Otolaryngological findings in patients with chronic respiratory paralysis after poliomyelitis.
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Adolescent↗
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Innominate artery compression syndrome. Presentation of 16 cases.
A series of 16 patients with tracheal compression by the innominate artery is presented. In more than half of the patients the symptoms began during the first few days of life with stridor varying severity, recurrent tracheobronchitis and apneic spells. In six cases requiring surgical treatment the immediate result was good. In ten mild cases treatment consisted of medical management and follow-up. The present study confirms that the great arteries can exert compression on the trachea, which can always be relieved by means of an operation which moves the arteries forward. Bronchoscopy is considered to be the only reliable means of diagnosis. This entity should be considered more often in the differential diagnosis in children less than 3 years of age with stridor, breathing difficulties, recurrent infections, apneic spells, and asthma.
Apnea↗
Neurogenic inflammation in rat trachea is accompanied by increased negativity of interstitial fluid pressure.
The present experiments were performed to investigate whether neurogenic inflammation in rat trachea (with edema formation and protein extravasation when the circulation is intact) induced by electrical field stimulation of neuropeptide-containing C fibers in the vagal nerve is accompanied by increased negativity of interstitial fluid pressure (P(if)). Increased negativity of P(if) in the trachea occurs in dextran anaphylaxis and mast cell degranulation and facilitates edema formation under these circumstances. Experiments were performed after circulatory arrest had been induced in pentobarbital anesthesia to prevent edema formation, which will raise P(if) and potentially cause underestimation of an increased negativity of P(if). After induction of circulatory arrest, the vagal nerve was isolated and placed in a stimulating electrode. The trachea was then exposed and covered with mineral oil, and measurement of P(if) was started as soon as possible thereafter. P(if) was measured with sharpened glass capillaries (tip diameter, 3 to 7 microns) connected to a servocontrolled counterpressure system. P(if) in the control group (n = 12) did not change throughout the observation period. Electrical stimulation of the left vagal nerve caused P(if) to fall in all experiments, from -1.1 +/- 1.1 mm Hg in the control condition to an average of -10.6 +/- 3.4 mm Hg (n = 9, P < .01). In some experiments, a continuous recording of P(if) was obtained, showing that the reduction of P(if) started within 30 seconds after onset of stimulation to reach and later remain at a stable level within a few minutes. The experimental protocol was repeated after the C fibers had been nearly depleted of neuropeptides with capsaicin.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Neurogenic inflammation and lowering of interstitial fluid pressure in rat trachea is inhibited by alpha-trinositol.
The effect of alpha-trinositol (D-myoinositol-1,2,6-triphosphate) on edema formation and capillary permeability in neurogenically induced inflammatory edema was investigated in rat trachea. Interstitial fluid pressure (Pif) was studied, since increased negativity of Pif contributes to edema formation in this situation. alpha-Trinositol was used because it inhibits edema formation, capillary leakage, and increased negativity of Pif in burn-injured skin. Pif was measured with sharpened glass capillaries (3 to 7 microns) connected to a servocontrolled counterpressure system after circulatory arrest (induced by intracardiac injection of saturated potassium chloride in pentobarbital anesthesia). This was done in order to avoid the edema formation associated with inflammatory reactions, which will raise interstitial fluid volume and Pif, causing the underestimation of an increased negativity of Pif. Neurogenic inflammation induced by electrical-field stimulation of the left vagal nerve (10 V, 20 Hz, 0.5 ms) lowered Pif from -1.4 +/- 0.6 mm Hg to -8.4 +/- 2.1 mm Hg (p < 0.01). Corresponding numbers after the intravenous administration of alpha-trinositol (40 mg/kg) before stimulation were -1.2 +/- 0.4 and -1.4 +/- 0.4 mm Hg, respectively (p > 0.05). Another series of animals with intact circulation was used to study the effect of vagal nerve stimulation and alpha-trinositol on edema formation (total tissue water and extravascular 51Cr-ethylenediamine tetraacetic acid-[EDTA] space) and albumin extravasation. These parameters increased significantly after vagal nerve stimulation, while intravenous alpha-trinositol (40 and 120 mg/kg), as given above, significantly attenuated this increase. Thus, alpha-trinositol prevented a lowering of Pif and the edema formation accompanying neurogenic inflammation in rat trachea.
