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PubMed1994

Protection against oxygen toxicity by tracheal insufflation of endotoxin: role of Mn SOD and alveolar macrophages.

Endotoxin and the cytokines, tumor necrosis factor and interleukin-1, are known to protect adult rats against O2 toxicity. However, whether the effect of endotoxin is mediated through its direct effect on lung cells or through cytokines is not clear. In this study, we demonstrated that endotoxin at a dosage of 5 micrograms/rat (14-20 micrograms/kg) attenuated O2-induced pulmonary injury and markedly prolonged the survival of rats exposed to 100% O2. Endotoxin was more protective when given by intratracheal insufflation or intravenous injection than by intraperitoneal injection. The endotoxin-induced O2 tolerance was associated with a selective enhancement of pulmonary manganese superoxide dismutase, but not Cu,Zn SOD, mRNA. In addition, depletion of 84% rat alveolar macrophages by liposome-encapsulated dichloromethylene diphosphonate, resulted in a marked reduction (86%) of endotoxin-induced release of tumor necrosis factor into the alveolar space. However, endotoxin was still protective in these alveolar macrophage-depleted animals.

Animals↗

PubMed1994

Respiratory aflatoxicosis: suppression of pulmonary and systemic host defenses in rats and mice.

Dietary aflatoxin B1 (AFB1) exposure impairs innate and acquired host defenses resulting in increased susceptibility to infections in domesticated animals. Experimental studies have confirmed this observation by demonstrating the immunosuppressive effects of AFB1 ingestion. In addition to being present in dietary components, AFB1 is also found in significant amounts in respirable particles of grain dust. To determine the effect of respiratory tract exposure to AFB1 on host defenses, rats and mice were exposed either by aerosol inhalation or intratracheal instillation to AFB1. Nose-only inhalation exposure of rats to AFB1 aerosols suppressed alveolar macrophage (AM) phagocytosis at an estimated dose of 16.8 micrograms/kg with the effect persisting for approximately 2 weeks. To determine whether another mode of respiratory tract exposure, intratracheal instillation, reflected inhalation exposure, animals were treated with increasing concentrations of AFB1 which also suppressed AM phagocytosis in a dose-related manner albeit at doses at least an order of magnitude more than that obtained by aerosol inhalation. Intratracheal administration of AFB1 also suppressed the release of tumor necrosis factor-alpha from AMs and impaired systemic innate and acquired immune defenses as shown, respectively, by suppression of peritoneal macrophage phagocytosis and the primary splenic antibody response. These findings demonstrate that experimental respiratory tract exposure to AFB1 suppresses pulmonary and systemic host defenses and indicates that inhalation exposure to AFB1 is an occupational hazard where exposure to AFB1-laden dust is common.

Administration, Inhalation↗

PubMed1991

Lung uptake of liposome-entrapped glutathione after intratracheal administration.

The intratracheal delivery of glutathione (GSH), in liposome-encapsulated form, prolongs retention of the drug in the rat lung. This study has been designed to determine the extent and time-course of pulmonary tissue uptake of administered 14C-labelled liposomes containing [3H]GSH. Liposomes, composed of dimyristoylphosphatidylcholine (DMPC), dipalmitoylphosphatidylcholine and distearoylphosphatidylcholine each with or without 30 mol% cholesterol showed a clearance greater than 80% from the bronchoalveolar lavage, 24 h after intratracheal instillation. Lung tissue content of 14C-lipid increased with time: by 72 h, 42-56% of the administered dose was recovered from the tissue. [3H]GSH was present in pulmonary tissue in relatively constant amounts throughout the 72 h, ranging from 14-35% of the administered dose. Vesicles composed of DMPC had a low entrapment for GSH. There were only minor differences in GSH entrapment efficiency and lung tissue uptake between vesicles of the other lipid compositions.

Animals↗

PubMed1982

Pleural plaques in asbestosis: effect of Candida albicans.

