PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Intubation, Intratracheal”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 667 records · Page 37Linked to original sources

Activities of superior pharyngeal constrictor and levator veli palatini muscles related to respiration in dogs.

OBJECTIVE: This study, using mongrel dogs, attempted to delineate the respiratory activity of two closure muscles of the velopharynx, the levator veli palatini (LVP) and superior pharyngeal constrictor (PC) muscles. METHOD: Fifteen mongrel dogs were given tracheotomies, with intratracheal tubes being connected to their respiratory circuits. Activities of the PC and LVP muscles were recorded electromyographically, and the effects of PaO2 and PaCO2 were analyzed along with the effects of lung inflation intratracheally with O2 and N2. RESULTS: Under hypoxic conditions, expiratory LVP activity was observed while PC activity diminished. The effects of lung inflation on both LVP and PC activities were also studied. The activities of both muscles were enhanced by lung inflation. CONCLUSION: It was thus suggested that the roles of both muscles during velopharyngeal closing movements are not the same.

Administration, Inhalation↗

A single intratracheal dose of the growth factor Fms-like tyrosine kinase receptor-3 ligand induces a rapid differential increase of dendritic cells and lymphocyte subsets in lung tissue and bronchoalveolar lavage, resulting in an increased local antibody production.

Repetitive doses of the growth factor Fms-like tyrosine kinase receptor-3 ligand (Flt3L) have resulted in increased numbers of dendritic cells (DC) in various organs, and the effect on protective or tolerogeneic responses in the gut wall has been documented in the literature. In this study, for the first time, Flt3L was locally applied in the trachea of rats using a single dose only. A dose-dependent increase not only of DC, but also of T lymphocytes (CD4(+) and CD8(+)), was seen with a maximum on day 3. The effects on the cells in the lung interstitium and the bronchoalveolar space showed some differences. The use of tetanus toxoid as a model Ag applied intratracheally after the local Flt3L stimulation resulted in increased levels of specific IgA and IgG in the lung. Thus, this novel approach of locally stimulating APCs by topical application of a DC growth factor before applying the Ag offers a new vaccination strategy.

Adjuvants, Immunologic↗

Carcinogenicity of single and multiple intratracheal instillations of cadmium oxide in the rat.

The carcinogenic effects of single or multiple exposures to intratracheally instilled cadmium oxide, resulting in total doses of 0, 25, 50, and 75 micrograms, were studied in groups of 41 to 48 male Fischer rats. Pulmonary-deposited cadmium oxide did not result in increased numbers of tumors, except in the mammary gland or in rats that had three or more tumor types. Cadmium oxide was not carcinogenic in the lung, liver, kidney, or prostate gland of rats.

Animals↗

The role of infection in the pathogenesis of acquired tracheal stenosis.

A rabbit model was developed to study the role of infection in the development of postintubation acquired subglottic and tracheal stenosis. Following a surgically induced tracheal mucosal injury, rabbits were divided into three groups. Five animals underwent intratracheal bacterial inoculation using Staphylococcus aureus, six rabbits were given prophylactic antibiotics, and five control animals received neither bacteria nor antibiotics. After 10 days the rabbits were assessed for both tracheal stenosis and bacterial infection within the respiratory tree. Animals receiving antibiotic prophylaxis had a mean stenosis of 50.8%, similar to the 63.4% observed in controls. Rabbits inoculated with SA had a mean stenosis of 85.0%, greater than both the other groups (P = .001:ANOVA). Considering all animals, those with respiratory infection (including two control rabbits) had narrower stenoses than those that remained noninfected (82.1% versus 52.5%; P = .001). These data suggest that bacterial infection in the upper respiratory tract might increase the severity of airway stenosis following prolonged endotracheal intubation.

Animals↗

Endotracheal tube with movable blocker to prevent aspiration of intratracheal bleeding.

