The major cyclooxygenase metabolite of arachidonic acid (AA) in endothelial cells is prostacyclin (PGI2). Although most primary prostaglandins constrict the pulmonary vasculature, PGI2 is a pulmonary vasodilator. In the pulmonary circulation, optimal matching of blood flow to oxygenated alveoli is achieved by regulating the distribution of intrapulmonary blood flow. Alveoli exposed to reduced oxygen tension produce increases in pulmonary vascular resistance (PVR) resulting from hypoxic pulmonary vasoconstriction. These vasoconstrictor influences are opposed by endogenous vasodilator substances such as PGI2. It has previously been shown that exogenous administration of 5,6- epoxyeicosatrienoic acid (5,6-EET) into the intact canine pulmonary circulation opposes increases in PVR and results in large increases in PGI2 synthesis. Therefore it is proposed that stimulation by 5,6-EET in the pulmonary circulation results in increased synthesis of the pulmonary vasodilator, PGI2 which may mediate the vasodilator activity of 5,6-EET.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Predoctoral Individual National Research Service Award (F31)
Project #
5F31HL010333-02
Application #
6351457
Study Section
Special Emphasis Panel (ZRG1-SSS-8 (58))
Program Officer
Colombini-Hatch, Sandra
Project Start
2000-02-01
Project End
Budget Start
2001-02-01
Budget End
2001-08-31
Support Year
2
Fiscal Year
2001
Total Cost
$12,124
Indirect Cost
Name
Saint Louis University
Department
Pharmacology
Type
Schools of Medicine
DUNS #
City
Saint Louis
State
MO
Country
United States
Zip Code
63103