Effect of chrysotile dust alone or together with Candida albicans administered intratracheally in guinea pigs was studied in the genesis of pleural plaques over a period of 12 months. A significant increase of mucopolysaccharides, phosphorus, calcium and -SH content was detected in pleural fluid of animals treated with chrysotile and Candida albicans together than in those treated with chrysotile or Candida albicans alone. The results suggest that an infection of Candida albicans accentuates the effect of chrysotile by altering the biochemical parameters preceding to the formation of pleural plaques.

Animals↗

PubMed2004

Effect of mechanical ventilation on cytokine response to intratracheal lipopolysaccharide.

BACKGROUND: Mechanical ventilation may cause lung injury through the excitation of an inflammatory response and the release of mediators, such as cytokines. The authors tested the hypothesis that intratracheal lipopolysaccharide amplifies the cytokine response to mechanical ventilation. METHODS: Rat lungs were intratracheally instilled with lipopolysaccharide followed by ex vivo mechanical ventilation for 2 h with low tidal volume of 7 ml/kg with 3 cm H2O positive end-expiratory pressure (PEEP), high tidal volume of 40 ml/kg with zero PEEP, medium tidal volume of 15 ml/kg with 3 cm H2O PEEP, or medium tidal volume and zero PEEP. RESULTS: In the absence of lipopolysaccharide, lung lavage concentrations of tumor necrosis factor and interleukin 1 beta but not macrophage inflammatory protein 2 were significantly higher in lungs ventilated at high tidal volume/zero PEEP than at low tidal volume. There was a marked increase in lavage tumor necrosis factor and macrophage inflammatory protein 2 concentrations in lungs ventilated at low tidal volume after exposure to intratracheal lipopolysaccharide at doses of 100 ng/ml or greater. However, in lungs ventilated at high tidal volume, this response to lipopolysaccharide was markedly reduced. In addition, the number of alveolar macrophages recovered in the lavage was significantly lower in lungs ventilated at high tidal volume. CONCLUSION: Ventilation strategy can modify lung cytokine responses to lipopolysaccharide, likely through an effect on the alveolar macrophage population.

Administration, Inhalation↗

PubMed2007

Alcohol intoxication inhibits pulmonary S100A8 and S100A9 expression in rats challenged with intratracheal lipopolysaccharide.

BACKGROUND: Alcohol is known to inhibit the recruitment of polymorphonuclear leukocytes (PMNs) into tissue sites including the lung. During infection and inflammation, recruited neutrophils (PMNs) release S100 proteins that function to promote the recruitment of additional phagocytes. METHODS AND RESULTS: This study investigated the effects of alcohol intoxication on S100 protein production in the lung in response to lipopolysaccharide (LPS). Animals were administered alcohol (5.5 g/kg) or saline 30 minutes before intratracheal challenge with LPS (100 microg/rat). Alcohol suppressed PMN recruitment into the lung following intratracheal LPS, which was associated with an inhibition of increase in S100A8 levels in both the bronchoalveolar lavage (BAL) fluid and lysates of cells recovered by BAL at 90 minutes and 4 hours post-LPS challenge. S100A8 and S100A9 mRNA expression in cells recovered by BAL was significantly up-regulated at both 90 minutes and 4 hours after the LPS challenge, and alcohol also suppressed this response. In addition, intratracheal LPS caused a transient increase in S100A8 mRNA expression in circulating leukocytes at 90 minutes after the challenge. Similarly, this LPS-induced up-regulation of S100A8 mRNA expression was inhibited in rats intoxicated with alcohol. CONCLUSION: These data show that alcohol inhibits the S100 protein response in the lung, which may serve as a mechanism underlying alcohol-induced suppression of PMN recruitment into the terminal airways during pulmonary infection.

Alcoholic Intoxication↗

PubMed1982

Distribution and clearance of 63Ni administered as 63NiCl2 in the rat: intratracheal study.

