Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0344329 (collapse)
 28,634 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of repetitive doses of beta-adrenoceptor stimulants on the resting tone and responsiveness of bronchopulmonary smooth muscle were studied in guinea pigs. Collapse time was used to assess bronchospasm in conscious animals while resistance and compliance measurements were used in the anesthetized guinea pigs. Repetitive administration of either isoproterenol or salbutamol, at effective bronchodilator doses, caused an exacerbation of the histamine-induced bronchospasm in the presence or absence of anesthesia. Repetitive administration of either prostaglandin E1, 20 micrograms/kg i.m., or aminophylline, 400 micrograms/kg i.m. did not enhance histamine-induced bronchospasm. Furthermore, in guinea pigs preselected for lack of histamine sensitivity, treatment with salbutamol caused a decrease in both dynamic compliance values and peak expiratory flow rate as well as an increase in resistance values. Trachea removed from guinea pigs treated with isoproterenol or salbutamol retained normal responsiveness to histamine and dibutyryl cAMP while the responsiveness to isoproterenol was reduced. These studies indicate that repetitive administration of beta-adrenoceptor stimulants can produce a specific desensitization of beta-adrenoceptors in pulmonary tissue and an alteration of resting baseline values of pulmonary mechanics measurements.
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PMID:Physiological consequences of beta-adrenoceptor desensitization in guinea pigs. 630 76

Seventeen dogs with clinical signs attributable to nonneoplastic obstruction of the larynx, trachea, or large bronchi underwent computed tomography (CT) imaging. In 16 of the 17 dogs, CT was performed without general anesthesia using a positioning device. Fifteen of these 16 dogs were imaged without sedation or general anesthesia. Three-dimensional (3D) internal rendering was performed on each image set based on lesion localization determined by routine image planes. Visual laryngeal examination, endoscopy, video fluoroscopy, and necropsy were used for achieving the cause of the upper airway obstruction. The CT and 3D internal rendering accurately indicated the presence and cause of upper airway obstruction in all dogs. CT findings indicative of laryngeal paralysis included failure to abduct the arytenoid cartilages, narrowed rima glottis, and air-filled laryngeal ventricles. Laryngeal collapse findings depended on the grade of collapse and included everted laryngeal saccules, collapse of the cuneiform processes and corniculate processes, and narrowed rima glottis. Trachea abnormalities included hypoplasia, stenosis, or collapse syndrome. The CT findings in tracheal hypoplasia consisted of a severely narrowed lumen throughout the entire length. Tracheal stenosis was represented by a circumferential decrease in tracheal lumen size limited to one region. Tracheal collapse syndrome was diagnosed by severe asymmetric narrowing. Lobar bronchi collapse appeared in CT images as a narrowed asymmetric lumen diameter. CT imaging of unanesthetized dogs with upper airway obstruction compares favorably with traditional definitive diagnostic methods.
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PMID:Computed tomographic imaging of dogs with primary laryngeal or tracheal airway obstruction. 2144 37

Flat trachea syndrome, commonly known as 'tracheobronchomalacia', is a central airway disease characterised by excessive expiratory collapse of the tracheobronchial posterior membrane due to weakness in the airway walls. Patients present with symptoms such as chronic cough, dyspnoea and recurrent respiratory tract infections, which are often attributed to more common conditions such as asthma and chronic obstructive pulmonary disease (COPD). The term 'Flat Trachea Syndrome' was first proposed by Niranjan and Marzouk in 2010 following a retrospective study of 28 patients with the condition who underwent surgery for it. The authors advocated the term due to the primary abnormality being collapse of the posterior membranous wall of the central airways as opposed to softening of the tracheal cartilage (tracheobronchomalacia), which they proposed is a misnomer. We present a rare case of a patient with flat trachea syndrome on a history of COPD who initially presented with recurrent respiratory tract infections.
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PMID:Flat trachea syndrome: a rare condition with symptoms similar to obstructive airway disease. 2572 28

Post-intubation tracheal stenosis was a late time complication after tracheotomy but the happening of dyspnea was unusual. Diagnosing tracheal stenosis after incubation, and figuring out the location and causes of the stenosis were important. Treatment of post-incubation tracheal stenosis relied on accurate diagnosis of the type of tracheal stenosis. Computed tomography (CT) and laryngoscope could be used for detecting the stenosis but not enough. Two patients who were already under the urgent tracheotomy over 1 year were reported. However apnea was found on these two patients for a long time after traheotomy. Obviously laryngeal obstruction appeared. CT virtual bronchoscope and laryngoscope examination showed that the cannula was obstructed and plenty of granulation tissue blocked the orificium. But the exact location of the cannula and the adjacent relationship of the tissue around the cannula was equivocal. Mimics 10.01 software was used to analyze the data of the CT scan and found that a pseudo cavity was formed by granulation tissue which partly blocked the cannula in 1 case; granulation tissue occupation and scar formation in the trachea were the reason of tracheal stenosis but not the collapse of the cartilage in case 2. The purpose of this report is to discuss the cause of dyspnea after emergency tracheotomy, its diagnostic method and their management. CT virtual bronchoscope and laryngoscope should be used as a regular examination after tracheotomy to clarify the location of cannula and avoid the failure of airway opening caused by the dislocation of cannula and the complication. Trachea tissue should be protected properly during and after the tracheotomy which might decline the rate of the tissue remodeling, tracheal stenosis and dyspnea after surgery. The clinical use of Mimics 10.01 made it possible to observe morphology more directly by invasive examination and provided a significant clue to make the operation plan so that it should be used widely. Meanwhile, the method to put the cannula into its right way under the guidance of rigid endoscope and the excision of granulation tissue by semiconductor laser should become one of the best treatments of this disease. Following the method above, laryngeal obstruction was relieved after the surgery. Postoperative follow-up lasted for 1 year and recurrence was not found.
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PMID:[Analysis of 2 cases of dyspnea happening after tracheotomy and the clinical application of Mimics 10.01]. 3033 60