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PubMed1983

[Serum gentamicin level after intratracheal application in ventilated patients with normal and reduced kidney function].

In a prospective study, serial serum determinations of gentamicin were made after its intratracheal application (40 mg/8 h) to 14 patients on ventilators (seven with normal renal function, seven with compensated, preterminal or dialysis-requiring renal failure). The patients with normal renal function had no therapeutic or toxicologically significant gentamicin concentration in their serum: less than 0.1 mg/l, in one case maximally 0.67 mg/l. But in patients with renal failure even the first gentamicin dose increased the serum level up to 1.5 mg/l. After repeated endotracheal application gentamicin accumulation in serum led to maximal values of 6.2 mg/l after the sixth and 7.5 mg/l after the seventh dose. The absorption of the drug from the tracheobronchial system differed between individuals. Thus serum concentrations were reached in patients with renal failure which are systemically effective and potentially toxic.

Adult↗

PubMed1996

Lung inflammation after exposure to nonfibrous silicates increases with chelatable [Fe3+].

Lung exposures to complexes of coordinated iron can be associated with a neutrophilic alveolitis. We tested the hypothesis that lung inflammation after intratracheal instillation of mineral oxides in rats increases with surface-complexed [Fe3+]. The 10 mineral oxides employed had measurable [Fe3+] complexed to the dust surface. The metal was incompletely coordinated, as demonstrated by the ability of the particles to catalyze electron transfer and generate thiobarbituric acid (TBA) reactive products of deoxyribose. After exclusion of those silicates containing structural iron within the crystal lattice, there was a significant correlation between the concentration of chelatable metal and TBA-reactive products (r = 0.82; p = .04). Four days after intratracheal instillation of the 10 mineral oxide particles into rats, lavage neutrophils and protein were significantly increased for all dusts compared to injected saline. Among those dusts with no structural iron, the correlation between chelatable iron concentrations and percentage neutrophils did not reach significance (r = 0.73; p = .10), but that between metal and lavage protein did (r = 0.80; p = .05). We conclude that (1) mineral oxides complex iron cations at the surface, (2) in vitro measures of oxidant generation increase with the concentration of surface iron among those dusts with no structural iron, and (3) acute inflammation following introduction of these particles into the lower respiratory tract also increases with surface iron concentrations among those mineral oxides with no structural iron.

Animals↗

PubMed1990

Errors in tracheal pressure recording in patients with a tracheostomy tube--a model study.

The recording of intratracheal pressure in patients breathing through a tracheostomy tube is marred by methodological problems. In model experiments it has been shown that the introduction of a recording catheter into the tracheostomy tube alters the recorded pressure by as much as 20-40%. To avoid such inaccuracy, a specially designed tracheostomy tube is proposed with an externally placed channel for introduction of the recording catheter. In in vivo measurements, recordings can be made at a distance of up to about 20 mm below the end of tube. Pressure recordings from this part of a model trachea are compared with results obtained from a reference pressure port 100 mm below the tube ending. The results show that it is possible to record expiratory pressure with good accuracy but that inspiratory pressure is still overestimated by 9-16%.

Airway Resistance↗

PubMedDate not supplied

Clenbuterol in the horse: confirmation and quantitation of serum clenbuterol by LC-MS-MS after oral and intratracheal administration.

