To investigate the regional variability in intrathoracic vascular pros
taglandin (PG) synthesis, we obtained vessel segments from porcine cor
onary artery (COA), thoracic aorta (AT), common carotid artery (CRA),
pulmonary artery (PA), pulmonary vein (PV), and inferior vena cava (IV
C). Vascular production rates of 6-keto-PGF(1 alpha) (an indicator for
PGI(2)), PGF(2 alpha) and PGE(2) were measured both in unstimulated s
tate and in arachidonic acid-stimulated state using immunosorbent assa
ys. Our results indicated that PGI(2) production rate in all vessel se
gments decayed with time after vessel dissection. In all vessel segmen
ts tested under unstimulated conditions, PGI(2) production rates were
about one order of magnitude higher than PGF(2 alpha) and PGE(2) produ
ction rates of the same specimens. Results from unstimulated, 1.5 hr p
re-incubated specimens indicated that i) PGI(2) production rates in CO
A, AT, and PV were greater than those in CRA, PA, and IVC; ii) PGF(2 a
lpha) 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 ii
i) PGE(2) production rates from the same specimens were not significan
tly different from one another. Arachidonic acid added at about 1.5 hr
after vessel harvest stimulated the PGI(2) and PGF(2 alpha) synthesis
rates by 3 to 15 folds. However, this arachidonic acid treatment caus
ed 70 to 300-fold increases in PGE(2) production rates, reaching level
s comparable to PGI(2). All three prostanoid production rates under st
imulated conditions were also variable among different intrathoracic v
essels. Although either physiological gas concentrations or local hemo
dynamic conditions alone can partially explain our results, which phys
iological parameter(s) actually causes these regional differences rema
ins to be verified.