Analysis of Variance↗
Antigen inhalation unmasks NK-2 tachykinin receptor-mediated responses in vagal afferents.
The majority of airway sensory innervation originates from afferent neurons whose somata reside in vagal (nodose and jugular) ganglia. Using guinea pigs immunized with chick ovalbumin, we have discovered that airway inflammation provokes phenotypic changes in the tachykinin responsiveness of nodose neurons. Bath application of substance P (SP; 0.1 to 10 microM) to nodose neurons isolated from guinea pigs with normal uninflamed airways did not elicit measurable changes in resting electrophysiological properties. In sharp contrast, 80% of nodose neurons isolated 24 h after in vivo aerosolized antigen challenge of the airway were depolarized by 100 nM SP. Inhalation of a nonantigenic protein did not evoke the expression of SP responses. Pharmacological analysis revealed that SP responses unmasked by airway inflammation were mediated by neurokinin-2 (NK-2) tachykinin receptors. There are several potential mechanisms for transduction of an "unmasking signal" from the inflamed airway to vagal afferent somata. The vagus nerve may relay the signal, either through anterograde transport and/or nerve impulse activity. Alternatively, a signal generated by airway inflammation may be carried by the circulation to the nodose ganglia. Unilateral vagotomy significantly reduced the percentage of SP-responsive neurons compared with intact controls, suggesting that the vagus nerve is required for unmasking of NK-2 responses.
Animals↗
Treatment of nosocomial pneumonia and tracheobronchitis caused by multidrug-resistant Pseudomonas aeruginosa with aerosolized colistin.
Gram-negative bacilli including multidrug-resistant (MDR) Pseudomonas aeruginosa are responsible for a significant proportion of episodes of nosocomial pneumonia. Since the development of new antibiotics with activity against gram-negative organisms has not kept pace with the increase in prevalence of MDR pathogens, there has been renewed interest in antimicrobial agents that had previously been used but had been abandoned because of toxic side effects. This report describes three patients with nosocomial pneumonia or tracheobronchitis due to multiresistant strains of P. aeruginosa for whom aerosolized colistin proved beneficial as supplemental therapy. Aerosolized colistin merits further consideration as a therapeutic intervention for patients with pulmonary infections due to MDR P. aeruginosa.
Administration, Inhalation↗
Respiratory tract infections increase susceptibility to neurogenic inflammation in the rat trachea.
This study reveals that respiratory tract infections make the tracheal mucosa of rats more susceptible to neurogenic inflammation, which is a type of inflammation mediated by neuropeptides released from sensory nerves. Neurogenic inflammation was produced in the tracheas of 2 groups of Long-Evans rats by electrical stimulation of the vagus nerve (5 V, 1 ms, 20 Hz for 5 min) or by an injection of capsaicin (15 to 200 micrograms/kg i.v.) or substance P (0.05 to 5.0 micrograms/kg i.v.). Rats of one group were pathogen-free; the others had serologic evidence of naturally occurring airway infections caused by Sendai virus, coronavirus, and Mycoplasma pulmonis. The stimuli produced neurogenic inflammation in both groups of rats, but the magnitude of this inflammation was much greater in the infected rats. The susceptibility of the infected rats to neurogenic inflammation was manifested by a 2.0 to 3.1 times larger increase in vascular permeability to Monastral blue, 5 times larger increase in number of neutrophils adhering to the endothelium of venules, and conspicuous morphologic changes in the tracheal epithelium. When pathogen-free rats acquired respiratory tract infections, they too became susceptible to neurogenic inflammation. Other experiments showed that infection by Sendai virus was essential for the change, although infection by M. pulmonis or coronavirus may also be necessary. The susceptibility to neurogenic inflammation outlasted the transient pathologic changes caused in the airway mucosa by the viral infections and may have been permanent.
