Prostacyclin synthesis in human and experimental atherosclerosis

Lipid composition of rabbit aortic wall following removal of endothelium by balloon catheter.

“…21 " 23 The finding that the arachidonic acid content of phospholipids was reduced in regrowth areas (Table 5) is consistent with other reports. In summarizing their observations in many specimens of atherosclerotic human and animal tissues, Sinzinger et al 24 reported a diminished formation of prostacyclin. Similar data were published by Dembinska-Kiec et al 25 indicating that atherosclerosis decreases prostacyclin formation in rabbit lungs and kidneys, thereby implying an alteration in the metabolism of arachidonic acid.…”

Alteration in prostacyclin and prostaglandin E2 production. Correlation with changes in human aortic atherosclerotic disease.

“…Our results report the amount of enzyme present per unit weight of microsome, and provide additional data to that obtained in previous experiments based on arterial rings (intact cells). 5 ' 610 " 13 Earlier observations showed that glutathione promotes the production of E-type PG rather than PGI 2 and that this effect is specific for GSH in comparison to the effects of other sulfur-containing molecules. 3738 The enzyme PG H-PG E 2 isomerase that catalyzes the isomerism of PGH 2 into PGE 2 requires glutathione as a cofactor.…”

“…As controls, we used aortic roots from young adults instead of apparently disease-free aortic areas from the patients. 10 " 13 Since age-matched controls were unavailable, our control group represents a compromise. We cannot completely rule out the possibility that there are significant differences in arterial wall arachidonic acid metabolism between the upper thoracic and the abdominal portion of the aorta.…”

“…Atherosclerotic arteries produce less PGI 2 than normal vessels. 8 " 13 Patients with ischemic heart disease have increased thromboxane Aj (the proaggregatory prostanoid) plasma levels and decreased PGI 2 production. 1415 It was postulated that atherosclerosis could originate from a defect in PGI 2 production in the arterial wall and the resulting unbalanced equilibrium between thromboxane Aj (TxA^ and PGI 2 levels in plasma.…”

“…Previous studies dealing with established lesions have failed to show a relationship to the type of atherosclerosis and PGI 2 production. 11 " 13 We have classified atherosclerotic lesions into three groups encompassing the very early stages of the development of atherosclerosis and here report the progressive, inverse PGI 2 and PGE 2 production changes in human aortas as atherosclerosis progresses histologically.…”