Intracellular elemental content of cardiac and skeletal muscle of normal and dystrophic hamsters

Smith, Nancy R.; Morris, Sidra S.; Richter, Michael R.; Cameron, Ivan L.

doi:10.1002/mus.880060703

Cited by 8 publications

(5 citation statements)

References 37 publications

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“…Our findings for Na + , Mg 2+ , P, Cl", and K + are very similar to the results of Smith and coworkers 43 in cryosections from myo and control hearts, rapidly frozen in vitro. However, contrary to their results, we found no evidence for an elevated S content in myo hearts.…”

Section: Subcellular Elemental Content In Cardiomyopathic Heartssupporting

confidence: 92%

Subcellular calcium content in cardiomyopathic hamster hearts in vivo: an electron probe study.

Bond

Jaraki

Disch

et al. 1989

Circulation Research

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In the Syrian cardiomyopathic hamster heart, abnormal cellular calcium regulation, resulting in cellular calcium overload, is believed to play a role in the pathogenesis of cardiac hypertrophy and failure. Alternatively, the primary abnormality may be coronary vasospasm, resulting in reperfusion-induced necrosis. According to the latter hypothesis, only those cells that suffer an ischemic insult would contain elevated calcium levels. To determine whether a generalized elevation in myocytic calcium exists in myopathic hamster hearts, we measured cellular and subcellular calcium concentrations by electron probe microanalysis in cryosections of 50-day and 96-day myopathic and control hearts, rapidly frozen in vivo. Total calcium content of ventricular homogenates from each group was also measured by atomic absorption spectrophotometry. No significant differences hi subcellular calcium were found by electron probe microanalysis among 50-day and 96-day myopathics and their age-matched controls. In 50-day myopathic and control hearts, mitochondria! calcium was 0.7±0.2 and 0.9±0.2, respectively, and A-band calcium was 3.0±0.4 and 2.6±0.4 nunol calcium/kg dry wt(±SEM). Results from 96-day animals were similar. Localized regions of elevated calcium were found only at sites of necrotic foci: in Na + -loaded cells (mitochondria: 4.7±1.3 (SEM) mmol/kg dry wt), in dying cells (mitochondria: 72±22 (SEM) mmol/kg dry wt) or as extracellular deposits (7-10 mol/kg dry wt). Total calcium content of hearts from myopathic hamsters, as determined by atomic absorption spectrophotometry, was also 13 times (50-day) and 50 times (96-day) higher than controls. These results demonstrate that there is a marked heterogeneity in cellular calcium content in myopathic hamster hearts, but the data do not support the hypothesis of a generalized cellular calcium overload. 9 In view of the early onset of many of these changes in Ca 2+ metabolism, it has been proposed that a general elevation of intracellular Ca 2+ may be an important initiating or aggravating factor in the etiology of the disease.10 " Alternatively, it has been proposed by Sonnenblick and coworkers 12 that the primary defect responsible for development of heart failure in myo hamsters may not be an abnormality in Ca 2+ handling by the myocytes themselves but an increased reactivity of the coronary arteries and arterioles. They and others have provided evidence for the existence, in myo hamsters, of coronary vasospasm in situ 13 31920 Ca 2+ content of isolated mitochondrial fractions has also been shown to be significantly elevated in myo hearts.1120 The approaches used in these studies are, however, limited in their ability to identify whether the observed elevation in cardiac and/or mitochondrial Ca 2+ is a homogeneous phenomenon throughout the heart. An alternative methodology, which avoids the problems associated with measurements of total tissue Ca 2+ by AA, is electron probe microanalysis (EPMA) of intracellular and subcellular concentrations of Ca 2+ and other elements in ...

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Section: Subcellular Elemental Content In Cardiomyopathic Heartssupporting

confidence: 92%

Subcellular calcium content in cardiomyopathic hamster hearts in vivo: an electron probe study.

