三氟拉嗪与骨骼肌和心肌的快速、钙触发损伤

Trifluoperazine and the rapid, Ca2+-triggered damage of skeletal and cardiac muscle.

作者信息

Duncan C J, Rudge M F

出版信息

Comp Biochem Physiol C Comp Pharmacol Toxicol. 1984;78(1):49-50. doi: 10.1016/0742-8413(84)90046-x.

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.

摘要

通过A23187、二硝基苯酚（DNP）、缺氧或钙反常现象，在哺乳动物和两栖动物的骨骼肌及心肌中实验性地提高了细胞内钙离子浓度（[Ca2+]i）。10^(-5) M的三氟拉嗪（TFP）未能在任何一种制剂中防止由升高的[Ca2+]i引发的典型快速损伤。得出的结论是，钙调蛋白与这种快速的超微结构损伤无关。单独使用TFP也会导致相同的损伤模式。它可能在骨骼肌和心肌细胞中起作用以提高[Ca2+]i。