Failure to detect changes in sarcolemma permeability in amphibian muscle following severe cellular damage.
1. Isolated amphibian hearts and pectoris cutaneous muscles were exposed either to DNP or to caffeine, thereby producing severe myofilament damage. 2. No accompanying change in sarcolemma permeability was detected by monitoring either CK or LDH release or Procion yellow entry in the heart, or by Procion entry in amphibian skeletal muscle. 3. The findings are in contrast with mammalian cardiac and skeletal muscles, and confirm that the pathways leading to myofilament degradation and to the breakdown in sarcolemma organization are separate.
D000818:Animals; D002110:Caffeine / Q000633:toxicity; D002463:Cell Membrane Permeability / Q000187:drug effects; D003402:Creatine Kinase / Q000378:metabolism; D004140:Dinitrophenols / Q000633:toxicity; D006321:Heart / Q000187:drug effects; D066298:In Vitro Techniques; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D010369:Pectoralis Muscles / Q000187:drug effects; D011896:Rana temporaria; D012508:Sarcolemma / Q000187:drug effects* / Q000201:enzymology / Q000648:ultrastructure
D004140:Dinitrophenols; D002110:Caffeine; D007770:L-Lactate Dehydrogenase; D003402:Creatine Kinase