Intra-airway Pressure Research Articles

Effects of long-term application of metoprolol and propranolol in a rat model of smoking.

Beta-blockers, especially selective β1 -adrenoceptor antagonists, are often used to treat cardiovascular disease, even when complicated by chronic obstructive pulmonary disease. The association of beta-blocker selectivity and treatment effects is disputed, and the curative effects and side-effects of various antagonists may differ. Herein we investigated the effects of 1months treatment with the selective β1 -adrenoceptor antagonist metoprolol and the non-selective β-adrenoceptor antagonist propranolol on pulmonary function and pathology in a 4-month rat model of passive cigarette smoke exposure and explored potential mechanisms of action. Lung function and general pathological changes were evaluated after 4months exposure to cigarette smoke, with metoprolol and propranolol treatment (50 and 25mg/kg per day, respectively; intragastrically) during the last month. Cytokine and mucin levels in bronchoalveolar lavage fluid (BALF) were determined by ELISA, whereas β1 - and β2 -adrenoceptor expression in the lungs was evaluated by immunohistochemistry and western blot analysis. Chronic treatment with metoprolol and propranolol did not exacerbate peak expiratory flow or intra-airway pressure in rats exposed to cigarette smoke. Propranolol significantly attenuated inflammatory cell infiltration, cytokine levels (tumour necrosis factor-α and interleukin-8) in BALF or mucus secretion, whereas metoprolol reduced only smooth muscle proliferation. Moreover, propranolol treatment was associated (albeit not significantly) with restoring β2 -adrenoceptor expression in airway epithelia. Propranolol had a more beneficial effect on cigarette smoking-induced lung damage than metoprolol in a smoking rat model that may be associated with restoration of endogenous β2 -adrenoceptor density in the airway epithelial cells.

Obesity, obstructive sleep apnoea, and diabetes mellitus: anaesthetic implications

Obesity is an epidemic in much of the Western World. The extent of this problem, combined with the increasing preference for ambulatory surgical procedures, has produced a difficult situation for many anaesthesiologists. Even the simplest anaesthetic procedures can become very complicated and potentially difficult in this population. Although there are numerous complications associated with obesity, perhaps obstructive sleep apnoea (OSA) and diabetes mellitus are among the more significant. Patients with OSA are often not ideal candidates for certain day-case procedures, but many outpatient procedures can be performed on patients with OSA as long as attention is paid to anaesthetic technique. Diabetic patients are prone to numerous complications in the perioperative period, including cardiac problems, but with careful management, they are able to undergo day-case surgical procedures safely.

A Prospective and Randomized Study for Improvement of Acute Asthma by Non-invasive Positive Pressure Ventilation (NPPV)

We hypothesized that non-invasive positive pressure ventilation (NPPV) would improve an acute asthma attack in mild to moderate cases without bronchodilator therapy. A total of 44 eligible patients with acute asthma of mild to moderate severity who had acute attacks were randomly allocated to a NPPV (n=30) or control group (n=14). Both groups received intravenous infusion of hydrocortisone prior to the study. Patients in the NPPV group were divided into two subgroups at random: a high- (n=16) and a low-pressure group (n=14). The former had a fixed expiratory positive airway pressure and inspiratory positive airway pressure of 6 cmH2O and 8 cmH2O, respectively, while the latter had levels of 4 cmH2O and 6 cmH2O, respectively. Effects on the following variables were assessed: FEV(1), oxygen saturation, heart rate, respiratory rate, scores of accessory muscle use and wheezing by auscultation, modified Borg scale score, and mean intra-airway pressure on the monitor. A total of 26 patients completed the study in the NPPV group. The mean percent change in FEV(1) significantly improved after 40 minutes in the high-pressure group compared with that in the control group (p<0.0001). Similar significant improvements in modified Borg scale score and physical examination findings were observed in the high- and low-pressure groups. None of the patients required re-hospitalization or return to the emergency room in either the NPPV or control group. We conclude that higher inflation pressure on NPPV led to clinical improvement in patients with acute asthma attacks of mild to moderate severity.

Significance of lung hyperinflation in chronic obstructive pulmonary disease

Lung hyperinflation is a critical characteristic of pathophysiological changes in chronic obstructive pulmonary disease (COPD), and is associated with the severity and prognosis of the disease. In an attempt to understand the importance of lung hyperinflation in the pathogenesis of chronic lung disease, we will discuss in this review the understanding of the disease, measurements of lung hyperinflation in COPD, clinical findings of lung hyperinflation in emphysema, potential mechanisms of lung hyperinflation, its potential reversibility and comparison of lung hyperinflation between asthma and COPD. Multiple factors may contribute to the development of lung hyperinflation, including compromised alveolar walls, increased intra-airway pressure, inflammation, goblet cell hyperplasia and metaplasia and tissue remodeling. The development of new technology to measure lung hyperinflation will be helpful in the diagnosis and monitoring of the disease. Improvement in lung hyperinflation should become one of the mos...

