Biological consequences of oxygen desaturation and respiratory effort in an acute animal model of obstructive sleep apnea (OSA).

Background: An animal model mimicking all the factors involved in obstructive sleep apnea (OSA) is useful for investigating mechanisms because the associated comorbidity usually present in such patients is an important limitation.

Aim: To test the hypothesis that hypoxia/normoxia and respiratory effort have different effects on the induction of inflammatory response and endothelial dysfunction in an acute rat model of OSA.

Methods: Four groups of anesthetized rats were studied (n=8): (1) sham; (2) apnea: obstructions (15s each, 60/h, for 3h); (3) apnea+O(2): obstructions and breathing oxygen-enriched air to avoid hypoxia and (4) intermittent hypoxia/normoxia.

Intratracheal transplantation of alveolar type II cells reverses bleomycin-induced lung fibrosis.

Rationale: Transplantation of stem cells has been proposed as a strategy for repair of lung fibrosis. Nevertheless, many studies have yielded controversial results that currently limit the potential use of these cells as an efficient treatment. Alveolar type II cells are the progenitor cells of the pulmonary epithelium and usually proliferate after epithelial cell injury.

Influence of portal blood on the development of systemic inflammation associated with experimental acute pancreatitis.

Background: The liver is a source of systemic proinflammatory mediators in acute pancreatitis. We have investigated the effects of blood from the pancreas and intestine in liver activation and lung inflammation during early stages of experimental acute pancreatitis in a rat model.

Methods: A portosystemic shunt and a mesosystemic shunt were created to prevent the passage of blood coming from the pancreas and the intestine, respectively, to the liver.

Oxygen in the alveolar air space mediates lung inflammation in acute pancreatitis.

During the early stages of acute pancreatitis, acute respiratory distress syndrome often occurs. This is associated with the release of proinflammatory mediators into the blood, but it remains unclear why these mediators induce inflammation especially in the lung. One of the first events occurring during the progression of acute pancreatitis is the induction of P-selectin expression in the endothelial cells of the lung.

Mobilization of xanthine oxidase from the gastrointestinal tract in acute pancreatitis.

Background: Xanthine oxidoreductase has been proposed to play a role in the development of local and systemic effects of acute pancreatitis. Under physiologic conditions, the enzyme exists mainly as xanthine dehydrogenase (XDH) but can be converted by proteolytic cleavage to its superoxide-generating form xanthine oxidase (XOD). In addition to its intracellular location XDH/XOD is also associated to the polysaccharide chains of proteoglycans on the external endothelial cell membrane.