Elastic and contractile properties of the myocardium in experimental cardiac hypertrophy of the rat Methodological and pathophysiological considerations

Jacob, R.; Brenner, Bernhard; Ebrecht, G.; Holubarsch, C; Medugorac, I.

doi:10.1007/bf02001421

Cited by 14 publications

(9 citation statements)

References 11 publications

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“…The papillary muscle at the posterior wall was freed from thin fibrous filaments and excised after silk ligatures were fixed to both ends of the muscle. The muscle preparations were mounted in a previously described myograph using stainless steel hooks (13,14,15).…”

Section: Methodsmentioning

confidence: 99%

“…Whereas tissue distensibility is not decreased in hypertrophy due to swimming training or experimental hyperthyroidism, considerable changes have been described in chronic pressure overload, particularly in renal hypertension (7,14,15,16). However, the structural basis of passive elastic properties has not been definitively clarified, neither in normal nor in hypertrophied myocardium.…”

Section: Introductionmentioning

confidence: 95%

“…Ventricular distensibility is influenced by anatomical dimensions, wall thickness and intrinsic myocardial passive elastic properties. In the hypertrophied heart, changes in geometric configuration can be accompanied by an increase in wall stiffness, the extent of which depends on the given experimental model (1,4,7,15,16). **) Supported by the Deutsche Forschungsgemeinschaft.…”

Section: Introductionmentioning

confidence: 99%

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Connective tissue content and myocardial stiffness in pressure overload hypertrophy A combined study of morphologic, morphometric, biochemical, and mechanical parameters

et al. 1983

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We investigated samples of left ventricular myocardium from Goldblatt II (4 and 8 weeks after operation) and spontaneously hypertensive rats (SHR; 40 and 80 weeks old) by histological and morphometric methods. From the same hearts, the distensibility of the left ventricular papillary muscle was analyzed by means of resting tension curves, and the collagen content of the whole left ventricular wall was determined by means of hydroxyproline concentration. In all groups, myocardial fibrosis was observed to accompany myocardial hypertrophy. The severity of fibrotic lesions increased with the duration of hypertension, and, in late stages, degenerative changes of cardiac myocytes were found. Morphometric determinations and chemical analysis of the hydroxyproline concentration revealed a decrease in myocardial muscle content, which was paralleled by an increase in collagen content when compared to the respective controls. In general, morphometric and chemical findings correlate with increased myocardial stiffness observed during mechanical measurements in isolated papillary muscle preparations from the same hearts. Differences were found, however, between chemical analysis and mechanical measurements in the 40-week-old SHR group, which may result from different patterns of collagen distribution between interstitium, perivascular spaces, and the walls of blood vessels. The comparison between histological, morphometric, chemical, and physiological data shows that (1) cardiac hypertrophy of Goldblatt and SH-rats is accompanied by myocardial fibrosis, and (2) changes in passive elastic properties of myocardium is better reflected in morphometric than in chemical analysis.

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Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 95%

Section: Introductionmentioning

confidence: 99%

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Connective tissue content and myocardial stiffness in pressure overload hypertrophy A combined study of morphologic, morphometric, biochemical, and mechanical parameters

et al. 1983

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“…The basic mechanisms, which govern the function of hypertrophied heart, are wen understood (30,31). As regards myofibrillar modulation of cardiac performance, the concept of polymorphic myosin provides a rational explanation of some until now rather empirical observations.…”

Section: The Myosin Isoenzyme Pattern and Myocardial Energeticsmentioning

confidence: 98%

The adaptive changes in the isoenzyme pattern of myosin from hypertrophied rat myocardium as a result of pressure overload and physical training

Rupp

1981

Basic Res Cardiol

135

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The distribution of cardiac myosin isoenzymes is altered as a result of pressure overload and physical training. Using polyacrylamide gel electrophoresis in sodium pyrophosphate, it was found that myosin from left ventricles of adult rats exists in three polymorphic forms, V1, V2 and V3. Cardiac hypertrophy due to renal hypertension (Goldblatt II) led to a shift of the isoenzymes towards V3, whereas swimming training resulted in an opposite redistribution. The isoenzyme V1 predominated, only traces of V2 and V3 were detectable. The changes in the isoenzyme distribution were reflected in an altered ATPase activity of myofibrils. In a representative sample of the Goldblatt rats, the activity was reduced by 11%, and the swimming training led to an increase by 10%. Changes in myofibrillar ATPase can, therefore, be traced to alterations in the isoenzyme pattern of myosin. The polymorphism of myosin has a two-faced aspect as regards cardiac performance. For example, a shift towards V3 is expected to increase the economy for tension development during isovolumetric contraction at the expense of a reduced maximum speed of ventricular contraction.