Clenbuterol is a beta2 agonist/antagonist bronchodilator, and its identification in post-race samples may lead to sanctions. The objective of this study was to develop a specific and highly sensitive serum quantitation method for clenbuterol that would allow effective regulatory control of this agent in horses. Therefore, clenbuterol-d9 was synthesized for use as an internal standard, an automated solid-phase extraction method was developed, and both were used in conjunction with a multiple reaction monitoring liquid chromatography-tandem mass spectrometry (LC-MS-MS) method to allow unequivocal identification and quantitation of clenbuterol in 2 mL of serum at concentrations as low as 10 pg/mL. Five horses were dosed with oral clenbuterol (0.8 microg/kg, BID) for 10 days, and serum was collected for 14 days thereafter. Serum clenbuterol showed mean trough concentrations of approximately 150 pg/mL. After the last dose on day 10, serum clenbuterol reached a peak of approximately 500 pg/mL and then declined with a half-life of approximately 7 h. Serum clenbuterol declined to 30 and 10 pg/mL at 48 and 72 h after dosing, respectively. By 96 h after dosing, the concentration was below 4 pg/mL, the limit of detection for this method. Compared with previous results obtained in parallel urinary experiments, the serum-based approach was more reliable and satisfactory for regulation of the use of clenbuterol. Clenbuterol (90 microg) was also administered intratracheally to five horses. Peak serum concentrations of approximately 230 pg/mL were detected 10 min after administration, dropping to approximately 50 pg/mL within 30 min and declining much more slowly thereafter. These observations suggest that intratracheal administration of clenbuterol shortly before race time can be detected with this serum test. Traditionally, equine drug testing has been dependent on urine testing because of the small volume of serum samples and the low concentrations of drugs found therein. Using LC-MS-MS testing, it is now possible to unequivocally identify and quantitate low concentrations (10 pg/mL) of drugs in serum. Based on the utility of this approach, the speed with which new tests can be developed, and the confidence with which the findings can be applied in the forensic situation, this approach offers considerable scientific and regulatory advantages over more traditional urine testing approaches.

Administration, Oral↗

PubMed1991

The frequency of spontaneously-occurring neoplasms in the male Syrian golden hamster.

The frequency of spontaneously-occurring neoplasms in the male Syrian golden hamster, often used as a control in carcinogenic studies, was examined. The hamsters were divided into 2 groups: Group 1 received 0.1 ml of the phosphate buffer vehicle intratracheally once a week for 15 w; Group 2 received 0.1 ml of Tween 60:ethanol:buffer (5.3:8.7:100 by volume) in the same manner. The mean survival days of hamsters' total life-span were 574.9 +/- 176.1 d in Group 1 and 427.7 +/- 178.1 d in Group 2. Tumor incidence rates were 10.6% (16/148) in Group 1 and 11.5% (13/113) in Group 2. The mean survival days for tumor-bearing hamsters in Group 1 was 692.0 +/- 80.7 d and was 650.8 +/- 74.2 d in Group 2. Most tumors increased with advancing hamster age. The most common neoplasm was adrenal gland tumors (Group 1 = 4.7%, Group 2 = 8.8%). The occurrence of other tumors in other organs was low. The Syrian golden hamster is a suitable animal model for evaluating chemical carcinogenicity.

Adrenal Gland Neoplasms↗

PubMed1980

Controlled delivery of an antitumor drug: localized action of liposome encapsulated cytosine arabinoside administered via the respiratory system.

Cytosine arabinoside in free or liposome encapsulated form was administered to the lungs of rats via intratracheal instillation. The free drug rapidly left the lung (T 1/2 = 40 min), while the encapsulated drug remained in the lung for a prolonged period (T 1/2 = 8 hr). Free cytosine arabinoside effectively inhibited DNA synthesis (measured by [14C]thymidine incorporation) in the intestine and bone marrow as well as in the lung. By contrast, liposome-encapsulated drug effectively inhibited DNA synthesis in the lung, but similar doses failed to inhibit DNA synthesis in other tissues. The metabolism of free and encapsulated drug were similar in that the same products resulted, namely the inactive catabolite uracil-beta-D-arabinofuranoside and the phosphorylated anabolites of cytoside arabinoside. These results suggest that the action of an antitumor drug can be confined to a single organ through the use of a liposomal drug delivery system.

Animals↗

PubMed1996

Efficacy of dead-space washout in mechanically ventilated premature newborns.

