Abstract:
:In this comparative study, rat hearts were perfused at 37 degrees C with three clearly defined protocols: the Ca2+ paradox, the O(2) paradox, and with 20 mM caffeine. Each protocol involved an initial priming (Ca(2+)(0) depletion or anoxia; stage 1) and subsequent full activation (Ca(2+)(0) repletion, caffeine or reoxygenation; stage 2) of the damage system of the sarcolemma. Creatine kinase release in stage 2 was completely inhibited (P < 0.001) in all three protocols when 420 mOsm was added to the perfusion medium throughout the experiments, or only during stage 1, or only during stage 2. Increasing the perfusion pressure in the Ca2+ paradox significantly (P < 0.001) exacerbated creatine kinase release, although this was still completely inhibited at 28 degrees C. Amiloride (1 mM) inhibited creatine kinase release completely at 40 cm of water pressure but only some 50% at 80 cm of water pressure. It is suggested that the transmembrane damage system needs to be uncoupled or deactivated by modifying its relationship with the cytosol or with the underlying cytoskeleton by hyperosmotic cell shrinkage for only one of the stages in all three protocols to block the damage pathway. Increased perfusion pressure has the opposite effect and exacerbates damage.
journal_name
Exp Mol Patholjournal_title
Experimental and molecular pathologyauthors
Harding RJ,Duncan CJdoi
10.1006/exmp.1999.2275keywords:
subject
Has Abstractpub_date
1999-10-01 00:00:00pages
91-8issue
2eissn
0014-4800issn
1096-0945pii
S0014-4800(99)92275-Xjournal_volume
67pub_type
杂志文章abstract::Formin-like 3 (FMNL3), a member of diaphanous-related formins subfamily, plays an important role in cytoskeleton reorganization, cell adhesion and cancer cell invasion in vitro. This study aimed to explore the expression of FMNL3 in colorectal carcinoma (CRC) cell-lines and tissues, and further evaluate its prognostic...
journal_title:Experimental and molecular pathology
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pub_type: 杂志文章,评审
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journal_title:Experimental and molecular pathology
pub_type: 杂志文章
doi:10.1006/exmp.1994.1005
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journal_title:Experimental and molecular pathology
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journal_title:Experimental and molecular pathology
pub_type: 杂志文章
doi:10.1006/exmp.1993.1037
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journal_title:Experimental and molecular pathology
pub_type: 杂志文章
doi:10.1006/exmp.1994.1035
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pub_type: 杂志文章
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journal_title:Experimental and molecular pathology
pub_type: 杂志文章
doi:10.1016/j.yexmp.2007.07.001
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journal_title:Experimental and molecular pathology
pub_type: 杂志文章
doi:10.1016/0014-4800(84)90010-8
更新日期:1984-08-01 00:00:00
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journal_title:Experimental and molecular pathology
pub_type: 杂志文章
doi:10.1016/j.yexmp.2004.02.002
更新日期:2004-08-01 00:00:00
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pub_type: 杂志文章
doi:10.1016/j.yexmp.2011.03.001
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journal_title:Experimental and molecular pathology
pub_type: 杂志文章
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更新日期:2015-12-01 00:00:00
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pub_type: 杂志文章
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journal_title:Experimental and molecular pathology
pub_type: 杂志文章
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更新日期:1992-04-01 00:00:00
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journal_title:Experimental and molecular pathology
pub_type: 杂志文章
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更新日期:2015-04-01 00:00:00