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钙反常期间离体灌注大鼠心脏的表面超微结构特征

Surface ultrastructural features of isolated perfused rat hearts during calcium paradox.

作者信息

Ashraf M, Onda M, Benedict J, Hirohata Y

出版信息

Scan Electron Microsc. 1981(Pt 3):109-14.

PMID:7330571
Abstract

Cellular damage caused by calcium (Ca++) paradox is of significant importance under both experimental and clinical conditions. Electron microscopy was used to study the surface changes of the isolated rat hearts perfused with normal Krebs-Henseleit (KH) medium, Ca++-free KH medium, Ca++-free KH medium followed by normal KH medium. The hearts perfused with Ca++-free medium and normal KH medium showed elongated parallel myofibrils with transverse ridges spaced at regular intervals. The major change in Ca++- free hearts consisted of wide cellular separation. For the Ca++- paradox hearts, wht myofibrils were twisted and narrowed at several locations. The myocardial fiber surfaces were bulged out, frequently with sarcolemmal ruptures and holes. Supercontraction of cells caused breaks in the sarcolemma and aggregation of mitochondria at the cell periphery. These results suggest that Ca++-depletion primarily affects the myocardial cell junctions which, following reintroduction of Ca++, accelerate the entry of Ca++ into the cells, supercontraction of cells and stretching of sarcolemma.

摘要

在实验和临床条件下,钙(Ca++)反常引起的细胞损伤都具有重要意义。利用电子显微镜研究了用正常克氏-亨氏(KH)培养基、无钙KH培养基、无钙KH培养基后接正常KH培养基灌注的离体大鼠心脏的表面变化。用无钙培养基和正常KH培养基灌注的心脏显示出拉长的平行肌原纤维,其横向嵴以规则间隔排列。无钙心脏的主要变化包括细胞间隙变宽。对于钙反常心脏,肌原纤维在几个位置扭曲变窄。心肌纤维表面向外凸出,经常出现肌膜破裂和孔洞。细胞的超收缩导致肌膜破裂和线粒体在细胞周边聚集。这些结果表明,钙耗竭主要影响心肌细胞连接,在重新引入钙后,加速钙进入细胞、细胞超收缩和肌膜拉伸。

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