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X-ray microanalysis of calcium in ischemic skeletal muscle cells

C S Zhong1, Y P Ling, Z Q Wu

  • 1Laboratory of Cell Ultrastructure, Shanghai Medical University.

Scientia Sinica. Series B, Chemical, Biological, Agricultural, Medical & Earth Sciences
|April 1, 1987
PubMed

Insights

Transient ischemia in rabbit muscle causes cell degeneration with calcium deposits in mitochondria and sarcoplasmic reticulum. Persistent ischemia shows less calcium accumulation in these organelles.

Area of Science:

  • Cellular Biology
  • Pathology
  • Biochemistry

Background:

  • Ischemia leads to cell damage and altered cellular processes.
  • Calcium homeostasis is critical for cell survival and function.
  • Understanding calcium's role in ischemic muscle injury is important.

Purpose of the Study:

  • To investigate the ultrastructural changes and calcium distribution in transiently and persistently ischemic rabbit muscle.
  • To identify the specific organelles involved in calcium accumulation during ischemia.

Main Methods:

  • Tissue sections of rabbit musculus latissimus dorsi subjected to transient and persistent ischemia were examined.
  • Ultrastructural analysis using electron microscopy was performed.
  • X-ray microanalysis was employed to determine elemental composition, specifically calcium concentration.

Main Results:

  • Both transient and persistent ischemia induced cell degeneration and necrosis.
  • Degenerated mitochondria with intramatrical deposits were observed in all ischemic samples.
  • Electron-dense granules, identified as degenerated mitochondria and sarcoplasmic reticulum, containing high calcium concentrations were found exclusively in transient ischemia samples.
  • Fluffy deposits in mitochondria contained low calcium levels.

Conclusions:

  • Calcium accumulation in degenerated and necrotic muscle cells during transient ischemia primarily occurs in mitochondria and sarcoplasmic reticulum.
  • The findings highlight the differential roles of organelles in calcium handling during varying ischemic conditions.
  • Further research into the mechanisms of calcium dysregulation in ischemic muscle is warranted.

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