A newly developed endotracheal tube with a movable blocker was found to be lifesaving in patients with copious and persistent intratracheal bleeding. The cases of 4 patients are presented. In 3 patients, severe intratracheal bleeding was attributed to the extensive bronchopulmonary laceration caused by blunt chest trauma. In the remaining patient, the bleeding was due to rupture of the sutured site in the right pulmonary artery; the rupture was caused by a postoperative bronchopleural fistula. In these patients, spread of blood was completely prevented and pulmonary resection was performed safely by using the blocker in this new device.

Adult↗

Transepithelial migration of neutrophils in response to leukotriene B4 is mediated by a reactive oxygen species-extracellular signal-regulated kinase-linked cascade.

The epithelial cells that form a barrier lining the lung airway are key regulators of neutrophil trafficking into the airway lumen in a variety of lung inflammatory diseases. Although the lipid mediator leukotriene B(4) (LTB(4)) is known to be a principal chemoattractant for recruiting neutrophils to inflamed sites across the airway epithelium, the precise signaling mechanism involved remains largely unknown. In the present study, therefore, we investigated the signaling pathway through which LTB(4) induces transepithelial migration of neutrophils. We found that LTB(4) induces concentration-dependent transmigration of DMSO-differentiated HL-60 neutrophils and human polymorphonuclear neutrophils across A549 human lung epithelium. This effect was mediated via specific LTB(4) receptors and was inhibited by pretreating the cells with N-acetylcysteine (NAC), an oxygen free radical scavenger, with diphenylene iodonium (DPI), an inhibitor of NADPH oxidase-like flavoproteins, or with PD98059, an extracellular signal-regulated kinase (ERK) inhibitor. Consistent with those findings, LTB(4)-induced ERK phosphorylation was completely blocked by pretreating cells with NAC or DPI. Taken together, our observations suggest LTB(4) signaling to transepithelial migration is mediated via generation of reactive oxygen species, which leads to downstream activation of ERK. The physiological relevance of this signaling pathway was demonstrated in BALB/c mice, in which intratracheal instillation of LTB(4) led to acute recruitment of neutrophils into the airway across the lung epithelium. Notably, the response to LTB(4) was blocked by NAC, DPI, PD98059, or CP105696, a specific LTB(4) receptor antagonist.

Animals↗

Tumorigenesis by a ferroactinolite mineral.

In lifetime exposure of male Fischer-344 rats to ferroactinolite fibers and to UICC amosite asbestos fibers by means of intratracheal and intrapleural treatments, oncogenesis was greater in the lung for the ferroactinolite and in the pleura for the amosite. The lack of correlation between the effects of the two methods of exposure suggests that in this instance intrapleural inoculation was not a good predictor of pulmonary response on the basis of mass dose. Another feature of the ferroactinolite was that pleural tumors resulted from intratracheal instillations. Conversely, lung tumors or tumorlike lesions were also induced by intrapleural inoculations of ferroactinolite. These facts suggest a greater in vivo transport for the ferroactinolite than for the amosite. Since there are far fewer mineral fibers per mass unit in the ferroactinolite the tumor yield per unit of mineral fibers was strikingly greater by both routes of administration for ferroactinolite than for amosite.

Animals↗

A genetically-defined riboflavin auxotroph of Actinobacillus pleuropneumoniae as a live attenuated vaccine.