Microgram amounts of nickel as 63NiCl2 were administered intratracheally to male rats. Regardless of time after instillation, the lungs and kidneys retained the greatest concentration of 63Ni, and 21 days after dose administration they were the only organs where 63Ni was still measurable. Urinary excretion was the main excretion route with 72% of the initial body burden eliminated by the urine at one day. By day 21, almost all 63Ni was excreted in the urine (96.5% of the initial body burden). The lungs retained 29% of their initial (35 min) burden at day 1, decreasing to 0.1% on day 21.

Animals↗

PubMed1982

Studies in transtracheal ventilation catheters.

A study was undertaken to assess the applicability of transtracheal ventilation in the instance of total upper airway obstruction. The effect of transtracheal jet ventilation through a variety of inflow catheters in the dog was studied. Arterial blood gas values, intratracheal pressure and minute ventilation were compared. Deflation of the airway through an array of outflow needles was independently assessed. Hypercapnia, decreased minute ventilation, and prolonged inspiratory and expiratory durations impaired use of the smallest catheters. A dual-lumen needle, to provide exclusive respiratory access and support was then designed based on the preliminary data. Prolonged transtracheal jet ventilation with a totally obstructed upper airway was successfully conducted in a live canine subject. A review of the literature is presented.

Airway Obstruction↗

PubMed1994

Performance characteristics of a novel reusable intermediate-volume low-pressure cuffed endotracheal tube.

STUDY OBJECTIVE: To evaluate the performance of the reusable intermediate-volume low-pressure cuffed "Super Safety Yellow" (Willy Rüsch AG, P.O. Box 1620, D-71332 Waiblingen, Germany) endotracheal tube with regard to cuff seal, tube tip position, and incidence of postoperative throat complaints. The "Super Safety Yellow" was compared with the "Super Safety Clear" (W. Rüsch AG), the "lo-pro (Mallinckrodt Laboratories, Cornamady, Athlone County, Ireland), and the "red rubber" (W. Rüsch AG) tubes. METHODS: Two hundred adult patients scheduled for minor surgery under standardized general anaesthesia were allocated to one of these tubes. Past-cuff leakage (indicator; orally instilled 0.2% indigocarmine) as well as intratracheal tube tip position (degree of being centred) were assessed by fibre-optic tracheoscopy. The semi-standardized interviews for the recording of postoperative sore throat were performed in double-blind fashion once a day, starting on the day of operation till p.o. day 3. STATISTICS: chi 2-test; significance: P < 0.05. MAIN RESULTS: A past-cuff leakage was found in three "red rubber" tubes. There were significant differences in tube tip position with the "Super Safety Clear" being best, and the "Super Safety Yellow" being worst centred (P = 0.010). The incidence of postoperative throat complaints showed a nonsignificant tendency in favour of the PVC-tubes. A significant number of such complaints were observed in women (P = 0.0004) and in obese patients (P = 0.011). By contrast, this incidence did not significantly differ with age, tracheal cross-sectional shape, tube tip position, use of atropine, and duration of intubation. CONCLUSION: Although resembling the "red rubber" tube in the incidence of postoperative throat complaints, the "Super Safety Yellow" may be an alternative to the currently used disposable tubes in anaesthesia. Its performance is comparable with regard to cuff seal and intra-cuff pressure. Additionally, it helps in reducing PVC waste and may lessen costs.

Adult↗

PubMed2001

Evidence of a no-effect level in silica-induced rat lung mutagenicity but not in fibrogenicity.

