Effect of Inhaled Nitric Oxide on Hemodynamics, Gas Exchange and Pulmonary Inflammation in Newborn Piglets with Escherichia coli Induced Septic Lungs.
- Author:
Yun Sil CHANG
1
;
Sun Young KO
;
Won Soon PARK
Author Information
1. Department of Pediatrics, Samsung Medical Center, Sungkyunkwan University School of MedicineSeoul, Korea.
- Publication Type:Original Article
- Keywords:
Nitric oxide inhalation;
Septic lung;
Gas exchange;
Hemodynamics;
Piglet
- MeSH:
Animals;
Anoxia;
Escherichia coli*;
Escherichia*;
Hemodynamics*;
Humans;
Hypertension;
Hypertension, Pulmonary;
Infant, Newborn*;
Lung*;
Nitric Oxide*;
Oxygen;
Peroxidase;
Pneumonia*;
Positive-Pressure Respiration;
Sepsis;
Vascular Resistance
- From:Journal of the Korean Pediatric Society
2003;46(8):777-783
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: The aim of this study was to evaluate the effect of inhaled nitric oxide(iNO) on gas exchange, hemodynamics and pulmonary inflammation in newborn piglets with E. coli induced septic lung. METHODS: Twenty three instrumented and ventilated piglets were randomized into three groups: CON(n=6), PCON(n=9), and PNO(n=8). In the piglets of the PCON and PNO groups, E. coli septic lung was induced by endotracheal instillation of E. coli. Ten ppm iNO was given continuously in the PNO group after endotracheal instillation of E. coli. All animals were mechanically ventilated for six hour with a peak inspiratory pressure of 30 cmH2O, frequency of 25 breaths/min, FiO2 1.0 and a positive end-expiratory pressure of 4 cmH2O. All measurements were made at one hour intervals during the experiment. At the end of the experiment, lung tissue was harvested for the analysis of myeloperoxidase activity, indicative of lung inflammation. RESULTS: All piglets with pulmonary instillation of E. coli developed E. coli sepsis. Piglets in the PCON group developed progresseve pulmonry hypertension, hypoxemia and hypercarbia compared to the CON group due to increased pulmonary vascular resistance, intrapulmonary shunt fraction and physiologic dead space fraction. iNO did not reverse pulmonary hypertension in the PNO group. However iNO significantly improved oxygenation, which was attributed to marked improvement of venous admixture and partial attenuation of increase in dead space fraction. Increased myeloperoxidase activity in PCON compared to CON was significantly attenuated in PNO. CONCLUSION: iNO improves oxygenation and lung inflammation in newborn piglets with E. coli induced septic lung.