Actinobacillus pleuropneumoniae is a gram negative pleiomorphic rod that is the causative agent of a severe, highly infectious and often fatal pleuropneumonia in swine. We have previously reported the construction of genetically-defined stable riboflavin auxotrophs by replacement of a portion of the APP riboflavin biosynthetic operon (ribGBAH) with an antibiotic cassette encoding resistance to kanamycin, and have demonstrated that such riboflavin auxotrophs are avirulent. In this study, we evaluated riboflavin auxotrophs of A. pleuropneumoniae for their ability to stimulate protective immunity against pleuropneumonia. An initial challenge experiment demonstrated that intramuscular vaccination with a live attenuated serotype 1A rib mutant, in a vaccine formulation that included a limiting amount of exogenous riboflavin, provided better protection against challenge with virulent A. pleuropneumoniae than either intratracheal immunization or intramuscular immunization with live bacteria in the absence of exogenous riboflavin. Subsequent studies in which the vaccine inoculating dose, concentration of exogenous riboflavin, and serotype of the vaccine strain were varied demonstrated that immunization with live avirulent riboflavin auxotrophs could elicit significant protection against experimental challenge with both homologous and heterologous virulent serotypes of A. pleuropneumoniae.

Actinobacillus Infections↗

Intratracheal N-acetylcysteine use in infants with chronic lung disease.

To evaluate the effect of intratracheal administration of N-acetylcysteine (Mucomyst) on the clinical status, pulmonary function and gas exchange in premature infants with chronic lung disease, we conducted a randomized, placebo-controlled, crossover trial. Ten mechanically ventilated infants (gestational age 27 +/- 1 week; postnatal age 22 +/- 6 days) with clinical and radiological evidence of chronic lung disease and increased airway secretion were enrolled in the study. Each infant received tracheal administration of 5% N-acetylcysteine for one week and saline placebo every 4 h for another week. N-acetylcysteine was associated with a 59 +/- 26% increase in total airway resistance by the third day of treatment (p less than 0.01). A two-fold increase in airway resistance associated with an increased frequency of bradycardia and cyanosis spells was seen in two of the infants following three days of N-acetylcysteine administration, with a rapid improvement in their condition when subsequently switched to saline. Overall, N-acetylcysteine administration had no effect on the variables measured. We conclude that intratracheal administration of N-acetylcysteine to liquefy airway mucus neither improves the clinical condition nor hastens recovery in premature infants with chronic lung disease and its administration may lead to increased total airway resistance and cyanotic spells. The present data do not support the use of N-acetylcysteine as a mucolytic agent in premature infants with chronic lung disease.

Acetylcysteine↗

Effect of intratracheal injection of mica dust on the lymph nodes of guinea pigs.

Histopathological changes in the tracheo-bronchial lymph nodes were studied up to 365 days in guinea pigs following intratracheal injection of a suspension of mica dust. In general, the cytotoxic effect provoked by dust was not pronounced as the majority of the swollen dust-laden macrophages retained their normal structure at the termination of the experiment and fibrotic lesions were limited to the formation of thick reticulin fibers. The poor fibrogenic response of mica dust has been attributed to its low cytotoxicity.

Aluminum Silicates↗

Adenoviral delivery of human and viral IL-10 in murine sepsis.

Adenovirus (Ad) gene therapy has been proposed as a drug-delivery system for the targeted administration of protein-based therapies, including growth factors and biological response modifiers. However, inflammation associated with Ad transduction has raised concern about its safety and efficacy in acute inflammatory diseases. In the present report, intratracheal and i.v. administration of a first-generation adenoviral recombinant (E1,E3 deleted) either containing an empty cassette or expressing the anti-inflammatory cytokines viral or human IL-10 (IL-10) was administered to mice subjected to zymosan-induced multisystem organ failure or to acute necrotizing pancreatitis. Pretreatment of mice with the intratracheal instillation of Ad expressing human IL-10 or viral IL-10 reduced weight loss, attenuated the proinflammatory cytokine response, and reduced mortality in the zymosan-induced model, whereas pretreatment with a control adenoviral recombinant did not significantly exacerbate the response. Pretreatment of mice with pancreatitis using adenoviral vectors expressing IL-10 significantly reduced the degree of pancreatic and liver injury and liver inflammation when administered systemically, but not intratracheally. We conclude that adenoviral vectors can be administered prophylactically in acute inflammatory syndromes, and expression of the anti-inflammatory protein IL-10 can be used to suppress the underlying inflammatory process.