Animals↗
Pseudomembranous tracheobronchitis caused by Aspergillus.
Four immunosuppressed patients with a rapidly evolving, febrile, respiratory distress syndrome were found at autopsy to have Aspergillus pseudomembranes of their lower tracheobronchial tree. Steroids, neutropenia, broad spectrum antibiotic use, and alcoholism appear to be predisposing risk factors. Bronchoscopy may reveal the pathology but antemortem diagnosis is difficult because of the low yield of sputum cultures and fulminant nature of the disease.
Adult↗
Ulcerative tracheobronchitis after lung transplantation. A new form of invasive aspergillosis.
Invasive aspergillosis is frequently a fatal disease in the setting of immunosuppression, including organ transplant recipients. The fungus usually affects lung parenchyma and may disseminate from there. We have recently noted tracheobronchitis in six patients with heart-lung and lung transplants, three of whom had deep mucosal ulceration and histologic evidence of invasive aspergillosis. This apparently new form of invasive disease is initially limited to the anastomosis site and large airways. Ulceration, necrosis, cartilage invasion, and formation of a pseudomembrane are the pathologic features. In two patients subsequent disseminated aspergillosis occurred with a fatal outcome. In the two single-lung recipients, disease was limited to the transplanted side emphasizing the importance of abnormal local defense mechanisms in the airways of lung transplant recipients. Routine bronchoscopic examination of the airways is important in early detection of this complication. Oral therapy with the new, antifungal agent itraconazole was successful in five of the six patients, with fatal relapse in one. A classification of the various forms of saprophytic, allergic, and invasive forms of aspergillus tracheobronchitis, to include this new entity, is proposed.
Adult↗
Plasma extravasation in the rat trachea induced by cold air is mediated by tachykinin release from sensory nerves.
Cold air was delivered to anesthetized, artificially ventilated, pathogen-free F344 rats via a tracheal cannula. Inhalation of cold air increased Evans blue dye extravasation in the trachea in a time-dependent (1 to 10 min) manner. Plasma extravasation increased after 3 min exposure to cold air and reached a maximum after 10 min exposure. The neutral endopeptidase inhibitor, phosphoramidon (2.5 mg/kg, intravenously), increased by 84% the plasma extravasation induced by inhalation of cold air for 1 min. The plasma extravasation evoked by 5 min exposure to cold air was abolished by the NK1 tachykinin receptor antagonist, CP-99,994 (4 mg/kg, intravenously); was reduced 30% by the B2 bradykinin receptor antagonist, HOE140 (0.1 mumol/kg, intravenously); and was not affected by H1 (pyrilamine, 10 mg/kg, intraperitoneally) or H2 (cimetidine, 10 mg/kg, intraperitoneally) histamine receptor antagonists or the cyclooxygenase inhibitor indomethacin (5 mg/kg, intravenously). In rats infected with Sendai virus, plasma extravasation evoked by inhalation of cold air was greater than in pathogen-free rats. Pretreatment with CP-99,994 (4 mg/kg, intravenously) inhibited completely the plasma extravasation induced by cold air in virus-infected rats. These findings indicate that cold air increases plasma extravasation in the rat trachea by a neurogenic mechanism that involves the release of tachykinins from sensory nerves. Kinin release may also play a role in this neurogenic inflammatory response.
Air↗
Oxygen therapy. Side effects and toxicity.
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Bronchitis↗
The site of leukocyte migration through the tracheal mucosa in the guinea pig.
The tracheal mucosa of the guinea pig was examined using light microscopy, thin section, and freeze-fracture replicas with transmission electron microscopy and scanning electron microscopy. These studies demonstrated that inflammatory cells en route to the mucosal surface migrate through the epithelium in file through solitary openings rather than randomly between epithelial cells. The fact that leukocytes migrate through these openings rather than randomly between epithelial cells has important implications. First, it provides a pathway for circulating cells to gain access to the surface of the airway where they can function as the first line of defense against inhaled material. Second, the movement of leukocytes through specified pathways rather than randomly between cells minimizes the number of openings required for cell transit so that fluid and solute movement can be more tightly controlled. Third, the prevention of random migration may also be important in minimizing the contact between the migratory cells and the epithelial sensory nerve net.