Going to extremes of lung volume

volume changes in the lung are the basis for life-sustaining respiration, yet in many regards, the lung is overengineered and the mechanical limits are most often not approached ([11][1]). For some activities, however, the entire volume range of the thorax and lung is necessary; for example,

胸部打撲による閉鎖性頚部気管断裂例

A case of cervical tracheal injury secondary to blunt trauma to the chest is reported. A 36-year-old male visited our hospital complaining of dyspnea and hemoptysis after having been run over on the back of the chest. Physical examination revealed no sign of trauma (wound nor subdermal hematoma) on the surface of the neck but there was subcutaneous emphysema in the cervical and thoracic area. A chest X-ray and computed tomography revealed pneumomediastinum, right pneumothorax, subcutaneous and deep neck emphysema and a fracture of the right clavicle. After post oral in tubation and the insertion of a thoracostomy tube, fiberoptic bronchoscopy was performed, which showed a disruption of the trachea just beneath the sternal notch.The patient was immediately taken to an operation room. Complete tracheal transection at the level of sixth ring was revealed, and was subsequently reconstructed by means of end-to-end anastomosis. Bilateral recurrent nerves were also damaged, but they were not repaired. The postoperative course was uneventful. Tracheostomy was done on the 14th postoperative day and the patient, with a sealed tracheobutton, was discharged on the 47th day.In this case, the mechanism of cervical tracheal disruption was thought to be compression between the manubrium of the sternum and the vertebral column and the dramatic increase in intraairway pressure because the glottis was closed when the chest was crushed.

Laryngospasm-induced pulmonary edema

We report the case of a 6-month-old child who developed acute pulmonary edema because of laryngeal spasm during orthopedic manipulations for congenital hip dysplasia. Laryngospasm was probably secondary to an unsuspected light level of anesthesia, maintained via face mask. No other predisposing factors, such as enlarged adenoid tonsils, laryngitis, epiglottitis, mechanical stimulation of the larynx or aspiration of foreign material were identified. Serious oxygen desaturation and bradycardia ensued, during inefficient attempts at positive pressure ventilation. After emergency intubation without muscle relaxant, copious pink secretions emerged from the airway. Negative pressure pulmonary edema was confirmed by chest X-ray, and short-lasting arterial desaturation despite positive pressure ventilation with high oxygen concentration. This type of pulmonary edema is caused by marked elevated negative intra-airway pressure, massive sympathetic discharge causing a blood shift from the systemic to the pulmonary circulation, and accentuation of physiological ventricular interdependence during forceful inspiratory effort against a closed glottis. As usual in such cases, pulmonary edema and laryngospasm resolved spontaneously without specific treatment, and extubation was carried out uneventfully two hours later. The child suffered no sequelae.

Properties of steady maximal expiratory flow within excised canine central airways.

Using our transistor model of the lung during forced expiration (J. Appl. Physiol. 62: 2013-2025, 1987), we recently predicted that 1) axially arranged choke points can exist simultaneously during forced expiration with sufficient effort, and 2) overall maximal expiratory flow may be relatively insensitive to nonuniform airways obstruction because of flow interdependence between parallel upstream branches. We tested these hypotheses in excised central airways obtained from five canine lungs. Steady expiratory flow was induced by supplying constant upstream pressure (Pupstream = 0-16 cmH2O) to the bronchi of both lungs while lowering pressure at the tracheal airway opening (16 to -140 cmH2O). Intra-airway pressure profiles obtained during steady maximal expiratory flow disclosed a single choke point in the midtrachea when Pupstream was high (2-16 cmH2O). However, when Pupstream was low (0 cmH2O), two choke sites were evident: the tracheal site persisted, but another upstream choke point (main carina or both main bronchi) was added. Flow interdependence was studied by comparing maximal expiratory flow through each lung before and after introduction of a unilateral external resistance upstream of the bronchi of one lung. When this unilateral resistance was added, ipsilateral flow always fell, but changes in flow through the contralateral lung depended on the site of the most upstream choke. When a single choke existed in the trachea, addition of the external resistance increased contralateral flow by 38 +/- 28% (SD, P less than 0.003). In contrast, when the most upstream choke existed at the main carina or in the bronchi, addition of the external resistance had no effect on contralateral maximal expiratory flow.(ABSTRACT TRUNCATED AT 250 WORDS)