No abstract

Bronchodilators are used widely in the acute exacerbations of chronic obstructive pulmonary disease (COPD), although their effectiveness is not clearly established. We used three bronchodilators in 20 patients with COPD who were being mechanically ventilated. Two of the bronchodilators, ipratropium bromide and salbutamol, were administered from metered-dose inhalers (MDI) through an adapter to the endotracheal tube, and the third, aminophylline, was administered in the form of intravenous infusion. Before administering each drug, peak airway pressure, end-inspiratory pressure, resistive pressure, and auto positive end-expiratory pressure (auto-PEEP) were measured, and inspiratory resistance (Rins) and compliance were calculated. Heart rate (HR) and blood pressure were also recorded, and arterial pH and blood gas determinations were made. These measurements were repeated 60 min after the administration of aminophylline, 15 and 60 min after administering salbutamol, and 30 and 60 min after administering ipratropium bromide. With these three drugs, airway pressures were reduced, as well as auto-PEEP and Rins, with respect to basal values (p less than 0.05). The changes in compliance were only significant with salbutamol (p less than 0.05). HR was only significantly modified with aminophylline (p less than 0.05). No blood gas change was observed with any of the three drugs. It can be concluded that: (1) the three drugs used in this study were equally effective in producing significant bronchodilation in patients on mechanical ventilation for severe acute exacerbation of COPD; (2) the administration of bronchodilators by MDI in intubated patients through a special adapter was as effective as the intravenous administration of aminophylline.

The combination of both drugs is more effective than ipratropium bromide alone at the doses used in this study.

Increased adiposity, through adipocyte hypertrophy, and/or hyperplasia, characterizes aging and obesity. Both are leptin-resistant states, associated with disturbed lipid metabolism, reduced insulin sensitivity and inflammation. Nevertheless, fat tissue dysfunction appears earlier in obesity than in normal aging. In contrast, lipodystrophy is accompanied by diabetes, and improving the fat cell capacity to expand rescues the diabetic phenotype. Fat tissue dysfunction is extensively studied in the diet-induced obesity, but remains relatively neglected in the aging-associated obesity. In the Wistar rat, as occurs in humans, early or middle aging is accompanied by an increase in adiposity. Using this experimental model, we describe the molecular mechanisms contributing to the white adipose tissue (WAT) hypertrophy. WAT from middle-old age rats is characterized by decreased basal lipogenesis and lipolysis, increased esterification, as demonstrated by the higher TAG and cholesterol content in visceral WAT, and the maintenance of total ceramide levels within normal values. In addition, we describe alterations in the adipose tissue plasma membrane lipid composition, as increased total ether-phosphatidylcholine, sphingomyelin, and free cholesterol levels that favor an enlarged fat cell size with aging. All these metabolic changes may be regarded as a survival advantage that prevents the aged rats from becoming overtly diabetic.

Our findings indicate that a BMCSs loaded bone matrix scaffold is capable of stimulating bone regeneration more effectively than isolated core decompression or in association with an acellular scaffold in a preclinical femoral head osteonecrosis model in sheep.