The Effects of Prostaglandin I2, Prostaglandin E1, and Nitroglycerin on Hemodynamics and Blood Gas Exchanges in Pulmonary Hypertension in Dogs.
10.4097/kjae.1998.35.4.633
- Author:
Hyun Hwa LEE
1
;
Mi Kyung YANG
;
Ok Hwan LIM
;
Sang Min LEE
;
Kwang Il SHIN
Author Information
1. Department of Anesthesiology, College of Medicine, Sung Kyun Kwan University.
- Publication Type:Original Article
- Keywords:
Blood Pressure:drug effect, pulmonary hypertension;
Lung:oxygenation;
Hormones: prostaglandin I2;
prostaglandin E1;
Pharmacology: nitroglycerin
- MeSH:
15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid;
Alprostadil*;
Animals;
Arterial Pressure;
Cardiac Output;
Dogs*;
Epoprostenol*;
Heart Rate;
Hemodynamics*;
Hypertension, Pulmonary*;
Nitroglycerin*;
Oxygen;
Pulmonary Artery;
Vasodilator Agents;
Ventricular Function, Right
- From:Korean Journal of Anesthesiology
1998;35(4):633-641
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGREOUND: The ideal drug for treatment of pulmonary hypertension would be a vasodilator which acts preferentially on the pulmonary vascular bed. The aim of this study was to compare the effects of prostaglandin I2 (PGI2) on central hemodynamics and right ventricular function with the more widely used vasodilators, prostaglandin E1 (PGE1) and nitroglycerin (NTG) and to investigate whether PGI2 is more selective to the pulmonary vascular bed compared with PGE1 and NTG in dogs. METHODS: We have used a method for producing sustained pulmonary hypertension in vivo by continuous infusion of U46619 adjusting the infusion rate until a mean pulmonary artery pressure (PAP) exceeded 25 mmHg. And the pulmonary and systemic effects of the three pulmonary vasodilators were compared at doses producing equivalent, lowered approximately 20% of mean arterial pressures (MAP) or mean PAP returned to baseline. RESULTS: After infusion of the three vasodilators, heart rate, cardiac output, and mean PAP/MAP ratio were significantly increased, but there was no statistical significant differences among the three vasodilators. PGI2 and PGE1 significantly increased (worsened) the PVR/SVR ratio, but NTG decreased. However there was no significant difference among the three vasodilators. After infusion of the three vasodilators, the arterial oxygen tension (PaO2), mixed venous oxygen tension (PO2), O2 deliver, and O2 uptake were increased, and shunt ratio (s/t(%)) were significantly decreased, but there were no significant differences among three vasodilators. CONCLUSIONS: PGI2, PGE1, and NTG all decreased both PVR and SVR. None of these vasodilatorswere more selective to the pulmonary vascular bed, myocardial performance, and improved gas exchange.
