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PubMed1990

Lung lavage and surfactant replacement for hydrochloric acid aspiration in rabbits.

Hydrochloric acid (0.1 N, 5.0 ml.kg-1 in total) was administered intratracheally to 28 adult rabbits anesthetized with pentobarbital and mechanically ventilated with pure oxygen. When the PaO2 decreased to 14.1 +/- 2.8 kPa (mean +/- s.d.), the PaCO2 increased to 8.9 +/- 2.5 kPa, and the minute ventilation (VE) decreased to 51 +/- 8% of the baseline value, animals were divided into 4 groups. The deteriorated values did not improve in the non-treated (control) animals, whereas the animals treated with lung lavage and surfactant replacement showed a significant increase in PaO2 to 35.1 +/- 12.2 kPa, and maintained lower PaCO2 and larger VE than the controls. These parameters showed no significant improvement with surfactant replacement alone, and deteriorated further with lung lavage alone. The minimum surface tension (gamma min) of the edema fluid that accumulated in the airways after acid administration was 22.5 +/- 1.7 mN.m-1, and was not lowered by adding surfactant preparation (10 mg.ml-1) whose original gamma min was less than 2 mN.m-1. We concluded that surfactant inhibition by edema fluid was a cause of respiratory failure, and that lung lavage followed by surfactant replacement might be of therapeutic value for acid aspiration.

Animals↗
PubMed1998

The role of leukocyte emigration and IL-8 on the development of lipopolysaccharide-induced lung injury in rabbits.

Leukocyte emigration and alveolar macrophage-derived cytokines may contribute to lung microvascular injury associated with adult respiratory distress syndrome. We have used mAbs against cell adhesion molecules on leukocytes (anti-CD18 and anti-CD49d) or against IL-8 to investigate these contributions. Intratracheal (i.t.) instillation of LPS (50 microg/kg) caused a significant increase in bronchoalveolar lavage polymorphonuclear leukocytes (PMNs) without an increase in mononuclear cells (MNCs) or an increase in lung permeability. Injection of LPS (10 microg/kg) i.v. at 24 h after i.t. LPS caused significant increases in bronchoalveolar lavage PMNs, MNCs, IL-8, and monocyte chemotactic protein-1, as well as increases in lung permeability. Rabbits that were administered i.t. LPS followed by i.v. LPS and treated with anti-CD18 mAb had a significantly lower lung permeability index and emigration of fewer PMNs but no change in MNC emigration compared with saline treatment. Anti-IL-8 mAb treatment resulted in a significantly lower lung permeability index with no change in PMN emigration compared with no treatment. These results suggest that PMN emigration is necessary but not sufficient for the development of LPS-induced lung injury, and that IL-8 plays a significant role in PMN-dependent lung injury, independent of PMN emigration.

Animals↗
PubMed1995

Intratracheally administered liposomal alpha-tocopherol protects the lung against long-term toxic effects of paraquat.

Paraquat is a broad-spectrum herbicide known to produce lung injury via oxidative stress-mediated mechanisms. Different pharmacological strategies have been explored to reduce the formation of these reactive oxygen species and/or prevent their toxic effects in the treatment of paraquat poisoning. The present study was carried out to investigate whether the antioxidant alpha-tocopherol, incorporated into liposomes and delivered directly to the lungs of rats, could protect the organ against the long-term toxic effects of paraquat. Plain liposomes (composed of dipalmitoylphosphatidylcholine, DPPC) or alpha-tocopherol liposomes (8 mg alpha-tocopherol/kg body weight) were administered intratracheally to animals 24 h prior to an intraperitoneal injection of paraquat dichloride (20 mg/kg) and rats were killed 0, 1, 4, 6, 8, 10, 12, 16, 19 or 24 days after paraquat treatment. Results of this study showed that lungs of animals treated with paraquat were extensively damaged, as evidenced by significant increases in lung weight and decreases in lung angiotensin converting enzyme (ACE) and alkaline phosphatase enzyme (AKP) activities. Moreover, paraquat treatment: resulted in a significant reduction in the number of neutrophils in the blood of rats with a concurrent increase in the pulmonary myeloperoxidase activity, suggestive of neutrophil infiltration in the lungs of treated animals. Pretreatment of rats with liposomes alone did not significantly alter the paraquat-induced changes of all parameters examined. On the other hand, pretreatment of rats with alpha-tocopherol liposomes, 24 h prior to paraquat challenge, attenuated paraquat-induced changes in ACE, AKP and myeloperoxidase activities but failed to prevent increases in lung weight. Thus, pretreatment of rats with liposome-associated alpha-tocopherol appears to protect the lung against some of the toxic effects of paraquat.