Exposure to silica can lead to fibrosis and the development of lung tumors in the rat. Based on these animal studies and on epidemiological data, silica has been classified as a human carcinogen. The initial mechanisms have not been finally clarified, but particle-induced tumor formation is at least closely associated with inflammation, the production of reactive oxygen species (ROS) and DNA damage. We investigated the dose-dependent effects of silica on the formation of the major DNA oxidation product 8-oxoguanine (8-oxo-Gua) in rat lung cells, on p53 (p53) and p53 mutant protein (p53 mut) synthesis, as well as on the amount of the surfactant phospholipids phosphatidylinositol (PI) and phosphatidylglycerol (PG) in the bronchoalveolar lavage fluids (BALF) as indicators of fibrotic processes in the lung. Rats were exposed by intratracheal instillation to various amounts of DQ12 quartz (0.15, 0.3, 0.6, 1.2, 2.4 mg/animal) and lungs were investigated after 21 and 90 days. PG decreased and PI increased quartz dose dependently. 8-oxoGua was significantly increased only after 1.2 and 2.4 mg quartz/animal. Cells expressing p53 protein were increased at 1.2 and 2.4 mg, p53 mutant protein only at 2.4 mg/animal. This indicates a no-effect level for mutagenicity at a low, but still fibrogenic quartz exposure.

Animals↗

PubMed1996

Intratracheal administration of DBcAMP attenuates edema formation in phosgene-induced acute lung injury.

Phosgene, a toxic gas widely used as an industrial chemical intermediate, is known to cause life-threatening latent noncardiogenic pulmonary edema. Mechanisms related to its toxicity appear to involve lipoxygenase mediators of arachidonic acid (AA) and can be inhibited by pretreatment with drugs that increase adenosine 3',5'-cyclic monophosphate (cAMP). In the present study, we used the isolated buffer-perfused rabbit lung model to investigate the mechanisms by which cAMP protects against phosgene-induced lung injury. Posttreatment with dibutyryl cAMP (DBcAMP) was given 60-85 min after exposure by an intravascular or intratracheal route. Lung weight gain (LWG) was measured continuously. AA metabolites leukotriene (LT) C4, LTD4, and LTE4 and 6-ketoprostaglandin F1 alpha were measured in the perfusate at 70, 90, 110, 130, and 150 min after exposure. Tissue malondialdehyde and reduced and oxidized glutathione were analyzed 150 min postexposure. Compared with measurements in the lungs of rabbits exposed to phosgene alone, posttreatment with DBcAMP significantly reduced LWG, pulmonary arterial pressure, and inhibited the release of LTC4, LTD4, and LTE4. Intratracheal administration of DBcAMP was more effective than intravascular administration in reducing LWG. Posttreatment also decreased MDA and protected against glutathione oxidation observed with phosgene exposure. We conclude that phosgene causes marked glutathione oxidation, lipid peroxidation, release of AA mediators, and increases LWG. Posttreatment with DBcAMP attenuates these effects, not only by previously described inhibition of pulmonary endothelial or epithelial cell contraction but also by inhibition of AA-mediator production and a novel antioxidant effect.

6-Ketoprostaglandin F1 alpha↗

PubMed1995

Is tracheal gas insufflation an alternative to extrapulmonary gas exchangers in severe ARDS?

Tracheal gas insufflation (TGI) of pure oxygen combined with mechanical ventilation decreases dead space and increases CO2 clearance. In the present study, TGI was used in six patients with ARDS who met extracorporeal membrane oxygenation criteria and who were severely hypoxemic and hypercapnic despite optimal pressure-controlled ventilation. This open clinical study aimed to investigate the effects of 4 L/min continuous flow of oxygen given via an intratracheal catheter. PaCO2 decreased from 108 +/- 32 to 84 +/- 26 mm Hg (p < 0.05), and no significant change in PaO2 (68 +/- 18 vs 96 +/- 43, p = 0.06). There was no change in airway pressures and hemodynamic variables. A slight increase in end-expiratory and end-inspiratory volumes with TGI possibly occurred, as seen on tracings from respiratory inductive plethysmography (Respitrace). We conclude that TGI improves tolerance of limited pressure ventilation by removing CO2, but it may induce changes in lung volumes that are not detected by ventilator measurements.

Adult↗

PubMed1997

Intraoperative monitoring of the motor pathway using transtracheal stimulation of the cervical spine in dogs.

