Elz J S, Nayler W G
Am J Pathol. 1984 Oct;117(1):131-9.
Hearts repleted with Ca2+-containing buffers after only a few minutes of Ca2+-free perfusioN display extensive ultrastructural damage and accumulate Ca2+. Ultrastructural damage includes separation of the intercalated disks, development of contracture bands, and splitting of the internal and external layers of the glycocalyx. In this study, the authors have used isolated spontaneously beating Langendorff perfused hearts to investigate whether Mn2+ alters the ultrastructural damage associated with Ca2+ repletion after Ca2+-free perfusion, previous studies having shown that it attenuates or abolishes the gain in Ca2+ which normally occurs under these conditions. Mn2+ added only at the time of Ca2+ repletion did not attenuate the ultrastructural damage. When Mn2+ (2 mM) was added during the Ca2+-free period or the Ca2+-free and Ca2+ repletion periods, however, the hearts were not as extensively damaged. The myofibrils were relaxed, and the intercalated disks were intact. However, splitting of the glycocalyx still occurred and was a prominent feature. These results indicate that splitting of the glycocalyx per se does not necessarily result in a massive gain in Ca2+ when Ca2+ is returned to Ca2+-depleted hearts. Possible mechanisms of action of Mn2+ are discussed.
在无钙灌注仅几分钟后，充满含Ca2+缓冲液的心脏就会出现广泛的超微结构损伤并积累Ca2+。超微结构损伤包括闰盘分离、挛缩带形成以及糖萼内外层分裂。在本研究中，作者使用离体自发搏动的兰根多夫灌注心脏来研究Mn2+是否会改变无钙灌注后与Ca2+再充盈相关的超微结构损伤，先前的研究表明它会减弱或消除在这些条件下通常出现的Ca2+增加。仅在Ca2+再充盈时添加Mn2+并不能减轻超微结构损伤。然而，当在无钙期或无钙和Ca2+再充盈期添加Mn2+（2 mM）时，心脏的损伤程度没有那么严重。肌原纤维松弛，闰盘完整。然而，糖萼的分裂仍然发生并且是一个显著特征。这些结果表明，当Ca2+回到缺钙心脏时，糖萼的分裂本身不一定会导致大量的Ca2+增加。文中讨论了Mn2+可能的作用机制。
