Atherosclerosis decreased prostacyclin formation in rabbit lungs and kidneys.
Metabolism of arachidonic acid (AA) was studied in perfused lungs and kidneys of normal and atherosclerotic rabbits by determination of PGE2, PGF2 alpha and the stable metabolites of PGI2 (6-keto-PGF1 alpha) and TXA2 (TXB2). PGI2 was the main AA metabolite formed by normal lungs and kidneys. Atherosclerosis reduced the formation of PGI2 by about 50 % in both organs. TXA2 formation was similarily decreased in lungs. In kidneys, the decrease in PGI2 formation was accompanied by an increase in PGE2 formation.
D000818:Animals; D001161:Arteriosclerosis / Q000378:metabolism*; D011464:Epoprostenol / Q000096:biosynthesis* / Q000378:metabolism; D007668:Kidney / Q000378:metabolism*; D008168:Lung / Q000378:metabolism*; D008297:Male; D011453:Prostaglandins / Q000096:biosynthesis*; D011458:Prostaglandins E / Q000378:metabolism; D011460:Prostaglandins F / Q000378:metabolism; D011817:Rabbits; D012636:Secretory Rate; D013931:Thromboxanes / Q000378:metabolism
D011453:Prostaglandins; D011458:Prostaglandins E; D011460:Prostaglandins F; D013931:Thromboxanes; D011464:Epoprostenol