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PubMed1994

Intratracheal but not intravascular interleukin-1 causes acute edematous injury in isolated neutrophil-perfused rat lungs through an oxygen radical-mediated mechanism.

Our goal was to determine whether administration of interleukin-1 (IL-1) intratracheally causes acute edematous injury in isolated rat lungs perfused only with neutrophils and physiologic buffer. We found that administration of native (50 ng) but not heated IL-1 intratracheally rapidly (60 minutes) increased (p < 0.05) lung weights and lung lavage Ficoll concentrations in isolated rat lungs perfused only with purified human neutrophils as compared with lungs given IL-1 intratracheally alone, lungs perfused with neutrophils alone, or untreated control lungs. In contrast, lung weights or lavage Ficoll concentrations did not increase (p > 0.05) when as much as 1 microgram of IL-1 was administered intravascularly with neutrophils. The mechanism of injury appeared to involve neutrophil-derived oxygen radicals, because acute edematous injury did not occur in isolated lungs given IL-1 intratracheally and then perfused with neutrophils previously heated at 48 degrees C for 10 minutes. The latter procedure decreased superoxide anion (O2-.) production but did not alter the adhesion or chemotactic properties of neutrophils in vitro. In parallel, incubation with IL-1 and human neutrophils did not lyse (as measured by chromium 51 release) cultured purified bovine pulmonary artery endothelial cells in vitro. Our results indicate that increased alveolar but not intravascular concentrations of IL-1 initiate a neutrophil-dependent, oxidant-mediated acute edematous lung injury.

Acute Disease↗

PubMed1992

Extracellular ATP stimulates elastase secretion from human neutrophils and increases lung resistance and secretion from normal rat airways after intratracheal instillation.

The effect of ATP on intracellular Ca2+ levels and elastase secretion in isolated normal human peripheral blood neutrophils was investigated as was its in vivo effect on lung resistance and mucous secretion. ATP (10(-5) M) increased [Ca2+]i from 61 +/- 3 to 165 +/- 15 nM in nonactivated neutrophils; elastase secretion was increased by 40% from nonactivated neutrophils but was unaffected in fMLP (10(-5) M) activated cells. Instillation of ATP (10(-5) and 10(-3) M) into the airways of brown Norway rats increased both lung resistance and secretion. These findings suggest that aerosolization of ATP into the cystic fibrosis-affected bronchial tree might be hazardous in terms of enhancement of parenchymal damage, which would result from neutrophil elastase release, and in terms of impaired respiratory lung function.

Adenosine Triphosphate↗

PubMed1996

Increased immune and inflammatory responses to dust mite antigen in rats exposed to 5 ppm NO2.

Immune hypersensitivity to house dust mite antigen (HDM) is a frequent cause of respiratory allergy. The objective of this study was to determine whether exposure to NO2, a common indoor air pollutant, modulates immune responses to HDM and influences immune-mediated lung disease. Brown Norway rats were immunized ip with 100 micrograms semipurified antigen and Bordetella pertussis adjuvant and challenged 2 weeks later with an intratracheal injection of 50 micrograms of a crude antigen preparation. Exposure to 5 ppm NO2 for 3 hr after both immunization and challenge procedures resulted in significantly higher levels of antigen-specific serum IgE, local IgA, IgG, and IgE antibody than air controls, and increased numbers of inflammatory cells in the lungs. Lymphocyte responsiveness to antigen in the spleen and MLN was also significantly higher in NO2-exposed animals. These data show that exposure to a common air pollutant can upregulate specific immune responses and subsequent immune-mediated pulmonary inflammation.

Air Pollutants↗

PubMed1998

Preliminary observations on the Colibri CO2-indicator.

The performance of a new colorimetric CO2-indicator (Colibri) was assessed in mini-pigs. It performed well during 8-hour procedures. Neither nitrous oxide, nor halothane, nor carbon monoxide, nor intratracheal application of drugs (epinephrine, atropine, lidocaine, and naloxone) interfered with its function. It gave a distinct color change at high ventilation frequencies up to 120/min. The only problem observed was difficulty in matching the colors displayed with the comparison color chart provided. The Colibri's performance seems at least equal to that of the EasyCAP detector, although both devices share some disadvantages (no alarms, semiquantitative, difficult reading in the dark). After initial control of endotracheal tube position by an esophageal detector device, both the Colibri and the EasyCAP seem suited for monitoring of ventilation and circulation if quantitative capnometry is unavailable.