The prosthetic dead space makes a significant contribution to the total dead space in low-birth-weight premature newborns receiving artificial ventilation in response to respiratory distress. Use of an endotracheal tube with capillaries molded into the tube wall enables washout of the dead space without insertion of a tracheal catheter. In 10 premature newborns (mean gestational age, 27.5 +/- 2.2 wk; mean weight, 890 +/- 260 g) receiving continuous positive-pressure ventilation (Paw = 12.7 +/- 1.8 cm H2O; FIO2 = 39 +/- 17%), tracheal gas insufflation (TGI) for CO2 washout was conducted using this technique. The flow of tracheal insufflation (0.5 L/min) was derived from the inspiratory line of the ventilator circuit and blown into the trachea. Intratracheal pressures showed little or no TGI-related modification ( < 1 cm H2O). A control system enabled TGI discontinuation in the event of a pressure rise. At constant ventilation pressure, PaCO2 decreased by 12.1 +/- 5.9 mm Hg (delta PaCO2 = -26 +/- 12%) under TGI, whereas PaO2 remained unchanged. While maintaining PaCO2 constant, peak inspiratory pressure (PIP) was decreased by 5.4 +/- 1.7 cm H2O (delta PIP = -22.0 +/- 8.3%). TGI showed immediate efficacy (PCO2 reduction of at least 5 mm Hg) in nine of the 10 newborns who then received chronic TGI (14 to 138 h). TGI appears to be an effective method, suitable for long-term clinical application, enabling a reduction in the aggressive nature of conventional ventilation.

Carbon Dioxide↗

PubMed2000

Mercaptoethylguanidine inhibits the inflammatory response in a murine model of chronic infection with Pseudomonas aeruginosa.

Chronic airway inflammation induced by Pseudomonas aeruginosa is the eventual cause of respiratory failure in most people affected by cystic fibrosis. Recent evidence implicates the involvement of free radical and oxidant stress in the pathogenesis of the inflammatory injury. Here we report the efficacy of a novel experimental therapeutic, mercaptoethylguanidine (MEG), which has combined actions as a selective inhibitor of the inducible nitric oxide synthase and as a scavenger of peroxynitrite, a potent oxidant formed in the reaction of nitric oxide and superoxide radical. Chronic pulmonary infection was established in FVB/N mice by intratracheal administration of 10(5) colony-forming units of P. aeruginosa in agar beads. Treatment with MEG (10 mg/kg/dose every 8 h i.p.) inhibited weight loss in the first 3 days and reduced histologic injury at 8 days postinfection. MEG also reduced myeloperoxidase activity, a marker of neutrophil infiltration, at 8 days and concentrations of the proinflammatory cytokines interleukin-1beta, tumor necrosis factor-alpha, and macrophage inflammatory protein 2 in whole lung homogenates. MEG-treated animals and controls had similar perioperative mortality and comparable colony counts of P. aeruginosa at 8 days, indicating that MEG did not exacerbate infection. Our data suggest that MEG may be an effective immunomodulatory therapy of pulmonary inflammation induced by chronic infection.

Anesthesia↗

PubMed1996

Assessment of in vivo attachment/phagocytosis by alveolar macrophages.

Alveolar macrophages (AMs) are recognized as an important first line of cellular host defense within the lung. Although mechanisms underlying AM response to microorganisms or particulates are well characterized in vitro, experimental approaches to the study of AMs in vivo are limited. To circumvent these limitations, a new assay was developed using fluorescently labelled liposomes or Pneumocystis carinii (PC) organisms which were administered intratracheally into mechanically ventilated rats. After 30 min, the lungs were lavaged and the percentage of administered liposomes or PC bound to AMs was determined by quantifying fluorescence. Factors known to enhance attachment/phagocytosis by AMs in vitro were assayed to determine their effect in vivo. For example, vitronectin (VN)-coated liposomes increased attachment from 25.2 +/- 2.4% to 47.2 +/- 3.0% (p < 0.001), while addition of VN increased the binding of PC to AMs from 16.5 +/- 1.7% to 24.5 +/- 2.2% (p < 0.05). Confocal laser microscopy of cells obtained by lavage provided morphologic evidence of attachment/phagocytosis by AMs. This model will permit the quantitative assessment of the interaction of fluorescently labelled liposomes or microorganisms with AMs in the lower respiratory tract of living animals.

Animals↗

PubMed2001

Catheters for tracheal gas insufflation.