Air Pollutants↗
PubMed2001

Inhibition by viozan of extravasation induced in rat trachea by capsaicin is mediated exclusively by beta 2-adrenoceptors.

The mechanism by which 2(3H)-benzothiazolone, 4-hydroxy-7-[2-[[2-[[3-(2-phenylethoxy)propyl]-sulphonyl]ethyl]amino]ethyl]-monohydrochloride (AR-C68397AA; viozan), a dual dopamine D2/beta2-adrenoceptor agonist which has shown promise in the treatment of chronic obstructive pulmonary disease (COPD), inhibits the extravasation of plasma protein induced by capsaicin in the tracheas of Brown Norway rats has been re-evaluated. Viozan (10-30 microg/kg given intratracheally; i.t.) inhibited dose-dependently the extravasation of plasma protein tagged with Evans Blue into rat trachea induced by capsaicin (10 microg/kg i.t.). Similar effects were seen with the selective beta2-adrenoceptor agonist, salbutamol (3-10 microg/kg i.t.), but the selective dopamine D2 receptor agonist, quinagolide (10-30 microg/kg i.t.), was inactive. The effects of viozan and salbutamol were abolished by propranolol (3 mg/kg) given intraperitoneally (i.p.) but unaffected by sulpiride (3 mg/kg i.p.). Thus, in c,ontrast to claims in the literature, a functional response to dopamine D2 receptor activation in a preclinical model of oedema arising from sensory nerve fibre activation in the rat lung could not be demonstrated. Moreover, no qualitative difference could be demonstrated between the response to a dual D2/beta2-adrenoceptor agonist and a selective beta2-adrenoceptor agonist. The observations call into question whether a dual D2/beta2-adrenoceptor agonist such as viozan would bring added benefit over established selective beta2-adrenoceptor agonists in the therapy

Adrenergic beta-2 Receptor Agonists↗
PubMed1990

Endotracheal epinephrine is unreliable.

When intravenous access cannot be obtained in an emergency, the endotracheal route of emergency drug administration can be used for epinephrine, atropine, and lidocaine. Optimal drug dosages for endotracheal administration as well as the amount and type of diluent are presently unknown. We compared central intravenous, peripheral intravenous, intraosseous, and intratracheal administration of epinephrine 1:10,000 in both normotensive and hemorrhagic shock dogs. The shock model consisted of 50% blood volume depletion over 15 min. Epinephrine was administered in a dose of 0.01 mg/kg (0.1 cc/kg) by the intraosseous route, central, and peripheral intravenous routes followed by a 5 cc normal saline flush. Intratracheal administration consisted of epinephrine 0.01 and 0.02 mg/kg diluted 1:1 and 1:2 with normal saline or sterile water and administered deep into the tracheo-bronchial tree using a 30-cm catheter. The effect of epinephrine was assessed by the response of the arterial blood pressure. Epinephrine was equally effective by the intraosseous, central intravenous, and peripheral intravenous routes in terms of time to onset of action, time to peak effect, and magnitude of effect on systolic, diastolic, and mean arterial pressures in both the shock and non-shock animals. The duration of effect was significantly longer (P less than 0.02) for the intraosseous route of administration. The endotracheal route of administration was unreliable and not reproducible in either the normotensive or shock animals. In 8/12 episodes in normotensive animals, including 5 trials with double doses of 0.02 mg/kg and dilutions of 1:1 and 1:2, and in 4/9 studies with shock animals including three with double doses, there was no discernable response of systolic or diastolic blood pressure.

Animals↗
PubMed2005

Respiratory toxicity of multi-wall carbon nanotubes.

