Prostacyclin (PGI 2 ) and prostaglandin E 2 (PGE 2 ) production was Investigated in human aortas (five controls and 27 with atherosclerotic lesions). The specific activities of PGI 2 and PGE 2 synthetase were studied using radioimmunoassays of PGE 2 and 6-keto-PGE 1( , of aortic microsomes incubated in the presence of additional substrate and cofactors. The atherosclerotic lesions were examined under the light microscope and were classified as Stage 1 when the disease was restricted to the intima and as Stages 2 and 3 when there were moderate or advanced lesions. Prostaglandin production for the control group (n = 5), Stage 1 (n = 7), Stage 2 (n = 10), and Stage 3 (n = 10) were as follows: 454 ± 15, 162 ± 81, 92 ± 90, and 65 ± 61 pmol 6-K-PGF 1u /50 mg proteln/10 minutes; and 15 ± 12, 399 ± 406, 227 ± 174, and 366 ± 362 pmol PGEj/50 mg protein/10 minutes (mean ± SD) respectively. We conclude that: 1) In normal aortas, PGE 2 production was low, while PGI 2 synthesis activity was elevated. The reverse situation was observed In aortas with atherosclerosis lesions (p < 0.05). 2) There was an inverse relationship between PGE 2 and PGI, production (p < 0.05).3) There was a direct hlstologlc relationship between lower PGI 2 production and atherosclerosis progression. A decided decline In 6-K-PGF,,, production was detected in aortas In the early stages (65% of control values). 4) By contrast, a progressive increase In PGE 2 production was found In Stage 2 and Stage 3 groups (p < 0.05). These results demonstrate that there are correlations between the changes In prostaglandin production and the morphological features of atherosclerosis development. Because of the pharmacologlc properties of prostaglandins, these changes in prostaglandin production may promote the development of atherosclerosis. (Arteriosclerosis 4:70-78, January/February 1984)

No abstract

No abstract