As an adjunct to mechanical ventilation, tracheal gas insufflation (TGI) injects gas flow into the trachea to flush carbon dioxide (CO2) from the anatomical and mechanical dead space, but the addition of TGI flow from a catheter may cause problems related to increased flow velocity at the catheter tip. Forward momentum and turbulence beyond the tip oppose expiratory flow and may cause or increase intrinsic positive end-expiratory pressure. If the catheter is placed within the endotracheal tube (ETT), the catheter itself acts as a resistive element to exhalation. Effects of the catheter presence (contact on or whipping against the airway) or local rapid gas flow effects on the tracheal mucosa are possible. Thus far, TGI has been delivered through a range of catheter sizes and styles. Two general design modifications have been incorporated in TGI systems to address the possible problems: embedding the catheter flow channel within the ETT, and directing the TGI flow cephalad. The LaBrune-Boussignac tube was designed with 6 or 8 channels embedded within the ETT, from which TGI flow exits laterally within the ETT at 1.5 cm from its tip. This avoids the use of a catheter and thus avoids local traumatic effects. A reverse-thrust catheter has been designed to direct flow within a sheath around the catheter tip; flow exits cephalad from a gap between the sheath and the catheter shaft. As part of a proposed ventilatory mode (intratracheal pulmonary ventilation) the reverse-thrust catheter delivers the tidal breath and, additionally, flushes CO2 and accelerates secretion removal during exhalation. A reverse-flow design ETT has been developed with two channels, one for tidal volume delivery and the other for TGI flow. The TGI channel is relatively large and flow is directed cephalad by a nozzle at the catheter tip. A recently developed bidirectional catheter allows the option of delivering TGI flow cephalad, towards the lungs or in both directions. Unfortunately, to be convenient, the use of specially designed catheters or ETTs requires the anticipation of TGI use. A complete system for the safe and convenient use of TGI in ventilated patients is not as yet available, but concerns about the safety and convenience of TGI delivery have been addressed with recent advances in catheter/tube design.

Catheterization↗

PubMed2003

Effect of polystyrene particles on lung microvascular permeability in isolated perfused rabbit lungs: role of size and surface properties.

The aim of this study was to investigate the role of particle number, total surface area, mass and surface chemical groups in (K(f,c)) changes. The lung effects of four different fine (110 nm) and ultrafine (24 nm) polystyrene particles have been tested in an isolated perfused rabbit lung model. Pulmonary microvascular permeability (K(f,c)) modifications were measured in response to intratracheal particle challenge. Polystyrene particles, mainly located in alveolar spaces and macrophages, induced a K(f,c) increase that was related to the total surface area and number of particles rather than to the instilled mass. Moreover, the positively charged amine-modified polystyrene particles were more effective in the K(f,c) response than the negatively charged carboxylate-modified polystyrene particles. We concluded that particle number and diameter that mathematically equally determined total surface area do not have the same importance in explaining the biological effects observed and that particle number could be an alternative to total surface area to describe the particle exposure. Furthermore, surface properties of polystyrene particles need to be considered to investigate the microvascular permeability changes measured in our model.

Animals↗

PubMed2004

Asthmalike symptoms following intratracheal exposure of Guinea pigs to sulfur mustard aerosol: therapeutic efficacy of exogenous lung surfactant curosurf and salbutamol.

The purpose of the present study was to investigate: (1) the acute effects of sulfur mustard on airway, lung, and surface tension of bronchoalveolar lavage fluid (BALfluid) in guinea pigs following intratracheal (i.t.) exposure to 1LD50 of an aerosolized solution of sulfur mustard in saline, and (2) the therapeutic efficacy of i.t. administration of the natural surfactant Curosurf and the broncholytic Salbutamol. Intratracheally aerosolized sulfur mustard solution induced two clinically relevant symptoms, that is, asthmalike symptoms reflected by an early bronchoconstriction and "late asthmatic responses" (LAR), and ARDS-like symptoms, that is, pulmonary edema and damage to the lung surfactant. The respiratory minute volume (RMV) was enhanced. Histologically, inflammation and severe epithelial injury in the upper airways were observed, whereas the lungs were homogeneously affected. The surface tension of BAL fluid derived at 24 h after sulfur mustard exposure was much higher (20 +/- 1 mN/m) than that of unexposed control animals (about 1.0 +/- 0.5 mN/m), indicating that the lung surfactant had been altered, and justifying treatment with exogenous surfactant. Intratracheal nebulization of a Salbutamol solution (10 microg/kg), or i.t. bolus administration of Curosurf (62.5 or 125 mg/kg), tended to reduce mortality, although Salbutamol appeared to be more effective than Curosurf in this respect. Although the present study does not give a definite answer to the question of whether the animal model used would be the most relevant for humans, a number of considerations in favor of i.t. aerosolization of sulfur mustard are discussed. Since it was noticed that sulfur mustard exposure induced damage to the lung surfactant, severe bronchoconstriction, and inflammation of the respiratory tract, the effectiveness of a combined treatment consisting of exogenous surfactant, anti-inflammatory drugs, and broncholytics is recommended to be further investigated.

