title: Variation in plasma platelet-activating factor degradation and serum lipids after acute myocardial infarction.
abstract: BACKGROUND
  Platelet-activating factor is a biologically potent phospholipid that may mediate cell damage in patients with myocardial ischemia. In plasma, its inactivation to lyso-platelet-activating factor is catalyzed by a specific, lipoprotein-associated acetylhydrolase. Because lipoprotein levels decrease after myocardial infarction, a possible reduction was suspected to occur in plasma degradation of platelet-activating factor.
  
  
  METHODS
  Degradation of platelet-activating factor was examined in an optimized assay of acetylhydrolase activity and in relation to the in vitro plasma half-life of platelet-activating factor. These, plasma lyso-platelet-activating factor and serum lipids, were measured in 12 men with acute myocardial infarction at presentation and at 2 and 7 days later.
  
  
  RESULTS
  Acetylhydrolase activity was depressed at day 2 and at day 7. The corresponding increase in plasma half-life of platelet-activating factor was minimal and insignificant. A significant linear relation existed between the half-life of platelet-activating factor and the reciprocal of acetylhydrolase activity at each time of study, indicating a hyperbolic relation between the two. By day 2, total and low-density lipoprotein cholesterol had decreased but showed no further change by day 7; high-density lipoprotein cholesterol had not decreased at day 2 but was depressed by day 7. Plasma lyso-platelet-activating factor had decreased by day 2 and had returned to its initial level by day 7.
  
  
  CONCLUSIONS
  Acute myocardial infarction is associated with depression of plasma acetylhydrolase activity, and because of the hyperbolic relation between the plasma enzyme activity and the half-life of platelet-activating factor, the latter shows negligible change. Hence, the mechanism for the inactivation of any platelet-activating factor that might be released as a consequence of tissue damage is preserved.
authors.affiliation: Department of Medicine, University of Western Australia, Perth.
authors.forename: C J
authors.initials: CJ
authors.lastname: Stephens
authors.forename: R M
authors.initials: RM
authors.lastname: Graham
authors.forename: M J
authors.initials: MJ
authors.lastname: Sturm
authors.forename: M
authors.initials: M
authors.lastname: Richardson
authors.forename: R R
authors.initials: RR
authors.lastname: Taylor
mesh_terms: D043203:1-Alkyl-2-acetylglycerophosphocholine Esterase; D002784:Cholesterol / Q000097:blood; D006207:Half-Life; D006801:Humans; D008055:Lipids / Q000097:blood*; D008075:Lipoproteins, HDL / Q000097:blood; D008077:Lipoproteins, LDL / Q000097:blood; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000201:enzymology*; D010741:Phospholipases A / Q000097:blood*; D010972:Platelet Activating Factor / Q000378:metabolism*
chemical_list: D008055:Lipids; D008075:Lipoproteins, HDL; D008077:Lipoproteins, LDL; D010972:Platelet Activating Factor; D002784:Cholesterol; D010741:Phospholipases A; D043203:1-Alkyl-2-acetylglycerophosphocholine Esterase