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Departments of Pharmacological and Physiological Science and Internal Medicine, St. Louis University School of Medicine, St. Louis, Missouri 63104
We recently
reported that canine pulmonary microsomes metabolize arachidonic acid
to all four regioisomeric epoxyeicosatrienoic acids (EET). 5,6-EET
dilates blood vessels in several nonpulmonary vascular beds, often in a
cyclooxygenase-dependent manner. The present study was designed to
determine whether 5,6-EET can decrease pulmonary vascular resistance
(PVR) in the intact pulmonary circulation. In isolated canine lungs
perfused with physiological salt solution, a constant infusion of
U-46619 (3.28 ± 0.99 nmol/min) increased PVR 62.1 ± 4.5%.
Administration of 5,6-EET
(10
5 M) into the perfusate
reduced the U-46619-mediated increase in PVR by 23.6 ± 6.1%. These
effects of U-46619 and 5,6-EET were limited to changes in resistance
solely in the pulmonary venous segment. In contrast, venous as well as
arterial segmental resistances were increased in 5-hydroxytryptamine
(5-HT)-treated lungs. However, in the latter instance, 5,6-EET reduced
arterial but not venous segmental resistance. 5,6-EET increased
pulmonary PGI2 synthesis from 70.5 ± 18.4 to 675.9 ± 125.4 ng/min. In the presence of indomethacin (104 M), 5,6-EET did not
increase PGI2 synthesis nor did it
decrease U-46619- or 5-HT-mediated increases in PVR. In canine
intrapulmonary vessels, 5,6-EET decreased active tension in veins
contracted with U-46619. 5,6-EET decreased active tension in arteries
but not veins contracted with 5-HT, consistent with results in the perfused lungs. These results demonstrate that 5,6-EET is a vasodilator in the intact pulmonary circulation. Its dilator activity depends on
the constrictor agent present, the segmental resistance, and cyclooxygenase activity.
thromboxane; prostacyclin; cyclooxygenase; pulmonary vasculature; segmental resistance
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