Eicosanoids in myocardial ischemia.
Arachidonic acid (AA) accumulation in the ischemic myocardial tissue. Its release and subsequent metabolization into several classes of eicosanoids and lipid peroxides occurs in parallel with the development of myocardial ischemic injury and may be initiated by the loss of energy-rich phosphates. The profile of eicosanoid release during ischemia and reperfusion differs both quantitatively and qualitatively from that seen under non-ischemic conditions. This is at least partially due to the presence of stimulated inflammatory cells and platelets with a considerable activity of AA-metabolizing enzymes as well as endothelial injury. Thus, cardiac eicosanoid release in nonischemic conditions is primarily beneficial, resulting in more effective adaption of its function to the needs of the circulation. Eicosanoid release in acute ischemia is primarily deleterious and enhances inflammatory reactions and functional disturbances.
Schrör
K
K
Institut für Pharmakologie, Heinrich-Heine-Universität, Düsseldorf, FRG.
Thiemermann
C
C
D000818:Animals; D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000378:metabolism; D003327:Coronary Disease / Q000378:metabolism*; D015777:Eicosanoids / Q000378:metabolism*; D006801:Humans; D009206:Myocardium / Q000378:metabolism*
D001095:Arachidonic Acids; D015777:Eicosanoids; D016718:Arachidonic Acid