Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0242706 (hyperoxia)
 5,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We compared the effects of treatment with methylprednisolone or the 21-aminosteroids, U-74389 and U-74006F (Tirilizad mesylate), on hyperoxic lung injury and the associated expression of mRNA for several adhesion molecules in rats. Inhalation of > 95% oxygen for up to 72 hr in Sprague-Dawley rats produced a marked increase in lung weight and an accumulation of fluid in the thorax when compared with air-breathing controls. Hyperoxia also induced a marked neutrophil-rich influx of inflammatory cells into the bronchial lumen as measured by bronchoalveolar lavage. Neutrophil numbers in bronchoalveolar lavage fluid peaked after 60 hr of exposure to s 95% oxygen; this was associated with a marked upregulation of mRNA for the adhesion molecules P-selectin and E-selectin but not VCAM-1. mRNA for ICAM-1 was constitutively expressed at high levels in both air-breathing controls and in the lungs of rats exposed to high concentrations of oxygen. Pretreatment with the 21-aminosteroids reduced hyperoxic lung damage and improved survival times in animals exposed to > 95% oxygen. However, treatment with methylprednisolone significantly decreased survival times. Treatment with U-74389 did not significantly (p > 0.05) inhibit the BAL neutrophilia and did not significantly (p > 0.05) reduce hyperoxia-induced increases in mRNA expression for P-selectin and E-selectin. The inhibition of hyperoxic lung damage coupled with improved survival seen in treated animals suggests that 21-aminosteroids may provide valuable treatments for pulmonary disorders in which oxidant damage has been implicated.
 ...
PMID:Attenuation of oxidant-induced lung injury by 21-aminosteroids (lazaroids): correlation with the mRNA expression for E-selectin, P-selectin, ICAM-1, and VCAM-1. 753 86

Recent studies have presented evidence that the processes of hypoxaemia and reperfusion are involved in several pathogenetic mechanisms of atherosclerotic lesions. The ability of hypoxaemia to activate circulating white blood cells (WBCs) and enhance WBC-endothelial cell (EC) interactions is suspected to be a major factor in deleterious processes in the blood vessel wall. Various groups have suggested that cell adhesion molecules (CAMs), such as ICAM-1, VCAM-1 and E-selectin and their leukocyte ligands are involved in intercellular activities of the relevant cell types. We studied the effects of different oxygen tensions, simulating normoxic conditions, hypoxia and hyperoxia in vitro with the help of an umbilical vein EC model in order to determine the effects of oxygenation on CAM presentation on vascular ECs with and without further cytokine and endotoxin (lipopolysaccharides; LPS) stimulation. Semiquantitative analysis of ICAM-1, E-selectin and VCAM-1 was performed using cell enzyme immunoassay techniques. The presentation of ICAM-1, E-selectin and VCAM-1 remained on the whole unaffected by both hypoxia and hyperoxic conditioning after both 7 and 24 h. Stimulation of ICAM-1 by cytokines and LPS was only marginally influenced by the oxygen tension. Cytokine induction of E-selectin was not affected after 7 h and was even reduced under hypoxia, compared to the control culture after 24 h, while stimulation was increased by hyperoxia. VCAM-1 was reduced in both the hypoxic and hyperoxic culture, while being maximally stimulated by cytokines and LPS after 7 h. In general, an effect of hypoxia was not found without any further stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Comparative studies on vascular endothelium in vitro. 2. Hypoxia: its influences on endothelial cell proliferation and expression of cell adhesion molecules. 754 71

