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[Changes in the myocardium damaged by strophanthin]
Abstract:
The mechanism of intoxication, produced with strophanthin (10 mg/kg) has been studied in myocardium of white rats. Area, perimeter and factor of form in mitochondria, ratio of the mitochondrial surface area with injured external membranes to the whole mitochondrial area, agranular sarcoplasmic network and T-system area, changes in myofilaments, Z-lines, length of sarcomeres have been estimated. Changes in succinate dehydrogenase, lactate dehydrogenase and in reduced forms of nicotinamide coenzymes activity has been investigated histochemically. Adenosine triphosphate (ATP) prevents appearance of ultrastructural and histochemical disturbances, produced with strophanthin. However, the protective effect of ATP is not sufficient. Adenosine monophosphate, penetrating across the cell membrane, is supposed to produce a greater curative effect.
Insights
Strophanthin intoxication damages rat heart cells, affecting mitochondria and muscle structure. Adenosine triphosphate (ATP) offers partial protection, but adenosine monophosphate may provide greater therapeutic benefits.
Area of Science:
- Cardiovascular toxicology
- Cellular biology
- Biochemistry
Context:
- Strophanthin is a cardiac glycoside known for its toxicity.
- Understanding its mechanism of action at the cellular level is crucial for potential therapeutic interventions.
- Myocardial tissue in white rats serves as the model system.
Purpose:
- To elucidate the cellular and subcellular mechanisms of strophanthin-induced cardiotoxicity.
- To investigate the protective effects of adenosine triphosphate (ATP) and adenosine monophosphate (AMP) against strophanthin toxicity.
- To assess histochemical changes in key cardiac enzymes and coenzymes.
Summary:
- Strophanthin intoxication in rat myocardium alters mitochondrial morphology (area, perimeter, form factor), increases damaged mitochondrial membrane ratios, and affects sarcoplasmic reticulum and T-system areas.
- Ultrastructural changes include alterations in myofilaments, Z-lines, and sarcomere length.
- Histochemical analysis revealed changes in succinate dehydrogenase, lactate dehydrogenase, and nicotinamide coenzyme activity.
- Adenosine triphosphate (ATP) partially mitigates these ultrastructural and histochemical disturbances.
- Adenosine monophosphate (AMP) is hypothesized to offer superior therapeutic effects due to its cell membrane permeability.
Impact:
- Provides detailed insights into the cellular pathology of strophanthin cardiotoxicity.
- Highlights the potential of nucleotide-based therapies, specifically AMP, for managing strophanthin poisoning.
- Contributes to the understanding of cardiac energy metabolism and drug-induced cellular damage.