title: Reduced prostaglandin release from the stunned porcine heart--significance for attenuated reactive hyperaemia.
abstract: OBJECTIVE
  Since both reactive hyperaemia and membrane phospholipids are altered even after short lasting ischaemic periods, the release of PGE2 and PGI2 in the basal state and during early reperfusion was examined to determine whether it was changed in the stunned myocardium. The effect of prostaglandin synthesis inhibition on reactive hyperaemia was also examined.
  
  
  METHODS
  The distal left anterior descending coronary artery was occluded for brief periods and coronary flow was recorded by Doppler flowmetry. In subgroups: (1) a shunt was established draining the ischaemic region for determination of myocardial prostaglandin release associated with 2 min of ischaemia before and after a 10 min occlusion; (2) prostaglandin synthesis was blocked between two 2 min occlusions by infusing indomethacin into the left anterior descending artery; and (3) segment lengths were measured in the left anterior descending artery region subjected to consecutive periods of 2, 10, and 2 min of ischaemia, and in a control region.
  
  
  METHODS
  21 pentobarbitone sodium anaesthetised pigs, weight 21-30 kg, were used.
  
  
  RESULTS
  30 min after the 10 min occlusion, systolic shortening was reduced by 38(18-57)% (median +95% confidence interval; p less than 0.05). Concomitantly, basal PGE2 and PGI2 release was reduced by 69(30-77)% (p less than 0.05) and 58(7-81)% (p less than 0.05), respectively. During early reperfusion after 2 min of ischaemia, PGE2 release was reduced by 53(17-86)% (p less than 0.05) after development of stunning, whereas PGI2 release remained unaltered. Blockade of prostaglandin synthesis did not affect reactive hyperaemia either in normal or in stunned myocardium.
  
  
  CONCLUSIONS
  Prostaglandin release from the stunned myocardium is reduced. Since indomethacin did not affect reactive hyperaemia, the attenuated PGE2 release during early reperfusion in stunned myocardium cannot explain the concomitant reduction in reactive hyperaemia.
authors.affiliation: University of Oslo, Ullevål Hospital, Norway.
authors.forename: K A
authors.initials: KA
authors.lastname: Kirkebøen
authors.forename: G
authors.initials: G
authors.lastname: Aksnes
authors.forename: A
authors.initials: A
authors.lastname: Ilebekk
mesh_terms: D015121:6-Ketoprostaglandin F1 alpha / Q000097:blood; D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D001810:Blood Volume / Q000502:physiology; D003326:Coronary Circulation / Q000502:physiology; D003327:Coronary Disease / Q000097:blood*; D015232:Dinoprostone / Q000097:blood*; D011464:Epoprostenol / Q000097:blood*; D005260:Female; D007213:Indomethacin / Q000494:pharmacology; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D013552:Swine
chemical_list: D015121:6-Ketoprostaglandin F1 alpha; D011464:Epoprostenol; D015232:Dinoprostone; D007213:Indomethacin