Animals↗
Importance of airway inflammation for hyperresponsiveness induced by ozone.
We studied whether ozone-induced airway hyperresponsiveness correlates with the development of airway inflammation in dogs. To assess airway responsiveness, we determined increases in pulmonary resistance produced by delivering acetylcholine aerosol to the airways. To assess airway inflammation, we biopsied the airway mucosa and counted the number of neutrophils present in the epithelium. Airway responsiveness and inflammation were assessed in anesthetized dogs before ozone exposure and then 1 h and 1 wk after ozone (2.1 ppm, 2 h). Airway responsiveness increased markedly at 1 h after ozone and returned to control levels 1 wk later in each of 6 dogs, but it did not change after ozone in another 4 dogs. Furthermore, dogs that became hyperresponsive also developed a marked and reversible increase in the number of neutrophils in the epithelium, whereas dogs that did not become hyperresponsive had no change in the number of neutrophils. For the group of dogs, the level of airway responsiveness before and after ozone exposure correlated closely with the number of epithelial neutrophils. The results suggest that ozone-induced airway hyperresponsiveness may depend on the development of an acute inflammatory response in the airways.
Acetylcholine↗
Airway hyperresponsiveness and inflammation induced by toluene diisocyanate in guinea pigs.
We examined the changes in airway responsiveness to increasing doses of an acetylcholine aerosol in anesthetized and ventilated guinea pigs 2, 6, or 24 h after exposure to 2 ppm toluene diisocyanate (TDI) or 2 h after exposure to air or 1 ppm TDI. Pulmonary resistance (RL) after the animals inhaled a buffered saline aerosol was used as baseline and was similar for air and TDI groups. The concentration of acetylcholine calculated to cause a 200% increase in RL was significantly lower for animals studied at 2 h (0.68%) or at 6 h (0.77%), but not at 24 h (2.39%), after TDI than for air animals (3.07%). The increase in airway responsiveness in the TDI-exposed animals was associated with histologic changes in the trachea and intrapulmonary airways. Exposure to 2 ppm TDI caused a patchy loss of cilia, shedding of epithelial cells into the airway lumen, and an influx of inflammatory cells into the trachea and other airways. In the lamina propria of the trachea, the concentration of extravascular polymorphonuclear leukocytes (PMN) was 13- to 26-fold greater in animals studied 2 or 6 h after exposure to 2 ppm TDI or at 2 h after 1 ppm TDI than in animals exposed to air. The concentration of PMN in the epithelium was significantly increased only in animals examined 2 h after 2 ppm TDI. Exposure to TDI also caused an influx of eosinophils into the tracheal mucosa. This influx occurred later and was more persistent than the influx of PMN. These results indicate that a single exposure to TDI can cause an increase in airway responsiveness that is associated with epithelial injury and acute airway inflammation.
Acetylcholine↗
Tissue macrophages associated with angiogenesis in chronic airway inflammation in rats.
Angiogenesis is a feature of chronic inflammation produced by Mycoplasma pulmonis infection of the respiratory tract. The mechanism of this angiogenesis is unknown, but cellular growth factors and matrix remodeling proteases produced by inflammatory cells are likely to be involved. The goal of this study was to determine the relationship between changes in the number, shape, and distribution of ED2-immunoreactive macrophages and the development of angiogenesis in the tracheal mucosa of Wistar rats after M. pulmonis infection. In pathogen-free rats, ED2-positive cells were scattered in the airway mucosa (261 +/- 42 cells/mm2 of surface, mean +/- SE). Most cells were irregularly shaped and had moderate ED2 immunoreactivity. No lymphoid tissue was present. The number of ED2-positive cells increased rapidly after infection, was 120% above baseline at 1 wk, and remained significantly increased throughout the 4-wk study (P < 0.05). Angiogenesis was first detected at 2 wk, and at 3 wk the vessel length density was nearly 8-fold the pathogen-free value. At 3 and 4 wk, focal sites of angiogenesis coincided with discrete clusters of round, strongly immunoreactive ED2-positive cells (1,340 +/- 124 cells/mm2) in polyp-like collections of mucosal lymphoid tissue. The close association of distinctive ED2-positive cells with angiogenic blood vessels suggests a relationship between a subset of tissue macrophages and the angiogenesis associated with M. pulmonis infection. The time course of the changes indicates that the initial influx of ED2-positive macrophages precedes the angiogenesis, and the rounding of the cells parallels the growth of new vessels.
