Source: Annual Congress 2002 - Clinical aspects of antibiotic and nonantibiotic therapy of pneumonia in the ICU
Disease area: Pulmonary vascular diseases

Abstract

Bacterial endotoxin induced pulmonary edema and pulmonary hypertension are severe expressions of the septic shock, and the multiple organ disfunction syndrome (MODS) are the major cause of death. Our previous study found that therapeutic inhalation of nitric oxide (INO) selectively dilates pulmonary vessels, in addition attenuated pulmonary edema and decrease of BP by endotoxin expose. In present study, INO (30 ppm) was administered in an endotoxin-induced acute pulmonary edema piglet (20-15 kg, n=24) model. Gas exchange, hemodynamics and the lung expression of NFKB, ET-1 and its receptors, COX-2 and i-NOS were investigated. Its aim to investigate:1/ if INO has anti-inflammatory effect in septic lung injury; 2/ the interaction of INO with pre-inflammatory proteins.
In a group that received INO and endotoxin infusion (INO+E) for six hours, the pulmonary artery pressure and PaO2 were better preserved than in a group that received endotoxin only (E control). However INO did not decrease the potent vasoconstrictor ET-1 level but decreased its receptor A. In addition the lung edema and lung expression of active NFKB, COX-2, i-NOS by endotoxin expose was attenuated in INO+E group than the E control group. In addition, the endotoxin-induced the decrease of BP, plasma protein level and urine flow, and the increase of abdomen leakage were mark less pronounced in INO+E group than in E control group. We conclude that earlier administration INO attenuate acute pulmonary reaction to endotoxin expose, and INO also has protective effect in extra pulmonary organs to antagonize endotoxin caused MODS.

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Citations should be made in the following way:
L. Chen, J. Da, F. Freden, G. Hedenstierna (Uppsala, Sweden). The anti-inflammatory effect of inhaled nitric oxide in septic shock. Eur Respir J 2002; 20: Suppl. 38, 231

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