Carbon nanotubes focus the attention of many scientists because of their huge potential of industrial applications, but there is a paucity of information on the toxicological properties of this material. The aim of this experimental study was to characterize the biological reactivity of purified multi-wall carbon nanotubes in the rat lung and in vitro. Multi-wall carbon nanotubes (CNT) or ground CNT were administered intratracheally (0.5, 2 or 5 mg) to Sprague-Dawley rats and we estimated lung persistence, inflammation and fibrosis biochemically and histologically. CNT and ground CNT were still present in the lung after 60 days (80% and 40% of the lowest dose) and both induced inflammatory and fibrotic reactions. At 2 months, pulmonary lesions induced by CNT were characterized by the formation of collagen-rich granulomas protruding in the bronchial lumen, in association with alveolitis in the surrounding tissues. These lesions were caused by the accumulation of large CNT agglomerates in the airways. Ground CNT were better dispersed in the lung parenchyma and also induced inflammatory and fibrotic responses. Both CNT and ground CNT stimulated the production of TNF-alpha in the lung of treated animals. In vitro, ground CNT induced the overproduction of TNF-alpha by macrophages. These results suggest that carbon nanotubes are potentially toxic to humans and that strict industrial hygiene measures should to be taken to limit exposure during their manipulation.

Administration, Inhalation↗
PubMedDate not supplied

Intratracheal pulmonary ventilation in premature infants and children with intractable hypercapnia.

The feasibility of intratracheal pulmonary ventilation (ITPV) was tested in five ventilated moribund neonatal and pediatric patients with uncontrollable hypercapnia: a 2-year-old child, a 52-day-old infant, and three premature infants (29, 29, and 26 weeks gestation; 1300 g, 1100 g and 890 g birth weight, respectively). ITPV was applied for 9.5, 8, 25, 58.5, and 47.5 hr, respectively. An intratracheal catheter (Cook Critical Care, Inc., Bloomington, IN) with a reversed continuous flow of gas at its tip (away from the lungs) allowed flushing of CO2 from the proximal dead space. Marked reductions in Paco2, ranging from 37% to 71% and improvement in pH were achieved within 4-6 hr of applying ITPV. During ITPV, the mean lowest Paco2 was significantly less than the pre-ITPV Paco2 (p < 0.0017), and the mean best pH was significantly higher than the pre-ITPV pH (p < 0.015). In four patients, despite significant reductions in Paco2, there was no substantial improvement in their baseline condition (shock and severe metabolic acidosis or coma) and they were switched back to conventional ventilation. This led to worsening hypercapnia to pre-ITPV values. These four patients subsequently died. It is possible that these patients were already too ill to derive significant benefit from the technique. One premature infant survived, was successfully weaned to conventional ventilation and was eventually discharged home. ITPV can alleviate uncontrollable hypercapnia in ventilated neonatal and pediatric patients.

Acidosis, Respiratory↗
PubMed1992

Epinephrine blood concentrations after peripheral bronchial versus endotracheal administration of epinephrine in dogs.

BACKGROUND AND METHODS: Emergency endotracheal drug administration has become an acceptable route for drug delivery during cardiopulmonary resuscitation. The purpose of the present study was to determine whether the site of endotracheal epinephrine injection is an important factor in its absorption. Epinephrine (1:1000), in a dose of 0.02 mg/kg diluted in 2 mL of saline, was given to ten anesthetized mongrel dogs. Each dog was studied twice: once when the epinephrine was injected into the endotracheal tube, and on another day, through the endotracheal tube via a flexible catheter wedged into a peripheral bronchus. Arterial blood samples for plasma epinephrine concentration determinations were collected, before and at 1, 2, 5, 10, 15, and 30 mins after each intratracheal drug administration. RESULTS: Both routes of epinephrine administration significantly increased plasma concentrations within 1 min of injection. Higher plasma epinephrine concentrations were achieved after peripheral bronchial epinephrine administration (maximal concentration 8.9 +/- 3.2 vs. 2.0 +/- 0.4 ng/mL), and the total dose absorbed was significantly (76.5 +/- 13.5 vs. 36.7 +/- 6.5 ng/min/mL, p < .05) higher. The time interval to reach maximal concentration was significantly shorter with the peripheral bronchial dosing than with the endotracheal route (1.3 +/- 0.2 vs. 2.7 +/- 0.5 min, p < .05). Neither group demonstrated a significant change in heart rate, and both had similar, minor decreases in BP for > 2 to 5 mins. There were no significant differences between the arterial blood gases of the two groups at various stages of the experiment. CONCLUSIONS: In dogs, epinephrine administered via the peripheral bronchial route has a clear pharmacologic advantage over the endotracheal route. This advantage may be more important during cardiopulmonary resuscitation conditions and other low flow states, and may account for the failure observed with the endotracheal route in recently published clinical reports.

