The Effects of Prostaglandin E1 and Hydralazine on Hemodynamics and Gas Exchange in Oleic acid induced Acute lung Injury.
10.4097/kjae.1988.21.3.462
- Author:
Pyung Hwan PARK
1
;
Yong Lack KIM
Author Information
1. Department of Anesthesiology, Korea University Medical School, Seoul, Korea.
- Publication Type:Comparative Study ; Original Article
- Keywords:
Oleic acid;
Lung injury;
Hemodynamics;
Gas exchange;
Prostaglandin E1;
hydralazine
- MeSH:
Acute Lung Injury*;
Alprostadil*;
Animals;
Capillaries;
Dogs;
Heart;
Heart Failure;
Hemodynamics*;
Humans;
Hydralazine*;
Lung Injury;
Oleic Acid*;
Oxygen;
Respiratory Distress Syndrome, Adult
- From:Korean Journal of Anesthesiology
1988;21(3):462-478
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Prostaglandin E1(PGE1) is a potent vasodillator of the systemic and coronary circulatory system, and when used in adult respiratory distress syndrome, PGE1 produces a decrease in pulmonary arterial pressure(PAP) and pulmonary vascular resistance(PVR), and increases cardiac output(CO) and arterial oxygen tension(PaO2). Another vasodilator hydralazine in patients with pulmonary hyertension and heart failure produces a decrease in PVR, and an increase in CO and inspite of an increase in CO, hydralazine maintains or increases the PaO2. The authors made a comparative studies on the effects of PGE1 and hydralarine on hemodynamics and gas exchange in experimentally induced acute lung injury. Oleic acid was infused in 8 dogs in order to induce acute lung injury and the effects on hemodynamics and gas exchange were measured every 30 minutes for 2hrs. After measuring Pre-PGE1 and Pre-hydralazine values, PGE1 and hydralazine were administered intravenously in order to evaluate and compare their effects. Doses for PGE1 and hydralazine were titrated until CO increased by 25%, heart rate(HR) increased by 15%, or mean arterial pressure(MAP) decreased by more than 20% from Pre-PGE1 and prehydralazine values. In PGE1 group, CO increased by 21%(p<0.01). MAP decreased by 14%(p<0.01). PVR decreased by 19%(p<0.01) and systemic vascular resistance(SVR) decreased by 29%(p<0.01). As CO increased with PGE1, intrapulmonary shunt(Qs/Qt) increased from 37% to 49%(p<0.01) and PaO2 fell from 109mmHg to 88mmHg(p<0.01). In hydralazine group, MAP, PVR, SVR and pulmonary capillary wedge pressure(PCWP) all decreased by 9%(p<0.01), 10%(p<0.05), 30%(p<0.0), 28%(p<0.01), respectively. CO increased by 41%(p<0.01) but the increase in Qs/Qt was only 5% inspite of a remarkable increase in CO, consequently PaO2 increased by 10% rising from 86mmHg to 94mmHg(p<0.01). Comparing the two groups, hydralazine resulted in a minor increase in Qs/Qt while there was a remarkable increase in CO. Moreover, it caused an increase in PaO2 and decrease in PCWP. The above results suggest that the effects of hydralazine are superior to those of PGE1 on the effects of hemodynamics and gas exchange in acute lung injury in dogs.
