NDLI: Amphipathic metabolites and membrane dysfunction in ischemic myocardium.

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Amphipathic metabolites and membrane dysfunction in ischemic myocardium.

Content Provider	Semantic Scholar
Author	Corr, Peter B. Gross, Richard W. Sobel, B. E.
Copyright Year	1984
Abstract	MANY laboratory and clinical observations have implicated altered lipid metabolism as a contributor to membrane dysfunction, electrophysiological derangements, malignant arrhythmia, and cellular injury in ischemic myocardium. Amphipathic metabolites, moieties with both hydrophobic and hydrophilic properties, are capable of exerting deleterious effects on biological membrane systems through multiple mechanisms. Because of their structure, amphiphiles can alter membrane function by inserting into the phospholipid bilayer, and, under some conditions, can act as detergents with resultant dissolution of membrane constituents including cholesterol and phospholipids. This selective review will consider the metabolism of fatty acids, fatty acid esters, and phospholipid catabolites which increase in ischemic myocardium and have been implicated as biochemical mediators of membrane dysfunction. Two reviews dealing with the biophysics of lipid alterations in membranes and alterations of carbohydrate and fatty acid metabolism during ischemia have been published recently (Liedtke, 1981; Katz and Messineo, 1981).
Starting Page	247
Ending Page	251
Page Count	5
File Format	PDF HTM / HTML
Alternate Webpage(s)	http://circres.ahajournals.org/content/circresaha/55/2/135.full.pdf
Alternate Webpage(s)	http://circres.ahajournals.org/content/circresaha/55/2/135.full.pdf?download=true
PubMed reference number	6086176v1
Volume Number	55
Issue Number	2
Journal	Circulation research
Language	English
Access Restriction	Open
Subject Keyword	Carbohydrates Cholesterol Detergents Esters Fatty Acids Lipid Metabolism Disorders Lipids Myocardium Phospholipids Review [Publication Type] Scientific Publication Thioctic Acid Tissue membrane catabolites fatty acid metabolism
Content Type	Text
Resource Type	Article

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