Animals↗
PubMed1994

Effects of induction and age-dependent enzyme expression on lung bioavailability, metabolism, and DNA binding of urban air particulate-absorbed benzo[a]pyrene, 2-nitrofluorene, and 3-amino-1,4-dimethyl-5H-pyridol-(4,3)-indole.

The effect of interactions between urban air particulates (UAP) and carcinogens on bioavailability, metabolism, and DNA binding was studied in the isolated perfused and ventilated rat lung. The availability of benzo[a]pyrene (B[a]P) varied from 29 to 60% after intratracheal doses of carcinogen particulates dissolving extremely slow and fast, respectively. Several cytochrome P450 enzyme (P450) inducers acting as 2,3,7,8-tetrachlorodibenzo[p]dioxin-receptor ligands have been identified in UAP extracts. beta-Naphthoflavone (BNF) was used to study how P450 induction alters the lung metabolism of carcinogens. Pretreatment increased the lung clearance for B[a]P 8-fold and for 2-nitrofluorene (2NF) by a factor of four from 0.55 +/- 0.06 ml/min to 2.37 +/- 0.62 ml/min. Studies with the intact lung and with isolated lung cells show that carcinogen metabolism and pharmacokinetics depend both on the route of exposure and dosage and on the distribution of specific enzymes. A cytochrome P450IIB1 enzyme was detected in lung epithelial cells where it catalyzes 9-hydroxylation of 2NF. This rat lung 2NF-9-hydroxylation capacity increases in parallel with the age dependent up-regulation of lung P450IIB1 expression. Both human and rat lung tissue have the capacity to form 9-hydroxy-2-nitrofluorene (9-OH-2NF) that is mutagenic. A BNF-inducible P450IA1 was detected in endothelial and alveolar type II cells. Consequently, aromatic hydroxylation dominated when 2NF was dosed directly into the lung circulation. Pretreatment of rats with BNF before intratracheal B[a]P dosage induced lung cytochrome P450IA1. The 7,8-dihydroxy-9,10-oxybenzo[a]pyrene-deoxyguanosine adduct and the total lung DNA adduct levels increased significantly from a peak level of 75 +/- 8 to 151 +/- 19 fmole/mg DNA in lungs from control and BNF pretreated rats, respectively. 3-Amino-1,4-dimethyl-5H-pyridol-(4,3)-indole (TRP-P1) is a potent mutagen and carcinogen identified in UAP extracts. Dietary BNF pretreatment of rats altered the [14C]TRP-P1 distribution as analyzed by whole-body autoradiography. An enhanced retention was observed in the small intestine, forestomach, esophagus, and lung. UAP catalyzes oxygen radical formation and deoxyguanosine-8-hydroxylation, which were inhibited when the UAP samples were extracted with organic solvents or when they were incubated in the presence of desferroxamine. We therefore postulate that a polycyclic aromatic hydrocarbon autooxidation pathway may be responsible for generation of hydrogen peroxide, which may be further converted to hydroxyl radicals through an iron-dependent reaction.

Aging↗
PubMedDate not supplied

Maganese retention in rat brain.

Manganese retention was observed in brains and in several other tissues of female Wistar rats after the intratracheal instillation of an inorganic manganese compound: manganese dioxide. Two categories of rats, younger (180 to 200g) and older (330 to 350g), were divided into a control group, in which animals received vehicle only (0.5 mL physiological saline), and an experimental group, in which rats received a dose of 0.48 mg of Mn/kg body weight (in 0.5 mL saline), twice a week for 3 months, for a total dosage of 11.80 mg of Mn/kg body weight. At the end of the exposure period, manganese retention in selected rat organs, brain, liver, kidney, and lung, was analyzed using atomic absorption spectrophotometry. At the end of the 6-wk or 12-wk manganese dioxide exposure period, analysis of variance of the manganese retention results revealed significant differences between Mn-exposed and unexposed rats in brain, kidney, and lung tissues (p<0.01) for both experimental age categories. Moreover, at the end of the 12-wk exposure period, significant results (p<0.05) between younger and older rats were obtained for both brain and kidneys. In both types of tissue, the manganese retention in the younger group was higher than that in older animals.

