Prostacyclin Increases Portal Venous Flow.
Abstract
Prostacyclin (PGI2) is a potent vasodilator and is a potential therapeutic agent to increase blood flow during several disease states. PGI2 is also elevated in plasma during sepsis or pancreatitis. The hemodynamic effect of PGI2 has not been investigated with regard to the portal venous system. In five anesthetized swine, cardiac output (CO), central venous pressure (CVP), femoral artery pressure (FAP), heart rate (HR), pulmonary artery pressure (PAP), portal venous flow (PoVF), and portal venous pressure (PoVP) were measured before and after increasing does of PGI2. The infusions were then repeated after atropine administration. The previously reported effects on the peripheral and pulmonary vascular systems were confirmed. After an injection of 0.5 to 5.0 microgram/kg of PGI2 into the left atrium, a significant decline in CO, FAP, and PAP occurred. Atropinization further depressed CO. The most marked effect of PGI2, however, was an increase in PoVF without a change in PoVP. This effect was more pronounced when atropine was administered. In anesthetized swine, PGi2, is a potent vasodilator in all vascular beds, including the portal venous system. These hemodynamic changes should be realized when exogeneous PGI2 is considered as a therapeutic agent or which endogenous PGI2 might increase in association with disease states like pancreatitis or sepsis.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jul 01, 1984
- Accession Number
- ADA145362
Entities
People
- C. C. Buchalter
- J. D. O'benar
- L. W. Traverso
Organizations
- Letterman Army Hospital