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Trifluoperazine and the rapid, Ca2+-triggered damage of skeletal and cardiac muscle
Abstract:
[Ca2+]i was raised experimentally in mammalian and amphibian skeletal and cardiac muscles by A23187, DNP, anoxia or the Ca2+ -paradox. Trifluoperazine (TFP) at 10(-5) M failed to protect against the characteristic and rapid damage triggered by elevated [Ca2+]i in any of the preparations. It is concluded that calmodulin is not implicated in this rapid ultrastructural damage. TFP alone also causes identical patterns of damage. It may be acting to raise [Ca2+]i in skeletal and cardiac muscle cells.
Insights
Elevated intracellular calcium ([Ca2+]i) causes rapid muscle damage, and trifluoperazine (TFP) does not prevent it. TFP may actually increase [Ca2+]i, contributing to muscle cell damage.
Area of Science:
- Muscle physiology
- Cellular biology
- Pharmacology
Background:
- Elevated intracellular calcium ([Ca2+]i) is known to cause rapid muscle damage.
- Calmodulin is a calcium-binding protein involved in various cellular processes.
Purpose of the Study:
- To investigate the role of calmodulin in rapid muscle damage induced by elevated [Ca2+]i.
- To determine if trifluoperazine (TFP) can protect against this damage.
Main Methods:
- Experimental elevation of [Ca2+]i in mammalian and amphibian skeletal and cardiac muscles using agents like A23187, DNP, anoxia, and the Ca2+-paradox.
- Administration of trifluoperazine (TFP) at 10(-5) M to assess its protective effects.
Main Results:
- TFP failed to protect any muscle preparations from the rapid, characteristic damage triggered by elevated [Ca2+]i.
- TFP alone induced similar patterns of muscle cell damage.
- The findings suggest calmodulin is not implicated in the rapid ultrastructural damage.
Conclusions:
- Calmodulin is not involved in the rapid ultrastructural damage of muscle cells caused by elevated [Ca2+]i.
- Trifluoperazine may exacerbate muscle damage by increasing intracellular calcium levels.