Table 1.

Shift of Prostanoid Synthesis Pattern in Atherosclerotic Vessels Because of Reduced Prostacyclin Synthase Activity

Stimulus/substrate	Atherosclerotic	Metabolites formed:
		6-keto-PGF1α	PGE2	PGF2α
Acetylcholine†	−	121 ± 43	47 ± 13	31 ± 8
(100 nmol/L)	+	48 ± 34*	129 ± 64*	41 ± 11
Angiotensin II†	−	113 ± 61	57 ± 34	28 ± 11
(50 nmol/L)	+	43 ± 27*	108 ± 38*	45 ± 21
Arachidonic acid†	−	167 ± 67	115 ± 58	33 ± 8
(10 μmol/L)	+	63 ± 27*	188 ± 54*	45 ± 15
14C-PGH2‡	−	75 ± 11	19 ± 11	4.5 ± 0.9
(100 μmol/L)	+	31 ± 7*	55 ± 14*	5.4 ± 2.1

^† Arteries were exposed to the stimuli for 30 minutes in an organ bath in the presence of 100 μmol/L N-methylarginine to inhibit NO formation. Prostanoids were extracted from the bath solution and quantitated by enzyme-linked immunosorbent assay. Data [in pg/mg wet tissue] represent means ± SEM from 10 independent experiments. Prostanoid release in unstimulated tissue was below the detection limit.

^‡ Radiolabeled PGH₂ was added to homogenized arteries. The percentage of conversion into different metabolites was determined after 3 minutes of incubation. Data [in percentage of ¹⁴C-PGH₂ conversion] represent means ± SEM from seven independent experiments.

* P < 0.01 (atherosclerotic versus normal tissue).