Growth of Bacteroides fragilis in rabbit tracheal organ culture: anaerobiosis and tissue respiration.
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Rabbit tracheal explants supporting growth of inoculated Bacteroides fragilis in air were shown to keep low oxygen tension. Treating the explants with sodium azide induced high oxygen tension and arrested reversibly the growth of B. fragilis. (+info)
Neurogenic inflammation in rat trachea is accompanied by increased negativity of interstitial fluid pressure.
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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) (+info)
Laryngotracheobronchitis: 2 years' experience with racemic epinephrine.
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A relatively new form of treatment of laryngotracheobronchitis, administration of racemic epinephrine by intermittent positive-pressure breathing, was begun in 1973 in the pediatric unit of a large community hospital. A review of 2 years' experience with this treatment, compared with the experience of the 3 years prior to its introduction, has shown that it has reduced significantly the necessity for tracheostomy, to nearly zero, and the duration of hospital stay. A total of 119 children (33.15% of those admitted) received this treatment, the average number of treatments required being 1.8. There were no important complications of treatment and no deaths. (+info)
Herpes simplex virus tracheitis in a patient with the acquired immunodeficiency syndrome.
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Herpetic tracheobronchitis and pneumonia occur basically in immunodepressed patients, but have rarely been reported in patients with the acquired immunodeficiency syndrome (AIDS). Some large reviews on pulmonary manifestations in AIDS report a small number of herpetic pulmonary infections, without determining any prevalence of this particular viral involvement. Predisposing factors are alteration of cell-mediated immunity and invasive procedures (such as endotracheal tube use) in debilitated patients. The case we report illustrates the occurrence of a herpetic tracheitis in an HIV-infected patient with severe P. carinii pneumonia, needing systemic corticotherapy and mechanical ventilation. It illustrates the risk of dissemination of herpes simplex virus (HSV) from a herpetic stomatitis to the lower respiratory tract, even after the endotracheal cannula has been removed. (+info)
Unilateral wheeze caused by pseudomembranous aspergillus tracheobronchitis in the immunocompromised patient.
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Unilateral wheeze in the immunocompromised patient with unremitting fever may be the first localising sign of aspergillus tracheobronchitis. Two such cases are presented. (+info)
A feline herpesvirus-1 recombinant with a deletion in the genes for glycoproteins gI and gE is effective as a vaccine for feline rhinotracheitis.
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Using a site-directed mutagenesis technique we constructed a new feline herpesvirus-1 recombinant strain containing a deletion in two genes encoding glycoproteins gI and gE. These proteins may have a role in virulence, the establishment of latency, and viral recurrence as shown in other herpesviruses of the varicella and simplex types. This recombinant was characterized and used to immunize juvenile cats against virulent virus challenge. Significant protection resulted from vaccination of cats by the subcutaneous route. (+info)
The effects of formoterol on plasma exudation produced by a localized acute inflammatory response to bradykinin in the tracheal mucosa of rats in vivo.
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1. The effects of formoterol, a beta 2-adrenoceptor agonist, on plasma protein exudation and microvascular permeability induced by topical, i.e. applied onto the tracheal mucosal surface, bradykinin (10 nmol; 20 microM, 5 min, 0.1 ml min-1) were studied in a perfused segment of trachea prepared in situ in anaesthetized rats. 2. Bradykinin increased the amount of plasma (fluorimetric assay for protein) in the perfusate (response; 10.98 +/- 0.357 microliters, n = 69; total increase in plasma over basal during 45 min after start of bradykinin application) and 2 responses at a 90 min interval were reproducible. Carbon labelling was seen in tracheal sections from animals that received i.v. colloidal carbon, indicating that bradykinin caused tracheal microvessels to leak (increase in microvascular permeability). 3. Five minutes after topical formoterol, 5 or 30 nmol (10 or 60 microM perfused for 5 min), the bradykinin response was significantly reduced. The effects of formoterol were not dose-related, i.e. were maximal at 5 nmol. The bradykinin response was at control levels 30 min after 5 nmol formoterol. After 30 nmol formoterol, the response was still reduced 120 min later. The bradykinin response was significantly reduced 60 min after systemic formoterol (i.p., 0.029 to 870 nmol kg-1) and, for 290 nmol kg-1 i.p. formoterol, this reduction was shown to last at least 150 min. 4 The bradykinin response was not prevented by supramaximal doses of topical (30 nmol) or i.p.(870 nmol kg-1) formoterol and carbon-labelled microvessels were seen in tracheal sections from all animals that received formoterol, although these were less in number and less densely labelled than in the absence of formoterol. There was a correlation between the plasma exudation response (ul) and the number of carbon-labelled vessels (Spearman's correlation coefficient 0.415, P<0.001).5 In animals pretreated with propranolol (3 pmol kg-1, i.v.), 29 nmol kg-1 formoterol, i.p., did not reduce the bradykinin response. However, propranolol itself markedly potentiated the bradykinin response which confounded the interpretation of its effects on formoterol.6 The study has shown, in a preparation of rat trachea in situ, that supramaximal doses of the beta2-adrenoceptor agonist, formoterol (a) produced a sustained, but incomplete, inhibition of plasma exudation (induced by topical bradykinin), and (b) did not prevent bradykinin-induced leaky microvessels. The data support the view that, at least in rodent airways, beta2-adrenoceptor agonists attenuate, but do not abolish, the microvascular permeability effects of bradykinin, a putative asthma mediator. (+info)
Glycoproteins gl and gE of feline herpesvirus-1 are virulence genes: safety and efficacy of a gl-gE deletion mutant in the natural host.
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Feline rhinotracheitis virus (FRV) is an important upper respiratory tract pathogen of cats. FRV is a member of the subfamily Alphaherpesvirinae and is designated feline herpesvirus-1 (FHV-1). Besides upper respiratory clinical signs, FHV-1 may cause generalized infections in neonates or abortions in pregnant queens. Recently we described a recombinant FHV-1 strain with a deletion in the genes for glycoproteins gl and gE (FHB beta-galglgE delta) and reported that cats vaccinated subcutaneously with high doses of the recombinant FHV-1 strain responded with only mild clinical signs and developed strong immunity against subsequent virulent virus challenge. Here we compare the intranasal and subcutaneous routes of administration of this strain and assess its ability to induce protective immunity and prevent virus shedding after challenge. Cats vaccinated subcutaneously or intranasally with high doses of the recombinant FHV-1 strain responded with only mild clinical signs and developed strong immunity against subsequent virulent virus challenge. This was especially evident when the mutant vaccine was administered oronasally. In contrast, intranasal administration of two other FHV-1 isolates induced severe clinical signs in cats. We conclude from testing this FHV-1 mutant in the natural host that deletion of gE and a portion of gl genes strongly reduces viral virulence but that immunogenicity is maintained. (+info)