Obesity is known to be a major risk factor of a whole range of cardiovascular, metabolic and respiratory disorders. It has been recognised that the pattern of regional fat distribution plays an important role in the pre-disposition of obese subjects to certain obesity-related complications. Derangement of parameters of lung function is determined to a large extent by the quantity and distribution of excess body fat with its potential to interfere with the mechanics of pulmonary physiology. Clinical, laboratory and epidemiological observations have established links between obesity and several breathing problems including obstructive sleep apnoea, obesity hypoventilation syndrome and asthma. However, in many respects, the pathophysiology of these links is not fully explored. In this article, the impact of obesity on pulmonary physiology and its association with the above-mentioned clinical conditions is discussed.
Bochdalek hernias occur as a result of a congenital defect in the diaphragm enabling abdominal viscera to enter the thoracic cavity restricting lung expansion and ventilation. Bochdalek hernias, in the majority of cases, present in neonates and very rarely in adults. To the best of our knowledge, there are only four published cases of Bochdalek hernia in the adult population causing respiratory failure. We present the case of an 87-year-old woman who had three admissions in the past 6 months with type II respiratory failure due to a Bochdalek hernia which we believe was congenital but had gradually increased in size over the years to cause progressive decompensation with acute exacerbations requiring non-invasive ventilation.
An approximately steady-state reduction of specific airway conductance was induced in healthy human subjects by means of an individualized inhaled methacholine loading dose followed by a maintenance dose regime. Tested against this background bronchoconstriction, the xanthine analogue SDZ MKS 492, when administered as a single oral dose of 40 mg, showed a significant bronchodilator action, which lasted for up to 5.5 h. Bronchodilatation was not seen after administration of 10 or 20 mg doses. SDZ MKS 492 inhaled as a dry powder had a bronchodilator action that was small, most evident with the 12 mg dose and transient. The peak relief of imposed bronchoconstriction was 29% and the apparent half-time of removal of SDZ MKS 492 from its site of action was 5-6 min. Inhaled SDZ 492 had a bitter taste that was not masked by inclusion of menthol and aspartame in the formulation. The bronchodilatation seen in laboratory animals can also be produced by SDZ MKS 492 in man when administered orally or by inhalation. Its magnitude correlates better with the plasma concentration of parent drug than with that of either of the identified metabolites. Dispositional processes in the lung abbreviate its action after administration by inhalation.
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