Although SEP monitoring of the spinal cord has been a well established method recently, not an ultimate, perfectly developed technique for monitoring of the motor system is known so far, particularly, because of the disturbing effect of narcotic drugs and relaxants on the motor evoked potentials. In this study the upper part of the spinal cord was stimulated in 14 anesthetized and relaxed dogs with a cathode attached to the intratracheal tube and an anode fixed to the cervical spinous processes. Single and serial stimuli were applied. Recordings were obtained from the exposed right femoral nerve and quadriceps muscle. Averaging was necessary when using serial stimulations. Responses were consequent and reproducible during regular anesthesia. The origin of the different responses in the spinal cord is discussed. The method seems to be appropriate for intraoperative monitoring of the thoracolumbar spine.

Anesthesia, General↗

PubMed2003

Role of endogenous adenosine in the acute and late response to allergen challenge in actively sensitized Brown Norway rats.

1. Endogenous adenosine has been suggested to amplify the response of airway mast cells to allergen in vivo. We have sought evidence for this by monitoring the acute and late-phase response to allergen in Brown Norway (BN) rats actively sensitised to ovalbumin (OA) and treated either with adenosine deaminase (ADA) linked covalently to polyethylene glycol (PEG-ADA; Adagen) to decrease adenosine availability or with erythro-9-(2-hydroxy-3-nonyl)adenine (EHNA), an inhibitor of ADA, plus S-(4-nitrobenzyl)-6-thioinosine (NBTI), an inhibitor of facilitated adenosine transport, to increase adenosine availability. 2. The cardiovascular effects of adenosine (0.01-3 mg kg(-1) i.v.) were significantly reduced in PEG-ADA-treated animals and augmented in EHNA/NBTI-treated animals. The difference in sensitivity to adenosine in the treated groups was 33- and 15-fold, at the level of 30% reduction in blood pressure and heart rate, respectively. 3. The acute response to allergen, given either intravenously or intratracheally, was quantified as bronchoconstriction. The late phase to allergen was measured as the influx and activation of immunoinflammatory cells into the bronchoalveolar lavage fluid 24 h after challenge. 4. Despite evidence of a substantial difference in adenosine availability following pretreatment with PEG-ADA or EHNA/NBTI, there were no differences in either the acute or late response to allergen in the actively sensitised BN rat. 5. Our data suggest no role for endogenous adenosine in determining the response to allergen under our experimental conditions.

Adenosine↗

PubMed1999

Tyloxapol confers durable protection against hyperoxic lung injury in the rat.

We tested the hypothesis that the nonlipid components of Exosurf, tyloxapol (TY), and cetyl alcohol (CA), protect against hyperoxic lung injury by induction of the animals' endogenous antioxidant defenses. Adult rats were intratracheally instilled with escalating doses of TY and CA (n = 20) or TY alone (n = 32) and immediately exposed to 100% oxygen. Intratracheal instillation of TY alone or in combination with CA protected against lethal hyperoxic injury in the rat in a dose-dependent fashion. To assess the effects of timing, rats were instilled with TY plus CA 24 hours before (n = 6) and 24 hours after (n = 6) exposure to 100% oxygen, with time to death determined. Rats were also instilled with TY alone at 0 hour (n = 6), 48 hours (n = 3), 96 hours (n = 3), and 186 hours (n = 4) prior to exposure to 100% oxygen. Lungs were assayed for superoxide dismutase, glutathione peroxidase, and catalase activities. Finally, the pharmacokinetics of TY in the rat lung were determined by instilling radiolabelled TY intratracheally. TY has a prolonged half-life in the rat lung, and protection against lethal hyperoxic injury was achieved by a single intratracheal dose delivered up to 186 hours prior to injury. Antioxidant enzymes were not induced in protected animals. We conclude that TY provides durable protection against hyperoxic lung injury without induction of antioxidant enzymes. It is present in the lung for sufficient duration to invoke a direct mechanism of protection, possibly as a radical scavenger. These findings raise the prospect of a therapeutic application for TY as prophylaxis in patients at risk for oxygen toxicity and adult respiratory distress syndrome.