Adenoviridae↗

Intratracheal poly (ADP) ribose synthetase inhibition ameliorates lung ischemia reperfusion injury.

BACKGROUND: We previously demonstrated that intravenous poly (ADP) ribose synthetase (PARS) inhibition protects against experimental lung ischemia reperfusion injury (LIRI) in an in situ, hilar occlusion model. This study determined its efficacy when administered intratracheally (IT). METHODS: Left lungs of rats were rendered ischemic for 90 minutes, and reperfused for up to 4 hours. Treated animals received INO-1001, a PARS inhibitor, intratracheally 30 minutes before ischemia, while controls were given IT vehicle at equivalent volumes. All groups contained at least 4 animals. Lung injury was quantitated utilizing vascular permeability to radiolabeled albumin, tissue myeloperoxidase (MPO) content, alveolar leukocyte cell counts, and arterial pO(2) at 4 hours of reperfusion. Electrophoretic mobility shift assays (EMSA) assessed the nuclear translocation of NFkappaB and AP-1 in injured left lungs, while ELISAs quantitated secreted cytokine induced neutrophil chemoattractant (CINC) and MCP-1 protein in bronchoalveolar lavage fluid. RESULTS: Intratracheal PARS inhibition was 73% (p < 0.0001) and 87% (p < 0.0001) protective against increases in vascular permeability and alveolar leukocyte accumulation, respectively, and improved arterial pO(2) (p < 0.0004) at 4 hours of reperfusion. Myeloperoxidase (MPO) activity in treated lungs was reduced by 70% (p < 0.02). The nuclear translocation of NFkappaB and AP-1 was attenuated at 15 minutes of reperfusion, and the secretion of CINC and MCP-1 (p < 0.05) protein into the alveolus was diminished at 4 hours of reperfusion. CONCLUSIONS: Intratracheal INO-1001 protects against experimental LIRI. The reduction in secreted chemokine protein at 4 hours of reperfusion appears to be mediated at the pretranscriptional level through attenuated NFkappaB and AP-1 activation. This route may optimize future donor organ management and improve lung recipient outcomes.

Animals↗

Deficient in vitro and in vivo phagocytosis of apoptotic T cells by resident murine alveolar macrophages.

Apoptotic lymphocytes are readily identified in murine lungs, both during the response to particulate Ag and in normal mice. Because apoptotic lymphocytes are seldom detected in other organs, we hypothesized that alveolar macrophages (AMphi) clear apoptotic lymphocytes poorly. To test this hypothesis, we compared in vitro phagocytosis of apoptotic thymocytes by resident AMphi and peritoneal macrophages (PMphi) from normal C57BL/6 mice. AMphi were deficient relative to PMphi both in percentage containing apoptotic thymocytes (19.1 +/- 1% vs 96 +/- 2.6% positive) and in phagocytic index (0.23 +/- 0.02 vs 4.2 +/- 0.67). This deficiency was not due to kinetic differences, was seen with six other inbred mouse strains, and was not observed using carboxylate-modified polystyrene microbeads. Annexin V blockade indicated that both Mphi types cleared apoptotic T cells by a mechanism involving phosphatidylserine expression. By contrast, neither mAb blockade of a variety of receptors (CD11b, CD29, CD51, and CD61) known to be involved in clearance of apoptotic cells, nor the tetrapeptide RGDS (arginine-glycine-aspartic acid-serine) blocked ingestion by either type of macrophage. To confirm these studies, apoptotic thymocytes were given intratracheally or i.p. to normal mice, and then AMphi or PMphi were recovered 30-240 min later. Ingestion of apoptotic thymocytes by AMphi in vivo was significantly decreased at all times. Defective ingestion of apoptotic lymphocytes may preserve AMphi capacity to produce proinflammatory cytokines in host defense, but could contribute to development of autoimmunity by failing to eliminate nucleosomes.

