration of the action potential is greatly prolonged in hypertrophy. A similar position is taken by Tritthart et al (25) based on their measurements of pressure-induced, right ventricular cardiac hypertrophy of the cat.…”

Section: Discussionsupporting

confidence: 79%

“…It is very likely that the significant increase in the time to peak force of the hypertrophied myocardium is due to the prolongation of the myocardial action potential (8,14). As shown by investigations of Antoni (2), an action potential prolongation directly causes a prolonged activation which results in a prolonged mechanical time to peak force and increased peak force.…”

Section: Discussionmentioning

confidence: 99%

“…The mechanical contraction data of the hypertrophied mammalian heart, however, especially the significant prolongation of the isometric time to peak (1, 6,14), suggest that some alterations in the transmembrane electrical activity of the myocardial cell may be involved here.…”

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confidence: 96%

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Analysis of myocardial action potential in left ventricular hypertrophy of Goldblatt rats

1979

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Action potentials were measured in hypertropl~ied rat myocardium by means of glass microelectrodes. Left ventricular hypertrophy was induced by experimental chronic coarctation of one renal artery without contralateral nephrectomy. The action potentials of the hypertrophied myocardium exhibit a marked prolongation without any significant changes in the transmembrane resting potential, in the amplitude, or in the maximum upstroke velocity of the action potential. The increase in the half-width of the action potential for the 6-week stage after the surgical procedure is 235%, for the 12-week stage 281%, and for the 24-week stage 314%. The prolongation of the action potentials was more marked when the degree of hypertrophy was more severe.After depression of the fast Na + inward current either by tetrodotoxin, by augmentation of the extracellular K + concentration, or by reduction of the extracellular Na + concentration, action potentials with similar marked broadening were still obtained in hypertrophied myocardium. The results under variation of the extracellular Ca ++ concentration and simultaneous inactivation of the fast Na* channels suggest that the slow transmembrane inward current is primarily carried by Ca ++ ions.The prolongation of the action potentials could be one cause of the significant increase in the time to peak force as well as the augmentation of isometric force found in this model of hypertrophied myocardium.In contrast to numerous available mechanical, biochemical and mor. phological data, few studies on electrical properties of hypertrophied cardiac muscle have been published: Most studies are concerned with electrocardiographic alterations under cardiac hypertrophy and correlate changes in ECG with changes in geometry of the hypertrophied heart without regard for possible alterations in the transmembrane electrical activity of the hypertrophied cardiac cell.

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Section: Discussionsupporting

confidence: 79%

Section: Discussionmentioning

confidence: 99%

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Analysis of myocardial action potential in left ventricular hypertrophy of Goldblatt rats

1979

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“…In order to attempt a correlation between mechanical performance and structural cellular conditions in experimentally produced cardiac pressure hypertrophy, an electron microscopic study was made at various stages of hypertrophy on the same material that was used for mechanical investigations (1). In this study, we limited our morphological investigations to the period of compensatory hypertrophy as the alterations in the myocardial cell itself were of the greatest interest for our original problem.…”

Section: Discussionmentioning

confidence: 99%

Time course of electron microscopic alterations in the hypertrophied myocardium of Goldblatt rats

Wendt-Gallitelli

Jacob

1977

Basic Res Cardiol

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In Goldblatt rats, electron microscopic investigations of morphological changes in heart tissue during the compensatroy stage of pressure induced cardiac hypertrophy were performed. Myocardial cellular size enlarged considerably within the first 4 weeks after renal artery coarctation. An enlargement of the T-tubular system is particularly striking. The ratio of myofibril volume to total cell volume is significantly increased from the 4th-24th week and can at least partially explain a rise in developed tension which occurs in spite of a frequent disarrangement of myofibrils. In later stages severe changes in the vessel walls take place and there is an augmentation of connective tissue which impairs a correlation between myocardial cell alterations and mechanical parameters.

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“…We suggest that differences in pressure load may be responsible for both regional variations in isomyosin distribution and for isomyosin changes in hypertensive animals. Ore Res 49: [1003][1004][1005][1006][1007][1008][1009]1981 HYPERTROPHY of the ventricular myocardium induced by pressure overload is accompanied by decreased rate of shortening (Spann et al, 1967;Hamrell and Alpert, 1977;Jacob et al, 1977). The reduced velocity of the hypertrophic myocardium has been demonstrated in chemically skinned ventricular preparations and must therefore reflect intrinsic changes in the contractile apparatus (Maughan et al, 1979).…”

Section: Isomyosin Distribution In Normal and Pressure-overloaded Ratmentioning

confidence: 99%

Isomyosin distribution in normal and pressure-overloaded rat ventricular myocardium. An immunohistochemical study.

Gorza¹,

Pauletto²,

Pessina³

et al. 1981

Circulation Research

110

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We have used affinity-purified antibodies reacting with guinea pig soleus muscle and ventricular myosin heavy chains to analyze the distribution of specific isomyosin in the ventricular myocardium of normal and renal hypertensive rats. Immunofluorescent staining of cardiac tissue sections with the two antimyosins revealed striking variations in reactivity among ventricular muscle fibers, reactive fibers being more numerous in the left compared to the right ventricle and in subendocardial compared to subepicardial layers. The response of the ventricular myocardium changed during development: all fibers were stained in the newborn rat, whereas most fibers were unreactive in 1-month-old animals. The number of reactive fibers increased again in subsequent stages leading to a mixed pattern in adult animals. The normal mixed pattern of reactivity was transformed into a uniformly positive pattern in hypertensive rats 2 months after surgery. This complete transformation was observed in 20 out of 23 hypertensive animals examined. These findings indicate that the two antimyosins cross-react with a particular type of ventricular myosin heavy chain, whose distribution varies in different muscle cells and whose relative concentration changes during development and during cardiac hypertrophy induced by systemic hypertension. We suggest that differences in pressure load may be responsible for both regional variations in isomyosin distribution and for isomyosin changes in hypertensive animals.

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Myocardial function in different models of cardiac hypertrophy. An attempt at correlating mechanical, biochemical, and morphological parameters

Cited by 4 publications

References 5 publications

Analysis of myocardial action potential in left ventricular hypertrophy of Goldblatt rats

Analysis of myocardial action potential in left ventricular hypertrophy of Goldblatt rats

Time course of electron microscopic alterations in the hypertrophied myocardium of Goldblatt rats

Isomyosin distribution in normal and pressure-overloaded rat ventricular myocardium. An immunohistochemical study.

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