Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034067 (emphysema)
 11,506 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pulmonary function can be reduced by beta-blockers. It has been established that no beta-blocker is entirely safe in patients with chronic obstructive lung disease. An alternative medication not expected to influence pulmonary function should first be considered. This side effect of beta-blockers develops mostly in patients with reversible bronchial obstruction, and it is much less pronounced in those with irreversible bronchial obstruction. Translated into terms of clinical diagnosis, this means that problems should be expected in patients with bronchial asthma and with asthmatic bronchitis, whereas those with chronic bronchitis and emphysema are much less likely to develop relevant symptoms. It has been demonstrated that beta-blockers with intrinsic sympathomimetic activity (ISA), such as pindolol, and beta 1-selective blockers have a less marked effect on pulmonary function than nonselective beta-blockers without ISA, such as propranolol. The untoward effect can be compensated by combination with a beta-mimetic agent; this mechanism is most effective during beta 1-selective blockade.
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PMID:beta-Adrenoceptor blockade and pulmonary function in patients suffering from chronic obstructive lung disease. 618 19

Ventilation, heart rate, and arterial blood gas tensions were measured at rest and during incremental exercise in 10 patients with emphysema after intravenous placebo or 7 mg metoprolol. Metoprolol reduced heart rate by 14% (P less than 0.001) and ventilation by 11% (P less than 0.01), but there was no significant difference in arterial O2 or CO2 tension (Pao2 and PaCO2, respectively). Metoprolol increased the time to exhaustion on a cycle ergometer (P less than 0.05) but did not improve the 12-min walking distance. A double-blind randomized crossover comparison of 4 wk treatment with atenolol (100 mg/day), metoprolol (100 mg/day), or matched placebo was performed in 12 patients with emphysema. Both beta-adrenoceptor antagonists reduced resting heart rate by 33% (P less than 0.001) and resting minute ventilation by 11% (P less than 0.025). There was no change in resting or exercise Pao2 or Paco2. During steady-state exercise on a cycle ergometer, atenolol and metoprolol reduced ventilation by 14 and 4%, respectively. This was accompanied by 11 and 5% reductions in O2 consumption (P less than 0.05) and 13 and 6% falls in CO2 production (P less than 0.05). There were no significant changes in tests of exercise tolerance, but forced expiratory volume in 1 s and forced vital capacity were reduced during beta 1-adrenergic blockade. beta 1-Blocking drugs reduce hyperventilation in emphysema by reducing pulmonary gas exchange without a change in arterial blood gas tensions. Increased airflow obstruction prevents this reduction being of therapeutic value.
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PMID:Effect of beta-adrenergic blockade on hyperventilation and exercise tolerance in emphysema. 686 97

The mechanism causing finger clubbing in patients with lung cancer (LC) is still unclear. We compared age, cigarette consumption, data on blood gas analysis and pulmonary function tests among patients with LC with clubbing (n = 30) and without clubbing (n = 28) and among patients with pulmonary emphysema (PE) with (n = 11) and without clubbing (n = 17). We also examined serum concentrations of transforming growth factor beta 1 (TGF beta 1) and insulin-like growth factor-I (IGF-I) in the patients and healthy volunteers (n = 21). There were no differences in age or cigarette consumption. LC groups showed normal levels of Pao2 and Paco2, suggesting that neither hypoxaemia nor hypercapnia caused clubbing in these patients. The level of serum TGF beta 1 in patients with LC with clubbing was significantly higher than in other groups (P < 0.005), whereas levels of IGF-I did not differ among the groups. Our data suggest that TGF beta 1 may play a role in the mechanism of clubbing in patients with LC.
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PMID:Elevated serum transforming growth factor beta 1 level in primary lung cancer patients with finger clubbing. 888 46

Peroral endoscopic myotomy (POEM) is a newly developed, less invasive treatment for esophageal achalasia that requires general anesthesia under positive pressure ventilation. In this retrospective case series, we describe the anesthetic management of 28 consecutive patients who underwent POEM for esophageal achalasia. Anesthesia was maintained with sevoflurane and remifentanil under positive pressure ventilation through a tracheal tube. Retained contents in the esophagus were evacuated just before anesthesia induction to prevent regurgitation into the trachea. The POEM procedure was performed using an orally inserted flexible fiberscope. Elevation of end-tidal carbon dioxide after initiating esophageal carbon dioxide insufflation was observed in all patients and was treated by minute adjustments to the ventilation volume. Scopolamine butylbromide-induced tachycardia in one patient was treated with landiolol hydrochloride, which is a short-acting beta 1-selective blocker. Minor subcutaneous emphysema around the neck was observed in one patient. POEM was successfully completed, and tracheas were extubated immediately after the procedure in all patients. Our findings suggest that prevention of aspiration pneumonia during anesthesia induction, preparation for carbon dioxide insufflation-related complications, and treatment of scopolamine butylbromide-induced tachycardia play important roles in safe anesthesia management of POEM for esophageal achalasia.
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PMID:Anesthetic management of peroral endoscopic myotomy for esophageal achalasia: a retrospective case series. 2535 41