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“…Regression of hypertrophy in these models has been associated with increased (13) and normal collagen concentration (20). As emphasized by others (30,31), factors in addition to increased afterload may affect the myocardial changes that occur in these models and comparison to other models of pressure-induced hypertrophy may be inappropriate.…”

Section: Resultsmentioning

confidence: 95%

Myocardial hydroxyproline and mechanical response to prolonged pressure loading followed by unloading in the cat.

Williams¹,

Mathew²,

Hern³

et al. 1983

J. Clin. Invest.

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A B S T R A C T To determine the myocardial response to prolonged pressure-loading and unloading, kittens weighing 0.8-1.2 kg underwent pulmonary artery banding, which initially elevated right ventricular (RV) systolic pressure by 10-15 mmHg. 52 and 76 wk later; RV weight/body weight had increased by -80%. Total RV hydroxyproline had increased significantly, whereas hydroxyproline concentration was unchanged from that of nonbanded animals of comparable age. In isometrically contracting RV papillary muscles, peak active force was significantly less at 76 wk (3.3±0.8 [SD] g/ mm2 than at 52 wk (5.1±0.8 g/mm2) or in nonbanded animals (4.8±0.8 g/mm2). Velocity of muscle shortening at comparable loads was unchanged after 52 wk but was significantly less after 76 wk. In nonstimulated, slowly stretched muscles, passive stiffness constants, a and ,B, derived from a = a(eft -1), where a is instantaneous stress and e is Lagrangian strain, were unchanged by banding. The band was removed after 52 wk in additional animals that were studied 24 wk later.In those animals with normal RV pressures at death, hypertrophy had regressed and hydroxyproline 'concentration was humans (1, 2) and experimental animals (3, 4) after removal of the hypertrophic stimulus. Unfortunately, this is not a universal occurrence and myocardial dysfunction may persist (1, 2, 5). The reasons for these therapeutic failures are unclear but myocardial fibrosis from prolonged overload often is incriminated as a major factor in the persistent dysfunction (6, 7). However, several studies have observed no increase in myocardial collagen or connective tissue concentration in patients dying with long-standing myocardial hypertrophy (8-10). An unanswered question and one that might contribute to these conflicting results regarding myocardial fibrosis is whether increased connective tissue that accompanies the hypertrophic process regresses when the stimulus for hypertrophy is removed. For example, connective tissue may increase proportionately to other myocardial constituents during hypertrophy but not regress or even continue to increase after removal of the stimulus, resulting in an increase in connective tissue concentration as muscle mass declines.Experimental studies of the hydroxyproline response to the development and regression of hypertrophy have produced conflicting data that may be due in part to differences in methods for producing hypertrophy. Baratosova (11) Engineering, Pennsauken, NJ). The compliance of the system without muscle but including the suture was 2 um/g and the equivalent mass of the lever system was 150 mg. Micrometers located above the lever permitted us to obtain isometric contractions (while varying muscle length by known amounts) or isotonic contractions under various afterloads (while maintaining initial muscle length constant).The muscle was stimulated at a frequency of 12/min and initially allowed to contract isotonically under a 0.5-g preload for 45-60 min at which time extent and rate of shortening were constant. Thereafte...

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Elastic and contractile properties of the myocardium in experimental cardiac hypertrophy of the rat Methodological and pathophysiological considerations

Cited by 14 publications

References 11 publications

Connective tissue content and myocardial stiffness in pressure overload hypertrophy A combined study of morphologic, morphometric, biochemical, and mechanical parameters

Connective tissue content and myocardial stiffness in pressure overload hypertrophy A combined study of morphologic, morphometric, biochemical, and mechanical parameters

The adaptive changes in the isoenzyme pattern of myosin from hypertrophied rat myocardium as a result of pressure overload and physical training

Myocardial hydroxyproline and mechanical response to prolonged pressure loading followed by unloading in the cat.

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