Animals↗
Organ culture with proinflammatory cytokines reproduces impairment of the beta-adrenoceptor-mediated relaxation in tracheas of a guinea pig antigen model.
The challenge of previously sensitized guinea pigs with aerosolized ovalbumin resulted in impairment of the beta-adrenoceptor-mediated relaxation as measured by the in vitro isometric assay of tracheas preconstricted with endothelin-1 or carbamylcholine. Numbers and affinities of beta-adrenoceptors in lung membranes of these animals were not altered under these conditions, although the antigen challenge caused an inflammatory response, as evident from the accumulation of inflammatory cells in the bronchoalveolar lavage fluids. In order to investigate the pathophysiologic role of inflammation in hyperreactive airways, isolated guinea pig tracheas were cultured with proinflammatory cytokines such as human recombinant tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), or interleukin-2 (IL-2). None of these cytokines affected the contractile response of tracheas to carbamylcholine. After preconstriction with carbamylcholine, the TNF-alpha- and IL-1 beta-pretreated tissues produced a significant reduction in the maximal relaxation induced by isoproterenol, whereas the IL-2 pretreatment had no effect. The reduction of the isoproterenol-mediated relaxation by the IL-1 beta treatment was time and dose dependent. Our present observations suggest that in vitro incubation of naive tracheas with proinflammatory cytokines is able to reproduce apparent beta-adrenoceptor impairment as seen in the airways of antigen-challenged guinea pigs of asthma model.
Animals↗
Dendritic cell influx differs between the subglottic and glottic mucosae during acute laryngotracheitis induced by a broad spectrum of stimuli.
Clinically, the subglottic and glottic mucosae may react differently, eg, during acute laryngotracheitis. In healthy rats, we showed previously that the composition of the mucosal immune system of the larynx also differs between these areas. Neutrophils, lymphocytes, and dendritic cells (DCs) are part of this mucosal immune system. In particular, DCs occupy a key function. They migrate into inflamed mucosae during the early phase of the immune response, which is normally characterized by an influx of neutrophils. Thus, they help to overcome the time lag between the innate and the adaptive immune responses. In the present study, the influx of DCs, neutrophils, and T lymphocytes into the subglottic and glottic mucosae of rats was examined at different time points after challenge with a broad spectrum of stimuli such as dead Moraxella catarrhalis, viable Bordetella pertussis, viable Sendai virus, and the soluble protein ovalbumin. The number of DCs increased rapidly after the application of the antigens. This increase was as rapid as the increase in neutrophils. Depending on the kind of antigen, their number in the mucosa increased up to 1,000 cells per 0.1 mm2 (Sendai virus). The comparison of different mucosal areas shows that an overwhelming number of immunocompetent cells entered the subglottic mucosa, whereas only a few cells migrated into the adjacent glottic mucosa. In conclusion, after inhalation of different kinds of antigens, the subset of immunocompetent cells investigated in this study entered the laryngeal mucosa in high numbers. The number of DCs entering the laryngeal mucosa was higher than the numbers of the other immune cells investigated. This finding underlines their function as first-line sentinels of the mucosal immune system of the larynx. The observation that the number of cells entering the laryngeal mucosa is location-dependent indicates the ability of adjacent laryngeal regions to react differently. This is similar to the clinical observation of a selective subglottic reaction during acute laryngotracheitis.
Acute Disease↗
Airway problems in children following prolonged endotracheal intubation.
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Asthma↗