Animals↗

Differential induction of squamous cell carcinomas and adenocarcinomas in mouse lung by intratracheal instillation of benzo(a)pyrene and charcoal powder.

Differential induction of squamous cell carcinomas, adenomas, and adenocarcinomas was observed in the lungs of male C57BL/6 and C3H/He mice after repeated intratracheal instillation of benzo(a)pyrene (BP) and charcoal powder suspended in 0.9% NaCl solution. when a high dose of BP (1.0 mg BP and 0.5 mg charcoal powder) was instilled intratracheally once a week for 8 weeks or when a low dose of BP (0.5 mg BP and 0.5 mg charcoal powder) was instilled once a week for 16 weeks, squamous cell carcinomas were induced in high incidence (77 to 87%) in the early period of observation, whereas pulmonary adenomas and adenocarcinomas were induced in low incidence (0. to 48%) in the late period of observation in both strains of mice. On the other hand, when a low dose of BP was instilled intratracheally once a week for 8 weeks, pulmonary adenomas and adenocarcinomas were induced in high incidence (76 to 91%), but squamous cell carcinomas were induced in low incidence (9 to 26%). These results show that a larger quantity of BP instilled intratracheally was needed for induction of squamous cell carcinomas than for induction of adenomas and adenocarcinomas in the lung of mice. Thus, when the carcinogen is administered to a single organ of a single mouse strain by the same route, different amounts of carcinogen have different effects on the incidences of various histological types of tumors.

Adenocarcinoma↗

Pulmonary cystic keratinizing squamous cell lesions of rats after inhalation/instillation of different particles.

Cystic keratinizing squamous cell lesions from three inhalation studies (Study A, B, C) and one intratracheal instillation study (Study D) in rats were reclassified and a certain number of lesions examined immunohistochemically for PCNA (proliferating cell nuclear antigen) as a marker of cellular proliferation. The following classification was used: squamous cell metaplasia with marked keratinization, keratinizing cyst, cystic keratinizing epithelioma, cystic keratinizing squamous cell carcinoma, keratinizing squamous cell carcinoma and non-keratinizing squamous cell carcinoma. In study A (inhalation of coal oven exhaust and subcutaneous injection of a high dose of DB (ah)A) 49.3% of rats developed cystic keratinizing squamous cell carcinomas. Inhalation of coal oven exhaust gas together with intratracheal instillation of crocidolite or subcutaneous injection of a low dose DB(ah)A (dibenz(ah)anthracene) resulted in cystic keratinizing squamous cell carcinomas in 23% to 24% of the rats. High incidences of cystic squamous cell carcinomas in the range of 31.9% to 76.4% were observed in rats of Study B1 after a 10-months exposure to tar/pitch condensation aerosol (different B(a)P (benzo(a)pyrene) concentrations) with added carbon black in some groups. After a 20-months exposure period to the same inhalation atmospheres (Study B2) the incidence of squamous cell carcinomas was increased up to 95.8%. Exposure of rats to various concentrations of unfiltered diesel exhaust (Study C) resulted in incidences of cystic keratinizing epitheliomas ranging from 2.5% (2.5 mg/m3) to 10.7% (7.5 mg/m3). Epitheliomas were also observed in 16.2% of carbon black and 16.0% of titanium dioxide exposed rats. Only a few cystic keratinizing squamous cell carcinomas occurred. In the intratrachel instillation study (Study D) increased incidences of cystic keratinizing epitheliomas occurred in rats exposed to native diesel exhaust particles (16.7%), high dose of extracted diesel exhaust particles (14.6%), extracted printex 90-carbon black particles (18.8%), and extracted printex 90-carbon black particles + B(a)P (18.8%). High indicences of cystic keratinizing squamous cell carcinomas were noted in rats that received 15 mg B(a)P (14.6%) or 30 mg B(a)P (72.7%) intratracheally. Immunohistochemical labeling of nuclei with PCNA demonstrated proliferative activity in one or two (and focally more than two) peripheral cell layers of cystic keratinizing epitheliomas and in more than three peripheral cell layers of cystic keratinizing squamous cell carcinomas and keratinizing squamous cell carcinomas. The wall of keratinizing cysts showed no or a weak reaction.