To investigate the pathogenesis of pulmonary oxygen toxicity, we examined the effect of hyperoxia on adhesion molecule expression in cultured human pulmonary artery endothelial cells (HPAEC) and human umbilical vein endothelial cells (HUVEC). Endothelial cell monolayers were exposed to either hyperoxic (90% O(2)-5% CO(2)) or normoxic (21% O(2)-5% CO(2)) conditions for various periods. The level of intercellular adhesion molecule (ICAM)-1 expression had increased in hyperoxia-exposed HPAEC and HUVEC at 48 h (194 +/- 38 and 233 +/- 56%, respectively; P < 0.001) and at 72 h (200 +/- 43 and 223 +/- 52%, respectively; P < 0.001) compared with normoxic conditions. These hyperoxia-induced ICAM-1 expressions were dose dependently attenuated by a protein kinase C inhibitor (H-7). In contrast, the levels of P-selectin and E-selectin expression in HPAEC and HUVEC were unchanged. The levels of ICAM-1 mRNA and the numbers of adherent neutrophils were increased in HPAEC and HUVEC at 48 and 72 h of hyperoxia. On the other hand, hyperoxia caused neutrophil H(2)O(2) production without affecting the level of CD11/CD18 expression. These results suggest that increased ICAM-1 expression in endothelial cells plays an important role in neutrophil accumulation during hyperoxia.
 ...
PMID:Effect of hyperoxia on adhesion molecule expression in human endothelial cells and neutrophils. 912 98

Recent evidence suggests that neutrophil recruitment may initiate cell apoptosis in ischemic tissues. We have recently shown that enterocyte apoptosis is increased following intestinal ischemia-reperfusion (IR) injury. The purpose of the present study was to examine the effect of hyperoxia on E-selectin expression, neutrophil recruitment and enterocyte apoptosis following intestinal IR in a rat. Male Sprague-Dawley rats were divided into three experimental groups: (1) sham rats underwent laparotomy without vascular occlusion and were ventilated with air (Sham) (2) IR rats underwent occlusion of both the superior mesenteric artery and portal vein for 30 min and were ventilated with air (IR), and (3) IR-O2 rats underwent IR and were ventilated with 100% started 10 min before reperfusion and continued for 6 h (IR-O2). Intestinal structural changes were determined 24 h following IR. Immunohistochemistry for E-selectin (using E-selectin cleaved concentrated polyclonal antibody) was performed to identify E-selectin immunoreactivity localized to the endothelium of venules. The recruitment of neutrophils was calculated per 100 venules. Immunohistochemistry for Caspase-3 was performed for identification of apoptotic cells. Non-parametric one-way ANOVA test was used for statistical analysis with p less than 0.05 considered statistically significant. A significant increase in E-selectin expression in the jejunum (6.1 +/- 2.2 vs. 2.5 +/- 1.0 E-selectin positive vessels/100 vessels, p < 0.05) and ileum (12.1 +/- 2.7 vs. 3.3 +/- 1.2 E-selectin positive vessels/100 vessels, p < 0.05) and a concomitant increase in neutrophil recruitment in the ileum (5.5 +/- 1.6 vs. 1.3 +/- 0.6 adhered PMN's per 100 venules) were observed in IR rats compared to sham animals and were accompanied by increased cell apoptosis (p < 0.05). Treatment with 100% oxygen resulted in a significant attenuation in E-selectin expression in the ileum (2.7 +/- 1.1 vs. 12.1 +/- 2.7 E-selectin positive vessels/100 vessels, p < 0.05), and neutrophil recruitment in the jejunum (2.5 +/- 1.4 vs. 7.7 +/- 1.9 adhered PMN's per 100 venules, p < 0.05) and ileum (1.5 +/- 0.7 vs. 5.5 +/- 1.6 adhered PMN's per 100 venules, p < 0.05) compared to IR animals, and was accompanied by decreased cell apoptosis (p < 0.05). Hyperoxia inhibits enterocyte apoptosis following intestinal ischemia-reperfusion. Down-regulation of E-selectin expression with subsequent decrease in neutrophil recruitment may be responsible for this effect.
 ...
PMID:Effect of 100% oxygen on E-selectin expression, recruitment of neutrophils and enterocyte apoptosis following intestinal ischemia-reperfusion in a rat. 1796 62