In addition to classical cholinergic and adrenergic neural mechanisms, a third division of autonomic control has been recognised in human airways. Non-adrenergic inhibitory nerves are the dominant inhibitory neural pathway in human airway smooth muscle and there is increasing evidence that VIP and a related peptide, PHM, may be the neurotransmitters. These peptides are probably cotransmitters of acetylcholine in the airways and may modulate cholinergic effects. A defect in this system could occur in asthma because inflammation may more rapidly inactivate these neurotransmitter peptides. Non-cholinergic excitatory nerves have also been described in animal airways, although their existence in human airways is less certain. The neurotransmitter may be substance P or a related peptide neurokinin A, which could be released by axon reflex. Another peptide, calcitonin gene-related peptide, is colocalized with substance P and appears to be much more potent in human airways. Non-adrenergic non-cholinergic mechanisms may also regulate mucus secretion and the bronchial microvasculature. The role of this nervous system in health and disease is still uncertain as there are no specific blockers available.
Two types of geometric imperfection typically need to be considered in the analysis and design of structural systems: global frame out-of-plumbness, also referred to as sway imperfections, and member out-of-straightness, also known as bow imperfections; the effect of local cross-section imperfections is generally accounted for through cross-section resistance checks. For modelling convenience, equivalent geometric imperfections are often employed to allow for the combined influence of initial geometric imperfections and residual stresses. For design by geometrically and materially nonlinear analysis with imperfections (GMNIA), amplitudes for equivalent bow imperfections for members are provided in EN 1993–1-14; however, no provisions exist for global sway imperfections. Therefore, equivalent sway imperfections suitable for use in the design of steel structures by GMNIA ϕ0,GMNIA are established herein. Two proposals for calculating ϕ0,GMNIA are presented: (1) ϕ0,GMNIA=ϕ0,geom+α/100, with ϕ0,geom representing the pure geometric sway imperfection, and (2) ϕ0,GMNIA=α/50. In both proposals, the varying degree and influence of residual stresses for different cross-section geometries and axes of buckling is captured by the imperfection factor α, as defined in EN 1993–1-1 for carbon steel and EN 1993–1-4 for stainless steel, respectively. A flow chart that provides guidance on the appropriate selection of frame and member imperfections to avoid duplication of the effects of residual stresses in design by GMNIA is also presented.
* Preface * Introduction * General * Basis of design * Materials * Durability * Structural analysis * Ultimate limit states * Serviceability limit states * Annex A - Method 1: interaction factors ky for interaction formula in clause 6.3.3(4) * Annex B - Method 2: interaction factors ky for interaction formula in clause 6.3.3(4) * Annex AB - additional design provisions * Annex BB - buckling of components of buildings structures * Design of joints * Cold-formed design * Actions and combinations of actions
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An intravenous infusion of platelet activating factor (Paf) in the guinea‐pig elicits an increase in bronchial responsiveness to the spasmogens, histamine and bombesin. Airways obstruction induced by bombesin in Paf‐treated animals is poorly reversed by isoprenaline compared to comparable airways obstruction induced by bombesin in vehicle‐treated animals. Isoprenaline induced a comparable dose‐related relaxation in vitro of tracheal smooth muscle isolated from Paf‐ and vehicle‐treated animals. No change in β‐adrenoceptor numbers or binding affinity was observed in lungs removed from Paf‐treated animals in comparison with those from vehicle‐treated animals, or after direct incubation with Paf in vitro. The reduced bronchodilator responsiveness to isoprenaline in Paf‐treated animals is not related to changes in pulmonary β‐adrenoceptor function. These results suggest that non‐spasmogenic elements may contribute to airways obstruction induced in hyper‐responsive animals.
There may be an overlap between the clinical pictures of asthma and chronic obstructive pulmonary disease which hampers a clear distinction between the two diseases. Most symptoms presented by patients do not clearly belong exclusively to either asthma or chronic obstructive pulmonary disease. By the nature of their discipline and training, general practitioners focus mainly on symptoms presented, which do not give a decisive answer in the differential diagnosis between the two diseases. Therefore, general practitioners must rely on objective parameters, such as determining the presence and degree of reversibility of airway obstruction, diurnal peak flow variability, bronchial hyper-responsiveness and allergy. This paper puts forward a pragmatic, primary care definition of asthma and chronic obstructive pulmonary disease.
Journal Article Airway receptors Get access P J Barnes P J Barnes Department of Thoracic Medicine, National Heart and Lung Institute, Dovehouse Street, London SW3 6LY, UK Correspondence: Professor P.J. Barnes, M.A., D.Sc., D.M., F.R.C.P. Search for other works by this author on: Oxford Academic Google Scholar Postgraduate Medical Journal, Volume 65, Issue 766, August 1989, Pages 532–542, https://doi.org/10.1136/pgmj.65.766.532 Published: 01 August 1989 Article history Received: 27 December 1988 Published: 01 August 1989