Administration, Inhalation↗

Diaphragmatic activity during REM sleep in the adult cat.

Diaphragmatic electromyograms from five adult cats were studied to determine whether diaphragmatic activity, like central respiratory activity, increases in rapid-eye-movement (REM) sleep. Breaths with inspiratory durations between 250 and 2,000 ms were analyzed. 1) There was a greater slope of the moving time average of diaphragmatic activity in REM than in non-REM (NREM) sleep. These greater slopes occurred whether the route of breathing was through the upper airways or through an endotracheal tube and may have resulted from early recruitment of motor units. 2) Mean diaphragmatic activity was also greater, but other variables (peak activity, the area under the curve of diaphragmatic activity, mean intratracheal pressures, inspiratory airflow rates, and tidal volumes) were not greater in REM than in NREM sleep. 3) Diaphragmatic activity was similar in REM sleep and active wakefulness. 4) Across states, slope of the moving time average varied with the duration of inspiration: greater slopes were associated with shorter breaths. These results are consistent with an increase in central respiratory drive in REM sleep that increases the rate of rise of diaphragmatic activity.

Airway Resistance↗

An in vivo model of beta-adrenoceptor desensitization.

Chronic use of beta2-agonists and increased production of inflammatory mediators during the late allergic reaction after antigen challenge results in the desensitization of beta-adrenoceptors in the airways and the accompanying rise in nonspecific airway hyperresponsiveness. In this study, we established an in vivo model of beta2-adrenoceptor desensitization in guinea pig airways by administration of IL-1beta intratracheally or chronic albuterol by inhalation. In the establishment of beta-adrenoceptor desensitization in response to both beta-agonist or inflammatory mediator, baseline pulmonary function responses were established to methacholine and isoproterenol-induced relaxation of methacholine bronchoconstriction. This was followed by the administration of IL-1beta (500 IU/d intratracheally for 2 days) or chronic albuterol (0.1 g/L by aerosol for 1 min three times a day for 10 days). After administration, the methacholine and isoproterenol-methacholine response was once again evaluated. Intratracheal administration of IL-1beta or chronic administration of albuterol significantly decreased (p < 0.05) the protective effect of isoproterenol on methacholine-induced bronchoconstriction, eliciting beta-adrenoceptor desensitization in vivo. The in vivo model will be very useful in monitoring the effect of other potential drugs on beta-adrenoceptor function in the airways.

Administration, Inhalation↗

Esophageal tracheal combitube, endotracheal airway, and mask: comparison of ventilatory pressure curves.

The esophageal tracheal Combitube (ETC) is a new airway especially designed for airway maintenance and ventilation in unconscious patients such as those requiring CPR. The ETC may be used as an esophageal obturator or an endotracheal airway. Previous studies yielded a significantly higher mean arterial oxygen tension (PaO2) during ventilation using an ETC in the esophageal position compared to a conventional endotracheal airway (ETA). To investigate this phenomenon, endotracheal and airway opening pressures were examined in 12 patients in randomized order during ventilation with an ETC in the esophageal position, with an ETA, and with a mask, respectively. In this study again the PaO2 was higher with ETC compared to ETA. The following differences in intratracheal pressure and flow could be found for ETC when compared to ETA: smaller rising pressure during inspiration, prolonged expiratory flow time, and formation of a small positive end expiratory pressure (PEEP). These factors may be responsible for the improved oxygen tension with ETC. Comparing mask to ETC ventilation, PaO2 did not differ; however, mean arterial carbon dioxide tension was higher during mask ventilation.

Adult↗