6,963 publications from this institution
Background Coronary microvascular dysfunction (CMD) is a common complication of ST‐segment–elevation myocardial infarction (STEMI) and can lead to adverse cardiovascular events. Whether CMD after STEMI is associated with functional left ventricular remodeling (FLVR) and diastolic dysfunction, has not been investigated. Methods and Results This is a nonrandomized, observational, prospective study of patients with STEMI with multivessel disease. Coronary flow reserve and index of microcirculatory resistance of the culprit vessel were measured at 3 months post‐STEMI. CMD was defined as index of microcirculatory resistance ≥25 or coronary flow reserve <2.0 with a normal fractional flow reserve. We examined the association between CMD, LV diastolic dysfunction, FLVR, and major adverse cardiac events at 12‐month follow‐up. A total of 210 patients were enrolled; 59.5% were men, with a median age of 65 (interquartile range, 58–76) years. At 3‐month follow‐up, 57 patients (27.14%) exhibited CMD. After 12 months, when compared with patients without CMD, patients with CMD had poorer LV systolic function recovery (−10.00% versus 8.00%; P <0.001), higher prevalence of grade 2 LV diastolic dysfunction (73.08% versus 1.32%; P <0.001), higher prevalence of group 3 or 4 FLVR (11.32% versus 7.28% and 22.64% versus 1.99%, respectively; P <0.001), and higher incidence of major adverse cardiac events (50.9% versus 9.8%; P <0.001). Index of microcirculatory resistance was independently associated with LV diastolic dysfunction and adverse FLVR. Conclusions CMD is present in ≈1 of 4 patients with STEMI during follow‐up. Patients with CMD have a higher prevalence of LV diastolic dysfunction, adverse FLVR, and major adverse cardiac events at 12 months compared with those without CMD. Registration URL: https://www.clinicaltrials.gov ; Unique Identifier: NCT05406297.
Part 1 Innervation of the Airways: Neuropeptides and Classic Innervation - Neural Structures in Human Airways Functional Autonomic Innervation of the Airways - The Cholinergic and Adrenergic Systems Neuropeptides in the Lower Airways Investigated by Modem Microscopy Neural Control of the Upper Respiratory Tract Peptide Biosynthesis and Secretion - Some Recent Developments and Unresolved Issues Vasoactive Intestinal Polypeptide in the Respiratory Tract Neuropeptide Y in the Airways Sensory Nerves and Tachykinins Pulmonary Endocrine Cells In Vivo and In Vitro Molecular Characterization of Autonomic and Neuropeptide Receptors Autonomic Receptors in the Upper and Lower Airways Tachykinin Receptor Antagonists Pulmonary Peptidases - General Principles of Peptide Metabolism and Molecular Biology of Angiotensin Converting Enzyme, Neutral Endopeptidase 24.11, and Carboxypeptidase M Peptidases in the Respiratory Tract - The Localization and Actions of Carboxypeptidase M. Part 2 Physiological Functions of Neuropeptides in the Airways: The Concept of Neurogenic Inflammation in the Respiratory Tract Modulation of Neurogenic Inflammation by Peptidase Control of Airway Vascular Beds Basophil and Mast Cell Activation - Neuropeptides and Nerves Inositol Triphosphate and Smooth Muscle Function Neuropeptides and Airway Macromolecule Secretion ATP as Neurally Released Modulator of Human Airway Ion Transport Effects of Neuropeptides on Neurotransmission in the Airways. Part 3 Pathophysiological Contribution of Neuropeptides to Disease: Neuropeptides and Asthma Inflammatory Mechanisms in Cystic Fibrosis Lung Disease Allergic Rhinitis Neuropeptides in Small Cell Lung Carcinoma Neuroregulation of Pulmonary Immunity - The Roles of Substance P and Vasoactive Intestinal Peptide Sensory Neuropeptides in an Animal Model of Hyperpnoea-induced Bronchoconstriction Nitric Oxide and Guanylyl Cyclases - Correlation with Neuropeptides Neuropeptides in Bronchoalveolar Lavage in Allergic Asthma Morphology of Neurogenic lnflammation in the Airways - Plasma Protein Movement Across the Airway Mucosa and Epithelium.
COPD is a major and increasing global health problem, which is currently the 4th commonest cause of death and predicted to become the the 5th commonest cause of disability in the world by 2020. While there have been major advances in the understanding and management of asthma, COPD has been relatively neglected and there are no current therapies that reduce the inevitable progression of this disease. However, because of the enormous burden of disease and escalating health care costs, there is now renewed interest in the underlying cellular and molecular mechanisms [1] and a search for new therapies [2], resulting in a re-evaluation of this disease [3].
