Effect of Inhaled Nitric Oxide on Pulmonary Function After Sepsis in a Swine Model.
Abstract
SEPSIS, A CONDITION that significantly affects the out come of severely injured patients, is characterized by a systemic inflammatory response that is mediated by various cytokines and activated leukocytes.' Pulmonary dysfunction as indexed by pulmonary arterial hyper- tension, decreasing compliance, and VA/Q mismatching leading to hypoxemia is a common sequeis of sepsis. The exact mechanism by which sepsis affects the pulmonary system is unknown. Activation of both leukocytes and endothelial cells in concert with the release of various compounds results in pulmonary vasoconstriction and increased vascular permeability leading to pulmonary failure, which often necessitates ventilatory support. 3 Inhaled nitric oxide (NO) has been reported to act as a selective pulmonary vasodilator without causing systemic vasodilation. This effect has been shown in various animal models of pulmonary arterial hypertension including those induced by thromboxane analogues, hypoxemia, and endotoxemia.The hypoxemia that accompanies endotoxemia has also been improved by NO.5 These beneficial effects of NO have been documented in patients with chronic obstructive pulmonary disease, adult respiratory distress syndrome (ARDS), congenital heart failure, and pulmonary arterial hypertension. JMD
Document Details
- Document Type
- Technical Report
- Publication Date
- Aug 01, 1994
- Accession Number
- ADA289625
Entities
People
- Avery A. Johnson
- Bryan S. Jordan
- Hiroshi Ogura
- Patrick J. Offner
- William G. Cioffi
Organizations
- United States Army Institute of Surgical Research