Prostacyclin increases portal venous flow
| Autor: | L W Traverso, J D O'Benar, C C Buchalter |
|---|---|
| Rok vydání: | 1984 |
| Předmět: |
Cardiac output
business.industry Portal venous pressure Central venous pressure Portal venous system Hemodynamics medicine.disease Biochemistry Sepsis Endocrinology Blood pressure Anesthesia medicine.artery Pulmonary artery cardiovascular system Medicine lipids (amino acids peptides and proteins) business |
| Zdroj: | Prostaglandins. 28:679-693 |
| ISSN: | 0090-6980 |
| DOI: | 10.1016/0090-6980(84)90177-1 |
| Popis: | Prostacyclin (PGI2) is a potent vasolidator and is a potential therapeutic agent to increase blood flow during several disease states. PGI2 is alos 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 doses 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 ug/kg of PGI2 into the left atrium, a significant decline in CO, FAP, and PAP occured. Atropinization further depressed CO. The most marked effecr of PGI2, however, was an increase in PoVF without a change in PoVP. This effect was more pronounced when atropine was administered. In anethetized swine, PGI2 is a potent vasodilator in all vascular beds, including the portal venous system. These hemodynamic changes should be realized when exogenous PGI2 is considered as a therapeutic agent or when endogenous PGI2 might increase in association with disease states like pancreatitis or sepsis. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|