Literature DB >> 3837825

Sarcolemmal disruption during the calcium paradox.

J A Post, P F Nievelstein, J Leunissen-Bijvelt, A J Verkleij, T J Ruigrok.   

Abstract

Reperfusion of an isolated heart with calcium-containing solution after a short period of calcium-free perfusion may result in irreversible cell damage (calcium paradox). The ultrastructure of the sarcolemma of the rabbit heart during the calcium paradox was studied by using fast freezing devices. This method excluded ultrastructural changes induced by chemical fixation and cryoprotection. In addition, thin-section and conventional freeze-fracture electron microscopy were used. During reperfusion with calcium-containing solution disruption of the sarcolemma was observed, which was attended with formation of unilamellar and multilamellar vesicles and aggregation of intramembrane particles. These ultrastructural changes are explained in terms of calcium- and proton-induced lateral phase separation and fusion processes in the lipid bilayer of the sarcolemma.

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Year:  1985        PMID: 3837825     DOI: 10.1016/s0022-2828(85)80009-2

Source DB:  PubMed          Journal:  J Mol Cell Cardiol        ISSN: 0022-2828            Impact factor:   5.000


  4 in total

1.  No evidence of oxygen free radicals-mediated damage during the calcium paradox.

Authors:  R Ferrari; C Ceconi; S Curello; A Cargnoni; T J Ruigrok
Journal:  Basic Res Cardiol       Date:  1989 Jul-Aug       Impact factor: 17.165

2.  The effect of hypothermia during the period of calcium repletion on the calcium paradox.

Authors:  T J Ruigrok; D de Moes; P van der Meer
Journal:  Basic Res Cardiol       Date:  1986 Jul-Aug       Impact factor: 17.165

3.  Possible role of phospholipase C in the induction of Ca(2+)-paradox in rat heart.

Authors:  S Persad; A Vrbanova; J T Meij; V Panagia; N S Dhalla
Journal:  Mol Cell Biochem       Date:  1993-04-21       Impact factor: 3.396

4.  Myosin heavy chain and cardiac troponin T damage is associated with impaired myofibrillar ATPase activity contributing to sarcomeric dysfunction in Ca2+-paradox rat hearts.

Authors:  Árpád Kovács; Judit Kalász; Enikő T Pásztor; Attila Tóth; Zoltán Papp; Naranjan S Dhalla; Judit Barta
Journal:  Mol Cell Biochem       Date:  2017-02-17       Impact factor: 3.396

  4 in total

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