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Ultrastructure of cardiocyte degeneration and myocardial calcification in the dystrophic hamster
Insights
In cardiomyopathic hamsters, electron microscopy revealed cellular damage and mitochondrial changes during acute lesions. Calcium deposition primarily occurred after cell damage, not before, suggesting secondary calcification.
Area of Science:
- Cardiovascular Biology
- Cellular Pathology
- Biochemistry
Background:
- The Bio 14.6 hamster model exhibits spontaneous cardiomyopathy.
- Acute lesioning stage is characterized by cardiocyte destruction and calcium elevation.
- Understanding cellular mechanisms is crucial for cardiomyopathy research.
Purpose of the Study:
- To investigate ultrastructural changes in cardiomyopathic hamster myocardium.
- To identify the timing and location of calcium deposition during acute lesions.
- To elucidate the role of mitochondria in cardiac calcification.
Main Methods:
- Electron microscopy of Bio 14.6 hamster myocardium.
- Analysis of cellular and organelle morphology during acute lesioning.
- Histological examination of calcium deposition.
Main Results:
- Most cardiocytes were normal, but necrotic foci with degenerative calcifying lesions were observed.
- Prenecrotic myocytes showed edema, sarcoplasmic reticulum/T-tubule distension, myofibrillar abnormalities, and mitochondrial changes.
- Calcium deposition was primarily seen within extruded mitochondria and on debris after sarcolemmal disruption, not in prenecrotic cells.
Conclusions:
- Cardiomyopathy involves significant mitochondrial alterations and cellular damage.
- Calcium deposition in this model appears to be a secondary event following sarcolemmal disruption.
- Mitochondrial calcification occurs in various cell types within advanced lesions.
Abstract:
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.