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大鼠心脏全心局部缺血期间缺血性挛缩的超微结构关联

Ultrastructural correlates of ischaemic contracture during global subtotal ischaemia in the rat heart.

作者信息

Harper I S, van der Merwe E, Owen P, Opie L H

机构信息

Research Institute for Medical Biophysics, Medical Research Council, Tygerberg, South Africa.

出版信息

J Exp Pathol (Oxford). 1990 Apr;71(2):257-68.

Abstract

The development of left ventricular ischaemic contracture and its correlation with ultrastructural and sarcolemmal permeability defects were studied in isolated rat hearts during global subtotal ischaemia. With acetate as substrate the hearts exhibited a rise in diastolic tension after 8-10 min at which time small foci of contracted myocytes were scattered throughout the myocardium. In hearts with 5% of the maximum diastolic tension (termed 5% contracture), the foci were situated predominantly in the subendocardium and papillary muscle. Contracted myocytes in these foci were capable of excluding ionic lanthanum thus demonstrating retention of normal sarcolemmal permeability properties. With 30% contracture ultrastructural damage had spread to the subepicardium and with further contracture there was an associated increase in the number and size of foci in all regions. In these foci, swelling of the tubular sarcolemmal system and occasionally of the sarcoplasmic reticulum appeared to precede myofibrillar contraction. At 50% contracture lanthanum influx into contracted cells became more frequent. Hearts developed full contracture by 15-18 min at which time most myocytes were contracted and retained lanthanum intracellularly. The heterogeneity of the response at a cellular level may offer a possible explanation for the lack of correlation between contracture and tissue ATP. A possible sequence of structural injury leading to impaired calcium homeostasis is also suggested.

摘要

在离体大鼠心脏全心局部缺血期间,研究了左心室缺血性挛缩的发展及其与超微结构和肌膜通透性缺陷的相关性。以醋酸盐为底物时,心脏在8 - 10分钟后舒张张力升高,此时收缩的心肌细胞小灶散布于整个心肌。在舒张张力达到最大舒张张力5%(称为5%挛缩)的心脏中,这些病灶主要位于心内膜下和乳头肌。这些病灶中的收缩心肌细胞能够排除离子镧,从而表明肌膜通透性特性正常。当挛缩达到30%时,超微结构损伤已蔓延至心外膜下,随着挛缩进一步加重,所有区域病灶的数量和大小均相应增加。在这些病灶中,管状肌膜系统偶尔还有肌浆网肿胀似乎先于肌原纤维收缩出现。当挛缩达到50%时,镧流入收缩细胞的情况变得更加频繁。心脏在15 - 18分钟时出现完全挛缩,此时大多数心肌细胞收缩并在细胞内保留镧。细胞水平反应的异质性可能为挛缩与组织ATP之间缺乏相关性提供一种可能的解释。还提出了导致钙稳态受损的结构损伤可能顺序。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0d3/1998717/11de3823f307/jexppathol00002-0121-a.jpg

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