Decreased serum levels of a factor stimulating prostacyclin synthesis in acute myocardial infarction.
To investigate the role of a factor in serum stimulating prostacyclin synthesis in acute myocardial infarction, we compared the activities of the factor among 7 patients with acute myocardial infarction (2.5 +/- 0.8 hrs and 80 +/- 17 hrs after the onset of symptoms), 12 patients with angina pectoris, and 7 normal subjects. In this study, we found that in patients with acute myocardial infarction, this activity is much lower immediately after infarction (2.5 +/- 0.8 hrs) than 80 +/- 17 hrs later, or in patients with stable angina pectoris, or in healthy volunteers. Since prostacyclin is antiaggregating and vasodilating, the deficiency in this ability during the very early phase of acute myocardial infarction may be related to the development of the thrombosis of acute myocardial infarction.
D015121:6-Ketoprostaglandin F1 alpha / Q000032:analysis; D000818:Animals; D011464:Epoprostenol / Q000096:biosynthesis*; D006801:Humans; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood*; D051381:Rats; D011919:Rats, Inbred Strains; D013997:Time Factors
D015121:6-Ketoprostaglandin F1 alpha; D011464:Epoprostenol