Electron microscopic observations and acid phosphatase activity in the ischemic rat heart
Autor: | L.P. McCallister, James R. Neely, Bryce L. Munger |
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Rok vydání: | 1977 |
Předmět: |
Male
medicine.medical_specialty Acid Phosphatase Ischemia Coronary Disease Sarcomere chemistry.chemical_compound Internal medicine medicine Animals Molecular Biology biology Glycogen Chemistry Myocardium Endoplasmic reticulum Acid phosphatase Anatomy medicine.disease Heart Arrest Rats Organoids Intercellular Junctions Endocrinology medicine.anatomical_structure Vacuolization biology.protein Lysosomes Cardiology and Cardiovascular Medicine Intercalated disc Perfusion |
Zdroj: | Journal of Molecular and Cellular Cardiology. 9:353-364 |
ISSN: | 0022-2828 |
DOI: | 10.1016/s0022-2828(77)80002-3 |
Popis: | Whole-heart ischemia was induced in isolated working rat hearts developing 75 to 90 mm Hg peak systolic pressures A decline in peak systolic pressure to 30 mm Hg was chosen to represent ventricular failure. For light and electron microscopy, hearts were fixed after pressure development had decreased to 60 mm Hg and also 12 to 24 min after ventricular failure and compared to control hearts with normal coronary perfusion. Lysosomal activity was assessed using the Gomori reaction for the demonstration of acid phosphatase. Twenty-four minutes after ventricular failure hearts showed a loss of glycogen stores, fragmentation of sarcomeres at the I band, disrupted sarcoplasmic reticulum and transverse tubules, vacuolization and decrease in matrix density of mitochondria, and separation of the intercalated disc at the level of the gap junctions. At 12 min the changes were more subtle. Ultrastructurally hearts appeared normal when fixed at peak systolic pressures of 60 mm Hg. The Gomori reaction for the demonstration of acid phosphatase showed only occasional deposits of reaction product in association with residual bodies and primary lysosomes in the nuclear pole zone of myocardial cells from control hearts and hearts fixed at 60 mm Hg. Hearts examined 12 min after ventricular failure showed an increase in electron opaque precipitate in association with residual bodies, vesicular structures, and the Golgi apparatus. At 24 min after ventricular failure the localization of acid phosphatase was not as intense. |
Databáze: | OpenAIRE |
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