Animals↗

PubMed1977

[Studies on pharmacokinetics and biotransformation of reproterol in animal and man (author's transl)].

Investigations on the pharmacokinetics and biotransformation in the rat, dog, rabbit and in humans were performed with 3H-or 14C-labelled 7-(3-[2-(3,5-dihydroxyphenyl)-2-hydroxy-ethlamino]-propyl)-theophylline (reproterol, Bronchospasmin). Following i.v. administration of reproterol, a similar course of the plasma levels as shown in both rat and dog. After oral administration to the rat, elimination occurs within 2 h following application; in the dog, however, a relatively constant plasma level persists for up to 24 h, which is then reduced during an elimination half-life of 12.4 h. Following i.v. as well as oral administration to the rabbit, phases of distribution and elimination persist over a considerable length of time. Plasma levels following oral administration remain relatively constant during a time period of 8--30 h, after which they decrease with a half-life of 70 h. Renal elimination in the dog and rabbit after i.v. application seems to be the main route of excretion (dog 57%, rabbit 66%), while in the rat there is 58% fecal elimination. Absorption ratios following oral administration amount to 13% in the rabbit and 18% in the rat and dog. The absorption ration in the rat following intratracheal application reaches 90%. This was particularly important in view of the anticipated use of reproterol as an aerosol. Tests on the quantitative organic distribution further showed that in the rat, the lund tissue has a particular affinity to reproterol. In man following i.v. administration, reproterol is rapidly distributed and eliminated. The highest plasma level reached within 2 h after oral administration, correlates well with the initial plasma level following i.v. administration. A great similarity was shown for the reproterol metabolism in rat, dog, rabbit and man. With complete metabolization, the same main metabolite is always formed.

Administration, Oral↗

PubMed2005

Nimesulide inhibits lipopolysaccharide-induced production of superoxide anions and nitric oxide and iNOS expression in alveolar macrophages.

The study was designed to investigate the effect of nimesulide on lipopolysaccharide (LPS)-induced proinflammatory oxidants production by rat alveolar macrophages (AMs). Effects of LPS and nimesulide on antioxidant defense and the expression of inducible nitric oxide synthase (iNOS) were also studied. It was found that nimesulide could scavenge superoxide anions (O2*-), nitric oxide (NO*) and total oxidant burden induced by LPS in AMs in vitro. Approximately 850 nmoles of nimesulide had activity equivalent to one IU of superoxide dismutase (SOD). Further, to confirm the in vitro observation, Male Wistar rats were orally administered with nimesulide (9 mg/kg b. wt. twice daily) for one week followed by intratracheal instillation of 2 microg LPS to stimulate lung inflammation. AMs from bronchoalveolar lavage fluid were collected 18 h after instillation of LPS. Nimesulide pretreatment could inhibit O2*-, NO() and lipid peroxidation in AMs. Nimesulide also suppressed LPS-induced iNOS expression in AMs in vivo and in vitro. Nimesulide could also normalize LPS-induced changes in the levels of superoxide dismutase (SOD), glutathione reductase (GR) and reduced glutathione (GSH) in AMs. Inhibition in production of oxidants in LPS-challenged AMs by nimesulide could be one of the pathways for its anti-inflammatory action.

Animals↗

PubMed1998

Endotracheal flumazenil: a new route of administration for benzodiazepine antagonism.

The purpose of this study was to determine if flumazenil is absorbed from broncho-pulmonary tissue after intratracheal administration and whether therapeutically significant plasma concentrations can be obtained. Six elective surgical patients received a dose of 1.0 mg flumazenil in 10 mL saline intratracheally during general anesthesia. Blood samples were drawn for 6 hours after administration and plasma concentrations were determined by gas chromatography-mass spectrometry (GC-MS). An average peak plasma flumazenil concentration of 65.9 +/- 43.1 ng/mL was attained within 1 minute after administration. No patients reported chest discomfort or dyspnea upon awakening and there were no other side effects noted. Administration of flumazenil via an endotracheal tube results in rapid attainment of therapeutic blood levels.