Endothelins (ETs) are expressed in several types of cell in human lung, including airway epithelial cells, pulmonary vascular endothelial cells, submucosal glands, and type II pneumocytes. There is evidence for increased expression of ET-1 in several pulmonary diseases, including asthma, fibrosing alveolitis, and pulmonary hypertension, suggesting that ET-1 may play a pathophysiological role. ET binding sites are widely distributed and are localized to airway and pulmonary vascular smooth muscle, fibroblasts, submucosal glands, and airway nerves, indicating that ETs may have widespread effects. ET-1 and ET-3 are potent constrictors of human airway smooth muscle via a direct effect on ET receptors in airway smooth muscle; these receptors are probably ETB receptors. ETs may have other effects on airway function, including constriction of bronchial vessels, increased plasma exudation, increased mucus secretion, airway smooth muscle hyperplasia, and possibly increased fibrogenesis; these effects may be mediated via ETA receptors. ET-1 is a potent constrictor of human pulmonary vessels, whereas ET-3 is less effective, suggesting a predominance of ETA receptors. Similarly, chemotaxis and mitogenesis of pulmonary vascular fibroblasts and smooth muscle are mediated via ETA receptors. These findings implicate ETs in various pulmonary diseases and suggest that ET antagonists may be useful in their treatment.
sinusitis; unidentified allergens (for example, occupational); dietary factors (for example, metabisulphite); drugs (for example, ji blockers
"Beta-adrenergic receptors and their regulation.." American journal of respiratory and critical care medicine, 152(3), pp. 838–860
We have characterized the effects of adenosine, the A1-receptor agonist N6-(L-2-phenylisopropyl)-adenosine (PIA) and the A2-receptor agonist 5'-(N-ethyl)-carboxamido-adenosine (NECA), in isolated human pulmonary vessels. Fresh human lung tissue was obtained from nine patients, and small pulmonary arteries (200-400 micron ID) were dissected and mounted in an organ bath. The effects of the adenosine antagonist 8-phenyltheophylline (8-PT) and endothelial denudation were also studied. Adenosine, NECA, and PIA (1-300 microM) all caused a dose-dependent vasodilation with log EC30 values of -4.31, -4.31, and -3.53, respectively. 8-PT (10 microM) caused a rightward shift of the adenosine dose-response curve, significantly decreasing the effect of adenosine (pKB = 6.3). Mechanical removal of endothelial cells had no significant effect on adenosine-mediated vasodilation. We also compared the effects of adenosine on eight large (7-10 mm ID) and eight small (200-400 micron ID) arteries and found no significant difference in the sensitivity to adenosine between these vessels. Our findings suggest that the pulmonary vasodilator effects of adenosine in humans are mediated through A2 receptors that are localized to vascular smooth muscle. Adenosine may function as a regulator of pulmonary vascular tone in humans and may have therapeutic potential.
Conference Abstract| January 01 1985 The Functional Association of Cholinergic and Non-Adrenergic Inhibitory Responses in Bovine Airway Smooth Muscle J. Palmer; J. Palmer 1Department of Medicine, Royal Postgraduate Medical School, Hammersmith Hospital, London W12 OHS Search for other works by this author on: This Site PubMed Google Scholar A. Sampson; A. Sampson 1Department of Medicine, Royal Postgraduate Medical School, Hammersmith Hospital, London W12 OHS Search for other works by this author on: This Site PubMed Google Scholar P. Barnes P. Barnes 1Department of Medicine, Royal Postgraduate Medical School, Hammersmith Hospital, London W12 OHS Search for other works by this author on: This Site PubMed Google Scholar Clin Sci (Lond) (1985) 68 (s11): 5P. https://doi.org/10.1042/cs068005Pa Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn MailTo Cite Icon Cite Get Permissions Citation J. Palmer, A. Sampson, P. Barnes; The Functional Association of Cholinergic and Non-Adrenergic Inhibitory Responses in Bovine Airway Smooth Muscle. Clin Sci (Lond) 1 January 1985; 68 (s11): 5P. doi: https://doi.org/10.1042/cs068005Pa Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsClinical Science Search Advanced Search This content is only available as a PDF. © 1985 The Biochemical Society and the Medical Research Society1985 Article PDF first page preview Close Modal You do not currently have access to this content.
Paper presented at the international conference of Thermodynamic Speciation Modelling, University of Salford, UK, 2003.
