Rudge M F, Duncan C J
Comp Biochem Physiol A Comp Physiol. 1984;79(3):393-8. doi: 10.1016/0300-9629(84)90533-4.
By measuring characteristic ultrastructural damage, the Ca2+-paradox has been demonstrated in isolated frog hearts, and in frog and mouse ventricle strips. During Ca2+-free perfusion (phase I), PCa of the sarcolemma is increased; 4 degrees C provides complete protection against these molecular changes in frog and a partial protection in mouse tissue. Re-introduction of extracellular Ca2+ (phase II) now causes typical Ca2+-triggered damage which is markedly reduced at 4 degrees C in both species but is not inhibited by leupeptin. Major sarcolemma damage occurs at this point.
通过测量特征性超微结构损伤,已在离体蛙心以及蛙和小鼠心室肌条中证实了钙悖论。在无钙灌注期间(阶段I),肌膜的钙通透性增加;4℃可完全保护蛙免受这些分子变化的影响,对小鼠组织则提供部分保护。重新引入细胞外钙(阶段II)现在会引发典型的钙触发损伤,在这两个物种中,4℃时这种损伤都会显著减轻,但不受亮抑蛋白酶肽的抑制。此时会发生主要的肌膜损伤。