Absorption↗

PubMed1988

Cyclosporin A inhibits the growth of Cryptococcus neoformans in a murine model.

Cryptococcus neoformans is a frequent opportunistic infectious agent in patients with decreased T-lymphocyte-mediated immune function, including those with acquired immune deficiency syndrome. Cyclosporin A (CsA), a potent inhibitor of T-lymphocyte function, was administered subcutaneously to mice to study the pathogenesis of C. neoformans infections in the setting of impaired T-cell function. Surprisingly, survival was prolonged indefinitely in animals that received immunosuppressive doses of CsA following either intratracheal or intravenous inoculations of C. neoformans. Furthermore, following intratracheal inoculation, mice treated with CsA cleared C. neoformans from their lungs more rapidly than did control mice. CsA directly inhibited the growth of C. neoformans when it was added to cultures in vitro at concentrations comparable to the blood levels achieved in experimental mice. Thus, CsA inhibited both in vitro and in vivo growth of C. neoformans. While these results must be extended to studies in humans, these data suggest that patients who now receive CsA-immunosuppressive therapy may be fortuitously protected against infections with C. neoformans. Furthermore, research into cyclosporin derivatives may yield compounds with less immunosuppressive properties and enhanced antifungal activity.

Animals↗

PubMed2003

Inhibitory effects of surfactant protein A on surfactant phospholipid hydrolysis by secreted phospholipases A2.

Hydrolysis of surfactant phospholipids by secreted phospholipases A(2) (sPLA(2)) contributes to surfactant dysfunction in acute respiratory distress syndrome. The present study demonstrates that sPLA(2)-IIA, sPLA(2)-V, and sPLA(2)-X efficiently hydrolyze surfactant phospholipids in vitro. In contrast, sPLA(2)-IIC, -IID, -IIE, and -IIF have no effect. Since purified surfactant protein A (SP-A) has been shown to inhibit sPLA(2)-IIA activity, we investigated the in vitro effect of SP-A on the other active sPLA(2) and the consequences of sPLA(2)-IIA inhibition by SP-A on surfactant phospholipid hydrolysis. SP-A inhibits sPLA(2)-X activity, but fails to interfere with that of sPLA(2)-V. Moreover, in vitro inhibition of sPLA(2)-IIA-induces surfactant phospholipid hydrolysis correlates with the concentration of SP-A in surfactant. Intratracheal administration of sPLA(2)-IIA to mice causes hydrolysis of surfactant phosphatidylglycerol. Interestingly, such hydrolysis is significantly higher for SP-A gene-targeted mice, showing the in vivo inhibitory effect of SP-A on sPLA(2)-IIA activity. Administration of sPLA(2)-IIA also induces respiratory distress, which is more pronounced in SP-A gene-targeted mice than in wild-type mice. We conclude that SP-A inhibits sPLA(2) activity, which may play a protective role by maintaining surfactant integrity during lung injury.

Airway Resistance↗

PubMed1985

[Effect of various tracheal diameter forms on airway pressure in experimental intratracheal injector ventilation].

Experimental catheter jet ventilation was performed on tracheal models of four sizes and six different shapes. Three coaxial jet positions were tested: centrally, adjacent to the wall and in a corner of the model. Driving gas pressure and size of the jet were kept constant. Airway pressure declines as the models increase in size. In the corner position, airway pressure is always less than in the centre position. In models with equal cross-section areas, airway pressure differs in all other shapes from that of the cylindrical shape. With this equipment, airway pressures between 9 and 14 cm H2O were achieved in cylindrically-shaped tracheas of a diameter of 15 resp. 20 mm. With the same transverse diameters, but with clinically relevant different tracheal shapes and jet positions, however, the values may vary from 18 cm H2O to less than 5 cm H2O.