Aerosols↗

PubMedDate not supplied

Recruitment of lymphocytes and dendritic cells from the blood to the bronchoalveolar space and the draining lymph nodes after a single intrabronchial application of the lipopeptide MALP-2.

OBJECTIVE: It has been shown previously that the synthetic macrophage-activating lipopeptide, MALP-2, is a potent stimulator of the respiratory immune system and an effective adjuvant in the induction of mucosal immune responses. In this study, the migration route of leukocytes from the blood to the bronchoalveolar space and then to the draining lymph nodes was investigated. METHODS: MALP-2 was intratracheally instilled into lungs of Lewis rats. Bronchoalveolar lavage cells as well as cell preparations of other lung compartments such as the marginal vascular pool, the interstitial pool and also the draining lymph nodes were examined 3 days later. RESULTS: The application of MALP-2 induced a pronounced leukocyte accumulation in the bronchoalveolar space and the lung interstitium but not in the marginal vascular pool. A tendency to increased lymphocyte and dendritic cell numbers was observed in the draining lymph nodes. CONCLUSION: Our data indicate the migration of blood cells into the lung interstitium and the bronchoalveolar space in response to MALP-2. Thus, the immune reaction induced by MALP-2 might be of relevance as an adjuvant treatment in inhalant vaccination strategies in the lung.

Animals↗

PubMed1984

Dispersion of a fluorescein dye-ampicillin mixture after intratracheal administration in calves.

The pulmonary and systemic dispersion of a dye mixture after intratracheal (i.t.) administration was characterized in young dairy calves. Five calves were given i.t. injections of a fluorescein and ampicillin mixture, and were then killed at 2, 5 or 15 min after treatment. The respiratory system, nasal pharynx area, nose, liver, kidney, stomach and esophagus were removed and examined. Sections were taken from lung areas for histopathological examinations and all tissues were photographed, using floodlight and ultraviolet light. There was uniform low-grade fluorescence throughout the lung, but the greatest fluorescence followed an anterior ventral dispersion. The dye was readily absorbed from the lung into the bloodstream, causing fluorescence in the liver, bile, kidney and urine. Coughing of the calves during the injection caused some of the mixture to be expectorated and swallowed, resulting in fluorescence in the esophagus, stomach contents, and nasal pharanges, turbinates and nostrils.

Ampicillin↗

PubMed2000

HMG-1 as a mediator of acute lung inflammation.

Acute inflammatory lung injury is often a delayed complication of critical illness and is associated with increased mortality. High mobility group-1 (HMG-1) protein, in addition to its role as a transcriptional regulatory factor, has recently been identified as a late mediator of endotoxin lethality. In the present studies, HMG-1 given intratracheally produced acute inflammatory injury to the lungs, with neutrophil accumulation, the development of lung edema, and increased pulmonary production of IL-1beta, TNF-alpha, and macrophage-inflammatory protein-2. In endotoxin-induced acute lung inflammation, administration of anti-HMG-1 Abs either before or after endotoxin exposure decreased the migration of neutrophils to the lungs as well as lung edema. These protective effects of anti-HMG-1 were specific, because pulmonary levels of IL-1beta, TNF-alpha, or macrophage-inflammatory protein-2 were not decreased after therapy with anti-HMG-1. Together, these findings indicate that HMG-1 is a distal mediator of acute inflammatory lung injury.