Animals↗

PubMed1988

Parameters of Mycoplasma pneumoniae infection in Syrian hamsters.

An animal model for evaluating the potency of Mycoplasma pneumoniae vaccines was developed with hamsters. Factors that influence hamster infection by M. pneumoniae were defined, and parameters for assessment of intensity of pulmonary disease were established. Colonization of hamster lungs was determined by culture, and intensity of lung disease was assessed histopathologically and expressed numerically as a lung pathological score. Intratracheal inoculation of the challenge was superior to the intranasal or aerosol route for inducing a consistent degree of lung disease. A challenge dose of 10(6) CFU inoculated intratracheally produced lung colonization and significant reproducible lung pathological scores in essentially all unvaccinated animals. The peak of infection, as determined by these criteria, was at about 2 weeks after challenge. Animals over 6 weeks of age were preferable for the test, since younger animals exhibited a lower lung pathological score even though they showed the same degree of lung colonization. The hamster assay developed provides a dependable experimental system for testing the protective potency of M. pneumoniae vaccines.

Administration, Inhalation↗

PubMed2006

Development of dry powder inhalation system of novel vasoactive intestinal peptide (VIP) analogue for pulmonary administration.

Vasoactive intestinal peptide (VIP) exerts a relaxing action on tracheal smooth muscle which is mediated through interaction with VIP receptors. The deficiency of VIP in the airways has been implicated in the pathogenesis of asthma. Thus, the administration of VIP may be useful for the therapy of pulmonary diseases. However, the therapeutic application of VIP is largely limited by its rapid degradation in addition to the systemic adverse effects due to the wide distribution of VIP receptors. To overcome these problems, we succeeded to synthesize a novel VIP derivative of VIP, [R15, 20, 21, L17]-VIP-GRR (IK312532), and to prepare its dry powder for the topical administration to the lung. The physicochemical properties of dry powder were evaluated by laser diffraction and cascade impactor. The laser diffraction analysis indicated that the carrier and fine particles had median diameter of 65.6 and 4.5 microm, respectively, and the air flow at the pressure of 0.15 MPa or higher resulted in the high dispersion and significant separation of fine particle containing peptide from the carrier molecule. The cascade impactor analysis clearly showed the high emission of dry powder from capsule and the deposition of peptide on stages 3 of the cascade impactor. The intratracheal administration of dry powder inhaler (DPI) of VIP or IK312532 brought about a significant decrease of maximal number of binding sites (Bmax) for [125I]VIP in anterior and posterior lobes of rat right lung, suggesting a significant occupancy of lung VIP receptors. This effect by IK312532-DPI compared with VIP-DPI lasted for a longer period. Thus, IK312532-DPI may be a pharmacologically useful drug delivery system for the VIP therapy of pulmonary diseases such as asthma.

Administration, Inhalation↗

PubMed1976

Predicting the risk of tumor occurrence under the effect of small doses of carcinogens.

Basic methodological approaches were formulated for determining the permissible levels of carcinogens in man's environment on the basis of current experimental oncological data dealing with the interaction of the organism and carcinogenic compounds. The tumor is proposed as a specific index of the harmfulness criterion of carcinogenic action. Under these conditions, both the frequency and the development time of tumors must be considered. Results are given of an experimental study of the carcinogenic activity of various doses of benz[a]pyrene (0.005, 0.02, 0.1, 0.5, and 2.5 mg) on rats by using a tenfold intratracheal administration. On the basis of mathematical models of the obtained dose-time-effect relationship, the risk of cancer occurrence due to small carcinogen doses is predicted. Small doses were not tested in the experiment. On the basis of the data obtained in the experiment, a maximally permissible concentration of benz a pyrene in the ambient air can be determined. A benz[a]pyrene dose of 0.02 mg is recommended as the basis of the calculation. The effect of this dose is shown at time periods longer than the limits of human life.

Animals↗