Catheterization↗

PubMed2003

Pharmacokinetics and tissue distribution of the nonadecapeptide Moli1901 in rats and mice.

1. Administration of aerosolized, radiolabelled Moli1901 (duramycin, 2622U90), a 19 amino acid polycyclic peptide, to rats resulted in the deposition of high amounts of radiolabel in the respiratory tract, with deposited radiolabel persisting almost unchanged through 7 days after dosing. Little to no radiolabel was present in the bloodstream of these rats. 2. Rats absorbed little radiolabel after p.o. administration, with nearly all of the dose excreted in the faeces by 2 days after dosing. 3. At 7 days following an intravenous dose, rats excreted 54% of the radiolabel in faeces and 5.4% in the urine, with 44% remaining in the carcass, primarily in the liver (33%). 4. Following an intratracheal instillation dose to rats, radiolabel was eliminated from the pulmonary system with a half-life of 64 days. Excretion was almost exclusively via faeces, with an elimination half-life of 52 days. Plasma and blood concentrations in these animals were uniformly <1 ng eq. ml(-1) at all sampling times. 5. Results in mice given intravenous and oral doses were consistent with those observed in rats. 6. Prolonged retention of Moli1901 in pulmonary tissue supports its use in the treatment of respiratory diseases.

Administration, Inhalation↗

PubMed1984

Pulmonary clearance of intratracheally administered 63Ni3S2 in strain A/J mice.

The pulmonary clearance of particulate 63Ni3S2 was evaluated in strain A/J mice following the intratracheal instillation of 3 microCi of 63Ni3S2 (1.66 micron, mass median diameter). Lung and tissue burdens were determined from serially sacrificed animals using scintillation counting techniques. Lung clearance over the 35-day observation period could be separated into two distinct components with initial and final phase biological half-times corresponding to 1.2 and 12.4 days, respectively. Radioactivity was detected in the blood, liver, kidney, and femur within 4 hr, and was eliminated at rates comparable to that in the lung. Excretion involved primarily urinary (60% of dose eliminated) but also fecal (40% of dose eliminated) pathways. The data are consistent with the relatively rapid translocation, solubilization, and elimination of particulate 63Ni3S2 from the body.

Animals↗

PubMed2000

[The fibrogenic effect of artificial ceramic fibres in experimental rats].

The fibrogenic effect of aluminosilicate ceramic fibres in rats administered intratracheally with a single dose of 25 mg was assessed on the basis of the lung hydroxyproline concentration and morphological changes in the lung parenchyma and mediastinum lymphatic nodes. Control groups were composed of rats administered with NaCl saline and crocidolite UICC. The rats were exposed for 6 and 9 months. It was found that after 6 and 9 months, aluminosilicate ceramic fibres (L-1, Langfaser, Thermowool and Kaowool) showed weak fibrogenic properties. The range of changes in reactivity, and the presence of fibres of fibrous connective tissue in granulomas, induced by ceramic fibres were lower than the range of changes and the contribution of connective tissue produced by asbestos and crocidolite UICC.

Aluminum Silicates↗

PubMed1976

Intratracheal instillation studies with 7H-dibenzo(c,g)carbazole in the Syrian hamster.

The morphologic effects and the retention and distribution times of single and multiple intratracheal instillations in Syrian hamsters of 7H-dibenzo[c,g]carbazole (DBC) and benzo[a]pyrene (BP) were compared. A single instillation of DBC induced slight changes in the hamster respiratory tract; however, five treatments caused tracheobronchial epithelial proliferation, cell hyperplasia, and occasionally, squamous metaplasia. The particle size of both carcinogens was approximately the same. BP in saline remained longer in the lungs than did DBC in saline. The shortest retention time was recorded when DBC was administered in aqueous solution, whereas multiple doses of DBC in aqueous solution did not markedly affect retention time. DBC passed from the lungs to the intestinal tract and was mainly excreted in the feces.

Animals↗

PubMed1990

Placental transfer of metals of coal fly ash into various fetal organs of rat.