Adjuvants, Immunologic↗

PubMed1996

Testicular toxicity evaluation of arsenic-containing binary compound semiconductors, gallium arsenide and indium arsenide, in hamsters.

The testicular toxicities of gallium arsenide (GaAs), indium arsenide (InAs) and arsenic trioxide (As2O3) were examined by repetitive intratracheal instillation using hamsters. GaAs (7.7 mg/kg) and As2O3 (1.3 mg/kg) were instilled twice a week a total of 16 times and InAs (7.7 mg/kg) was instilled a total of 14 times. GaAs caused testicular spermatid retention and epididymal sperm reduction, though the degrees were less severe than those in rats shown in our previous experiment. InAs and As2O3 did not show any testicular toxicities. Serum arsenic concentration in GaAs-treated hamsters was less than half of that in As2O3-treated hamsters in which no testicular toxicities were found. Serum molar concentration of gallium was 32-times higher than that of arsenic in GaAs-treated hamsters. Therefore gallium may play a main role in the testicular toxicity of GaAs in hamsters.

Animals↗

PubMed2001

Asbestos causes apoptosis in alveolar epithelial cells: role of iron-induced free radicals.

Asbestos causes asbestosis and malignancies by mechanisms that are not fully understood. Alveolar epithelial cell (AEC) injury by iron-induced reactive oxygen species (ROS) is one important mechanism. To determine whether asbestos causes apoptosis in AECs, we exposed WI-26 (human type I-like cells), A549 (human type II-like cells), and rat alveolar type II cells to amosite asbestos and assessed apoptosis by terminal deoxynucleotidyl transferase-mediated deoxyuridine-5'-triphosphate-biotin nick end labeling (TUNEL) staining, nuclear morphology, annexin V staining, DNA nucleosome formation, and caspase 3 activation. In contrast to control medium and TiO2, amosite asbestos and H2O2 each caused AEC apoptosis. A role for iron-catalyzed ROS was suggested by the finding that asbestos-induced AEC apoptosis and caspase 3 activation were each attenuated by either an iron chelator (phytic acid and deferoxamine) or a.OH scavenger (dimethyl-thiourea, salicylate, and sodium benzoate) but not by iron-loaded phytic acid. To determine whether asbestos causes apoptosis in vivo, rats received a single intratracheal instillation of amosite (5 mg) or normal saline solution, and apoptosis in epithelial cells in the bronchoalveolar duct regions was assessed by TUNEL staining. One week after exposure, amosite asbestos caused a 3-fold increase in the percentage of apoptotic cells in the bronchoalveolar duct regions as compared with control (control, 2.1% +/- 0.35%; asbestos, 7.61% +/- 0.15%; n = 3). However, by 4 weeks the number of apoptotic cells was similar to control. We conclude that asbestos-induced pulmonary toxicity may partly be caused by apoptosis in the lung epithelium that is mediated by iron-catalyzed ROS and caspase 3 activation.

Animals↗

PubMed1975

Vitamin A (retinyl acetate) and benzo(alpha)pyrene-induced respiratory tract carcinogenesis in hamsters fed a commercial diet.

Male Syrian hamsters fed a commercial diet were given a series of 12 intratracheal instillations of 3 mg benzo (alpha) pyrene adherent to 3 mg Fe2O3 in 0.2 ml 0.15 M NaCl at weekly intervals. After the last instillation, the hamsters were randomly assigned to receive either 100, 1600, or 3300 (later reduced to 2400) mug retinyl acetate per week in divided intragastric doses. Hamsters in the 2400-mug retinyl acetate group had a significantly higher incidence of respiratory tract tumors than those in the group given 100 mug retinyl acetate per week. Liver vitamin A stores increased dramatically in the groups given 1600 and 2400 mug retinyl acetate and corresponded to the administration of retinyl acetate p.o. Serum vitamin A values were not consistently related to retinyl acetate administration or to hepatic stores of vitamin A.

Adenocarcinoma↗