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The effects of vagal stimulation on pulmonary vascular permeability were studied in guinea pigs in vivo using 125I-labeled albumin as a marker of plasma extravasation. Bilateral vagus nerve stimulation (NS) significantly increased the plasma leakage index in both parenchyma and tracheobronchial tissues. The NS-induced plasma leakage in the parenchyma was unaffected by the alpha-adrenoceptor antagonist phentolamine, the muscarinic receptor antagonist atropine, the ganglionic blocker hexamethonium, or pretreatment with 6-hydroxydopamine or capsaicin, but it was significantly potentiated by the beta-adrenoceptor antagonist propranolol. NS-induced tracheobronchial vascular leakage was markedly inhibited by pretreatment with atropine, hexamethonium, or capsaicin, although it was unaffected by pretreatment with phentolamine, propranolol, or 6-hydroxydopamine. By itself, NG-nitro L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide (NO) synthase, had no effect on pulmonary vascular leakage, but it significantly enhanced the NS-induced plasma leakage to parenchyma in a dose-related and L-arginine-reversible manner. Elevation of blood pressure to a similar extent as that induced by L-NAME by a phenylephrine infusion had no significant effect on the increased plasma leakage induced by NS. These results suggest that vagal stimulation increases plasma extravasation in lung parenchyma through the release of unidentified transmitter(s) in a process that is modulated by endogenous NO and catecholamines (via activation of beta-adrenoceptors), and that different mechanisms are involved in the vagally induced plasma extravasation in the pulmonary and tracheobronchial vascular beds.
No abstract is provided for this article.
No abstract is provided for this article.
Long-acting bronchodilators are the most effective treatments currently available for managing patients with COPD.Long-acting muscarinic antagonists and β 2 -agonists are equally effective in producing bronchodilation, reducing symptoms, improving quality of life, and preventing exacerbations and are well tolerated.They probably work mainly by relaxing smooth muscle of peripheral airways to reduce gas trapping.Although both drug classes have non-bronchodilator effects that might be beneficial, this has not been clearly established in COPD patients.Remarkably, long-acting β 2 -agonists and long-acting muscarinic antagonists have additive bronchodilator effects, although this has not always translated into greater clinical benefit.Nevertheless, long-acting β 2 -agonist/long-acting muscarinic antagonist fixed-dose combinations are more effective than the single components and inhaled-corticosteroid/long-acting β 2 -agonist combinations.Although there is some rationale for triple therapy with long-acting β 2 -agonist/long-acting muscarinic antagonist/inhaled-corticosteroid, it remains to be shown that this would be more effective than long-acting β 2 -agonist/long-acting muscarinic antagonist combinations, although may be indicated for COPD patients with frequent exacerbations and with overlapping features with asthma, including increased blood eosinophils.It is unlikely that new classes of bronchodilators will be developed for COPD and what is needed is effective and safe antiinflammatory treatments.(BRN Rev.
An earlier prototype model for kink-banding in constrained layered structures, compressed in a layer-parallel direction, is summarized and extended. Important ingredients include layer-parallel stiffness, interlayer friction, overburden pressure and layer bending stiffness. The Maxwell stability criterion is proposed as a useful lower bound for failure loads and displacements. Predictions of angle of rotation, band orientation across the layers, kink band width, and initiation and propagation loads, are compared with simple preliminary small scale experiments on confined specimens comprising layers of paper.
