Tobacco Induced Diseases moves to BioMed Central.

This Editorial marks the transfer of Tobacco Induced Diseases to BioMed Central's publishing platform.

A comparison of biologically variable ventilation to recruitment manoeuvres in a porcine model of acute lung injury.

BACKGROUND: Biologically variable ventilation (return of physiological variability in rate and tidal volume using a computer-controller) was compared to control mode ventilation with and without a recruitment manoeuvre - 40 cm H2O for 40 sec performed hourly; in a porcine oleic acid acute lung injury model. METHODS: We compared gas exchange, respiratory mechanics, and measured bronchoalveolar fluid for inflammatory cytokines, cell counts and surfactant function. Lung injury was scored by light microscopy. Pigs received mechanical ventilation (FIO2 = 0.3; PEEP 5 cm H2O) in control mode until PaO2 decreased to 60 mm Hg with oleic acid infusion (PaO2/FIO2 <200 mm Hg). Additional PEEP to 10 cm H2O was added after injury. Animals were randomized to one of the 3 modes of ventilation and followed for 5 hr after injury. RESULTS: PaO2 and respiratory system compliance was significantly greater with biologically variable ventilation compared to the other 2 groups. Mean and mean peak airway pressures were also lower. There were no differences in cell counts in bronchoalveolar fluid by flow cytometry, or interleukin-8 and -10 levels between groups. Lung injury scoring revealed no difference between groups in the regions examined. No differences in surfactant function were seen between groups by capillary surfactometry. CONCLUSIONS: In this porcine model of acute lung injury, various indices to measure injury or inflammation did not differ between the 3 approaches to ventilation. However, when using a low tidal volume strategy with moderate levels of PEEP, sustained improvements in arterial oxygen tension and respiratory system compliance were only seen with BVV when compared to CMV or CMV with a recruitment manoeuvre.

The pulmonary surfactant: impact of tobacco smoke and related compounds on surfactant and lung development.

Cigarette smoking, one of the most pervasive habits in society, presents many well established health risks. While lung cancer is probably the most common and well documented disease associated with tobacco exposure, it is becoming clear from recent research that many other diseases are causally related to smoking. Whether from direct smoking or inhaling environmental tobacco smoke (ETS), termed secondhand smoke, the cells of the respiratory tissues and the lining pulmonary surfactant are the first body tissues to be directly exposed to the many thousands of toxic chemicals in tobacco. Considering the vast surface area of the lung and the extreme attenuation of the blood-air barrier, it is not surprising that this organ is the primary route for exposure, not just to smoke but to most environmental contaminants. Recent research has shown that the pulmonary surfactant, a complex mixture of phospholipids and proteins, is the first site of defense against particulates or gas components of smoke. However, it is not clear what effect smoke has on the surfactant. Most studies have demonstrated that smoking reduces bronchoalveolar lavage phospholipid levels. Some components of smoke also appear to have a direct detergent-like effect on the surfactant while others appear to alter cycling or secretion. Ultimately these effects are reflected in changes in the dynamics of the surfactant system and, clinically in changes in lung mechanics. Similarly, exposure of the developing fetal lung through maternal smoking results in postnatal alterations in lung mechanics and higher incidents of wheezing and coughing. Direct exposure of developing lung to nicotine induces changes suggestive of fetal stress. Furthermore, identification of nicotinic receptors in fetal lung airways and corresponding increases in airway connective tissue support a possible involvement of nicotine in postnatal asthma development. Finally, at the level of the alveoli of the lung, colocalization of nicotinic receptors and surfactant-specific protein in alveolar cells is suggestive of a role in surfactant metabolism. Further research is needed to determine the mechanistic effects of smoke and its components on surfactant function and, importantly, the effects of smoke components on the developing pulmonary system.

Identification of leptin receptors in lung and isolated fetal type II cells.

Leptin is a cytokine involved in regulation of the satiety response. Receptors for this protein have been identified in brain as well as many other peripheral tissues. Some of the highest levels of receptor concentration occur in the lung. Considering the cellular diversity of lung, neither the localization nor the function of leptin in pulmonary tissues has been delineated. The purpose of the present study was to determine if fetal and adult rabbit lung displayed specific binding for leptin, to identify the binding sites, and to explore a potential functional role for leptin in lung surfactant production. Frozen sections of adult and fetal rabbit (24th gestational day) lung were prepared and incubated with increasing concentrations of [125I]leptin in the presence or absence of 1-microM-unlabeled leptin. Sections were removed and radioactivity measured. Concurrently, sections were coated with nuclear Trac emulsion and incubated in the dark at -30 degrees C. Lung showed specific binding for leptin. Microscopically, [125I]leptin was localized to acinar-lining epithelium of developing fetal lung. Larger cells within the epithelial layer appeared to bind leptin more avidly than adjacent cells. Antibodies to the leptin receptor were used to identify binding sites in adult lung and isolated fetal lung type II cells. In adult lung, both the K20 (against the extracellular amino-terminal) and the M18 antibody (against the intracellular carboxy-terminal) displayed several binding sites. In contrast, the isolated fetal type II cells showed only a single binding site for both antibodies. The apparent molecular mass of the receptor using the K20 antibody appeared to be approximately 125 kD. A protein of similar mass bound the M18 antibody suggesting that functional receptor is present in lung and expressed by fetal type II cells. Incubation of isolated fetal type II cells with leptin (0.01-10 microg/ml) stimulated [3H]choline incorporation in disaturated phosphatidylcholine. These results show that fetal and adult lung bind leptin specifically, and fetal type II cells in particular, may be responsive to leptin stimulation of phospholipid production. Leptin may therefore be important in regulating maturation of cells of the fetal lung.