Elevated levels of the receptor for advanced glycation end products, a marker of alveolar epithelial type I cell injury, predict impaired alveolar fluid clearance in isolated perfused human lungs.
(49/1061)
Effect of inhalation of nebulized NO donor substance on acute hypoxic lung injury in newborn piglets.
(50/1061)
BACKGROUND: Birth asphyxia may result in multiple organ dysfunction such as lung injury. Inhalation of nebulized nitric oxide precursor can selectively reduce pulmonary hypertension. However, it is unknown whether such precursors can alleviate lung injury induced by hypoxia. We evaluated the effect of inhalation of nebulized nitroglycerine and sodium nitroprusside on acute hypoxic lung injury in newborn piglets. METHODS: Acute hypoxic lung injury was induced by inspiring 10% O2 for 1 hour. Twenty-four anaesthetized and mechanically ventilated piglets (5-7 days old) were randomly divided into four groups: (1) group S, not hypoxic; (2) group C, nebulized saline after hypoxia; (3) group NTG, nebulized nitroglycerine after hypoxia; (4) group SNP, nebulized sodium nitroprusside after hypoxia. Respiratory dynamic compliance and resistance of respiratory system were recorded at baseline, 0.5 hour and 1 hour of hypoxia; then 0.5 hour, 1 hour, 3 hours and 5 hours following hypoxia. After nebulization, arterial blood was collected for measuring methaemoglobin and nitrate/nitrite levels. Right lung tissue, wet-dry ratio and myeloperoxidase level were determined. White blood cell count (WBC), total surfactant phospholipids (TPL) and disaturated phosphatidyl choline (DSPC) of the bronchoalveolar lavage fluid (BALF) were calculated. Left lungs were used for examining pathological changes. RESULTS: No significant difference was observed in respiratory dynamic compliance, resistance of respiratory system, wet-dry ratio, levels of methaemoglobin and nitrate/nitrite after nebulization, TPL or DSPC/TPL among four groups. WBC in BALF in groups NTG and SNP significantly decreased as compared with group C: similarly for myeloperoxidase level in lung tissue. Lung histological findings showed infiltration of neutrophils in groups NTG and SNP decreased significantly as compared with group C. CONCLUSION: Inhalation of nebulized nitroglycerine or sodium nitroprusside can alleviate the infiltration of neutrophils, while it affects neither the metabolism of phospholipids nor water content in the lungs. (+info)
Post-transcriptional regulation of urokinase-type plasminogen activator receptor expression in lipopolysaccharide-induced acute lung injury.
(51/1061)
Pulmonary LPS exposure plays a key role in exacerbation of lung diseases such as chronic obstructive pulmonary disease and asthma. However, little is known about the effects of repeated LPS exposure in the lung microenvironment. We have developed a novel murine model of pulmonary LPS tolerance induced by intratracheal (i.t.) administration of LPS. First, we show that pulmonary LPS exposure does not induce whole-body refractoriness to systemic LPS, because i.t. administration followed by i.p. administration did not decrease plasma TNF-alpha. However, a local refractory state can be induced with two i.t. LPS exposures. Pulmonary LPS tolerance was induced by i.t. administration of 100 ng LPS at time 0 and 48 h. Nontolerant mice received PBS at time 0 and LPS at 48 h. Bronchoalveolar lavage levels of TNF-alpha were significantly attenuated in tolerant mice vs nontolerant mice (1597 pg/ml vs 7261 pg/ml). TNF-alpha mRNA was significantly reduced in bronchoalveolar lavage cells (5-fold) and lung tissue (10-fold). No reduction was seen in neutrophil numbers in the bronchoalveolar lavage fluid, myeloperoxidase activity, or expression of neutrophil chemoattractants CXCL1 and CXCL2, reflecting the specificity of the response. The reduction in TNF-alpha was accompanied by a significant increase in soluble receptors, TNF-SRI (159 pg/ml vs 206 pg/ml) and TNF-SRII (1366 pg/m vs 2695 pg/ml). In conclusion, pulmonary LPS tolerance results in a specific reduction in TNF-alpha expression, while the neutrophilic response is unaffected. This response may be a mechanism to limit tissue damage by reducing TNF-alpha levels, while still maintaining the antimicrobial capacity of the lung. (+info)
Inhibition of neuronal nitric oxide synthase in ovine model of acute lung injury.
(55/1061)