Granulocytes, platelet-activating factor, and myocardial injury.
نویسندگان
چکیده
منابع مشابه
Platelet-activating factor acetylhydrolase prevents myocardial ischemia-reperfusion injury.
BACKGROUND Platelet-activating factor (PAF) is one of the most potent biological mediators of tissue injury. PAF acetylhydrolase (PAF-AH) is a recently isolated naturally occurring enzyme that hydrolyzes PAF and renders it inactive. We hypothesize that inhibition of PAF with PAF-AH will reduce myocardial ischemia-reperfusion (I/R) injury in vivo. METHODS AND RESULTS The coronary ligation mode...
متن کاملOpposing effects of platelet-activating factor and lyso-platelet-activating factor on neutrophil and platelet activation.
Platelet-activating factor (PAF) is a potent, bioactive phospholipid that acts on multiple cells and tissues through its G protein-coupled receptor (GPCR). PAF is not stored but is rapidly generated via enzymatic acetylation of the precursor 1-O-hexadecyl-2-hydroxy-sn-glycero-3-phosphocholine (lysoPAF). The bioactivity of PAF is effectively and tightly regulated by PAF acetylhydrolases, which c...
متن کاملPlatelet-activating factor.
Platelet-activating factor is a phospholipid with diverse potent physiological effects. Its actions are achieved at concentrations as low as IO-‘” M in some systems and almost always by lo-’ M as an intercellular messenger. The molecular structure of PAF was discovered through parallel investigations of two different biological activities: a factor in the blood of rabbits undergoing anaphylaxis...
متن کاملPlatelet-activating factor.
Our ability to chemically characterize and synthesize this autacoid of allergy and inflammation has given us a unique opportunity to study these important molecules in a highly disciplined fashion. It has also opened the door to a vista of research approaches to define PAF's normal physiologic role as well as its actions as an immunopathologic mediator. Recent work is described.
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ژورنال
عنوان ژورنال: Circulation
سال: 1989
ISSN: 0009-7322,1524-4539
DOI: 10.1161/01.cir.79.6.1401