Bond

Jaraki

Disch

et al. 1989

Circulation Research

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“…23 The results of the present study clearly show that the Ca accumulation in cardiac muscle was significantly diminished in dystrophic hamsters treated with DDB. This was demonstrated both by direct chemical analysis (Table 1) and quantitated histological examination (Fig.…”

Section: Discussionsupporting

confidence: 64%

The effect of DDB on dystrophic hamsters: An in vivo and in vitro study

et al. 1987

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Dimethyl-4, 4'-dimethoxy-5, 6, 5'-6'-dimethylenedioxybiphenyl-2, 2'-dicarboxylate (DDB) is a synthetic analogue of Schizandrin C, an active compound isolated from a Chinese herb, Fructus schizandrae. We administered this compound to dystrophic hamsters in vivo for 31 days. This led to a 61% reduction of the calcium content, an 86% reduction of the area of calcium deposits, and a 52% reduction of the area of necrosis of cardiac muscle. However, skeletal muscle necrosis was not significantly improved. No clear change in plasma creatine kinase (CK) was observed. In an in vitro incubation study, the rate of CK release and tetanus tension of the extensor digitorum longus muscle of dystrophic hamsters were not substantially changed by the addition of DDB. This study suggests that DDB has some effect on cardiac necrosis, and that it might be useful for treatment of the cardiac involvement in patients with muscular dystrophy or other conditions with accompaning Ca accumulation.

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“…These authors suggested that the calcium increase is an early and widespread phenomenon occurring even in normal cells. Because ultracryomicrotomy of quenchfrozen tissue is required to prevent loss and redistribution of diffusible elements (see Moore et al, 1984, for review), it would appear that the data obtained by Smith et al (1983) might reflect more accurately the status of cytoplasmic calcium within the dystrophic myocardium. The results obtained in the present study (i.e., absence of detectable calcium except in mineralizing foci following necrosis) are compatible with the interpretation proposed by Smith et al (1983).…”

Section: Discussionmentioning

confidence: 97%

“…In an attempt to circumvent these problems, several investigators have turned to EPMA of thin sections to determine whether detectable changes of calcium and other electrolytes are present in dystrophic muscle, permitting correlation of any changes with specific tissue and cellular components. Smith et al (1983) used EPMA to analyze the electrolyte content of unfixed cryosections of cardiac and skeletal muscle of Bio 53.58 dystrophic hamsters. Significant elevations of S were detected in all myocytes of CM hamsters, but increased Na, C1, Ca, and P were present only in "damaged" fibers.…”

Section: Discussionmentioning

confidence: 99%

Ultrastructure of cardiocyte degeneration and myocardial calcification in the dystrophic hamster

Burbach

1987

Am. J. Anat.

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The myocardium of the Bio 14.6 cardiomyopathic hamster was examined with the electron microscope to identify cellular and organelle changes during the acute lesioning stage, a period typified by concomitant cardiocyte destruction and calcium elevation. Most cardiocytes retained their normal histologic and ultrastructural features, but scattered foci of altered and necrotic cells were observed in association with degenerative calcifying lesions. Prenecrotic alterations of myocytes included cellular edema; varying degrees of distension of sarcoplasmic reticulum and T-tubules; contraction bands and other myofibrillar abnormalities; mitochondrial clustering and hyperplasia; a wide spectrum of mitochondrial changes such as altered sizes, shapes, and cristal patterns, and increases in the number and size of osmiophilic matrix inclusions. Morphologic features consistent with substantial calcium excess were not observed in most altered but prenecrotic cells. Instead, calcium deposition within extruded mitochondria and upon degenerating organelle debris was observed only after cardiocyte disruption. Some calcifying cell remnants were phagocytized by macrophages, whereas large calcified plaques and other deposits remained in the interstitium. Mitochondrial calcification in vascular smooth muscle cells and fibroblasts was evident in highly calcified lesions. These observations suggest that most of the morphologically identifiable calcium deposition present in this cardiomyopathy results from secondary calcification subsequent to sarcolemmal disruption.

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Intracellular elemental content of cardiac and skeletal muscle of normal and dystrophic hamsters

Cited by 8 publications

References 37 publications

Subcellular calcium content in cardiomyopathic hamster hearts in vivo: an electron probe study.

Subcellular calcium content in cardiomyopathic hamster hearts in vivo: an electron probe study.

The effect of DDB on dystrophic hamsters: An in vivo and in vitro study

Ultrastructure of cardiocyte degeneration and myocardial calcification in the dystrophic hamster

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