Fly ash (100 mg/kg body weight) was administered intratracheally to 14-day pregnant rats for 6 consecutive days. On day 20 of gestation the translocation of metals present in the fly ash to various maternal and fetal organs was studied. Fly ash administration to pregnant mothers retarded the growth of fetal heart and kidney as determined by their weights. Fly ash instillation increased organ levels of nearly all the metals studied in both mother and fetus. Most of the metals present in coal fly ash were transferred in significant amounts through placenta to several fetal organs. However, the pattern of their distribution into various fetal organs was different for different metals.

Animals↗

PubMed2002

Lung expression of cytochrome P450 1A1 as a possible biomarker of exposure to diesel exhaust particles.

Polycyclic aromatic hydrocarbons (PAH) and reactive oxygen species (ROS) derived from diesel exhaust particles (DEP) are implicated in the pathophysiology of respiratory diseases. Cytochrome P450 (Cyp) 1A1 can be induced by several kinds of PAH and produce ROS. We determined whether acute inhalation exposure to DEP induced the expression of Cyp 1A1 in murine lung. Intratracheal instillation of DEP dose-dependently increased the lung expression of Cyp 1A1 at the levels of both mRNA and protein, whereas DEP decreased expression in the lung of aryl hydrocarbon receptors in a dose-dependent manner. In contrast, charcoal particles as the control did not affect the expression of these molecules. These results suggest that the lung expression of Cyp 1A1 can be a biomarker of acute inhalation exposure to DEP and may be implicated in an accelerated production of ROS and the subsequent aggravation of lung injury.

Animals↗

PubMed1981

DNA modification in rat lungs following intratracheal or subcutaneous administration of 4-nitroquinoline-1-oxide, benzo[a]pyrene or 2-aminoanthracene.

Benzo[a]pyrene (BP)-, 2-aminoanthracene (2AA)- and 4-nitroquinoline-1-oxide (4NQO)-mediated DNA modification were investigated in rat lungs by using alkaline sucrose gradient sedimentation. The exposure-route, the physicochemical nature of the administered compound and the number of treatments were all important in determining the extent of DNA modification. 4NQO produced qualitatively similar modification whether instilled intratracheally (i.t.) as a suspension or injected subcutaneously (s.c.) in a soluble form. BP and 2AA produced no DNA alteration when injected s.c; they did, however, modify DNA sedimentation when instilled as a suspension, but not until 24 h after treatment. Furthermore, BP caused no DNA modification at any sampling time when instilled in a lipid solvent. In contrast to the DNA modification observed at 24 h after a single i.t. treatment with a BP suspension, no such alteration was detected 12 or 24 h after the last of 5 similar daily treatments. These results are discussed with respect to mechanisms of differential transport, clearance and metabolism of administered carcinogens.

4-Nitroquinoline-1-oxide↗

PubMed1997

Xanthine oxidase decreases production of gut wall nitric oxide.

Multiorgan failure is often the lethal outcome of intratracheal aspiration of acidic gastric juice. The pathogenesis of multiorgan failure may involve a systemic imbalance between pro-inflammatory and anti-inflammatory factors. In an anesthetized rat model, intratracheal instillation of HCl elicited intestinal inflammation which was exaggerated by xanthine oxidase (XO) and attenuated by nitric oxide (NO). We hypothesized that XO may mediate injury in part by suppression of NO formation. Therefore, we measured intestinal tissue concentrations of the stable NO oxidative metabolites (NO2- and NO3-) following intratracheal (IT) instillation of NaCl or HCl alone or in combination with interventions aimed at increasing or decreasing XO activity. Compared with IT NaCl (control treatment) jejunal tissue NO2- and NO2- + NO3- concentrations were increased by allopurinol pretreatment, which inhibits XO, and were decreased by systemically administered XO, as well as by IT HCl. The decreased NO2- and NO2- + NO3- concentrations found following IT HCl were completely reversed by either allopurinol or by systemically administered L-arginine (the precursor of NO). We conclude that manipulation of the pro-inflammatory XO system has a reciprocal effect on the intestinal anti-inflammatory NO system in either the undamaged or the endobronchially acidified lung model.

Animals↗