To investigate the regional variability in intrathoracic vascular prostaglandin (PG) synthesis, we obtained vessel segments from porcine coronary artery (COA), thoracic aorta (AT), common carotid artery (CRA), pulmonary artery (PA), pulmonary vein (PV), and inferior vena cava (IVC). Vascular production rates of 6-keto-PGF1α (an indicator for PGI2), PGF2α, and PGE2 were measured both in unstimulated state and in arachidonic acid-stimulated state using immunosorbent assays. Our results indicated that PGI2 production rate in all vessel segments decayed with time after vessel dissection. In all vessel segments tested under unstimulated conditions, PGI2 production rates were about one order of magnitude higher than PGF2α and PGE2 production rates of the same specimens. Results from unstimulated, 1.5 hr pre-incubated specimens indicated that i) PGI2 production rates in COA, AT, and PV were greater than those in CRA, PA, and IVC; ii) PGF2α production rates from the same specimens were higher in PV than in AT, CRA, and IVC, while these in PA were higher than in IVC; and iii) PGE2 production rates from the same specimens were not significantly different from one another. Arachidonic acid added at about 1.5 hr after vessel harvest stimulated the PGI2 and PGF2α synthesis rates by 3 to 15 folds. However, this arachidonic acid treatment caused 70 to 300-fold increases in PGE2 production rates, reaching levels comparable to PGI2. All three prostanoid production rates under stimulated conditions were also variable among different intrathoracic vessels. Although either physiological gas concentrations or local hemodynamic conditions alone can partially explain our results, which physiological parameter(s) actually causes these regional differences remains to be verified.
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