Aging↗
PubMed2002

Halofuginone does not reduce fibrosis in bleomycin-induced lung injury.

Halofuginone, a coccidiostatic alkaloid, has anti-fibrotic properties, and may be useful as a therapeutic agent in lung fibrosis. To test this hypothesis we investigated the effect of halofuginone on bleomycin-induced lung fibrosis in Sprague-Dawley rats. Treatment groups included: (1) a single intratracheal (IT) instillation of 1.2U bleomycin, and intraperitoneal (IP) injection of halofuginone (0.5 mg/dose), every other day; (2) IT 1.2U bleomycin and IP distilled water (D.W.), every other day; (3) IT 0.8U bleomycin and daily IP halofuginone (0.5 mg/dose); (4) IT 0.8U bleomycin and daily IP D.W.; (5) IT saline and IP halofuginone, every other day; (6) IT saline and daily IP D.W.; (7) IT 0.625U bleomycin and oral halofuginone (10 mg/kg rodent lab chow); (8) IT 0.625U bleomycin and standard lab chow. Animals were studied 14 days after IT instillation. Lung injury was evaluated by total and differential cell count in bronchoalveolar lavage fluid, by a semi-quantitative morphological index of lung injury, and by biochemical analysis of lung hydroxyproline content. Overt signs of lung injury were apparent in bleomycin-treated rats by all measures. These changes were not affected by treatment with halofuginone, irrespective of the treatment regimen used. This study does not support the use of halofuginone to prevent or ameliorate lung fibrosis.

Angiogenesis Inhibitors↗
PubMed1997

Pulmonary endocrine cell hyperplasia and papilloma in rats induced by intratracheal injections of extract from particulate air pollutants.

We investigated the effect of intratracheal injections of an extract of suspended particulate matter (SPM) obtained from the urban ambient air of Tokyo, upon the development of proliferative lesions of pulmonary endocrine cells (PECs) in the rat. We also examined the modification effects of nitrogen dioxide, sulfur dioxide, or both of them on the PEC lesions. Male F344 rats were divided into six experimental groups of 5 animals each. Twenty animals were treated with intratracheal instillations of SPM admixed with carbon once a week for 4 weeks with or without additional gaseous exposure (6 ppm nitrogen dioxide or 4 ppm sulfur dioxide) 16 hrs a day for 11 months. Five animals were given intratracheal injections of carbon suspended in saline and the other five were untreated. The subcardiac lobes of the right lung were fixed with 4% paraformaldehyde, and embedded in paraffin. PEC hyperplasias and papillomas were counted in 200 serial sections, 4 microns thick. The average incidences of PEC hyperplasia in the untreated animals and in those treated with carbon were 194 and 200/cm3, respectively. The average incidences of PEC hyperplasia in the animals exposed to SPM tar only, SPM tar plus nitrogen dioxide and sulfur dioxide, SPM tar with nitrogen dioxide and SPM tar with sulfur dioxide were 376, 378, 372 and 349/cm3, respectively. These were significantly higher than the levels of the control animals, and additional gaseous stimuli had no effect on the incidence of PEC hyperplasia. Besides PEC hyperplasia, a few PEC papillomas were found in the animals treated with SPM tar, regardless of gaseous exposure, but in the control animals no papilloma was evident. Thus, compounds in airborne particulates are considered to be responsible for the development of PEC hyperplasias and papillomas.

APUD Cells↗
PubMed1995

Concentrations of metal elements in mouse organs after intratracheal administration of coal fly ash.

Size-density fractionated coal fly ash particles, 1-5 microns in diameter and 2.4-2.8 g/cm3 in density, were administered to mouse lungs intratracheally. The change in the concentrations of metal elements in the lungs, kidneys, livers and spleens was measured by inductively coupled plasma atomic emission spectroscopy and atomic absorption spectroscopy up to 16 weeks after administration. In the lungs, each elemental concentration increased 1 week after administration and decreased thereafter with time after administration. For example, the concentrations of Al were 1018 +/- 272 micrograms/g tissue at 1 week and decreased thereafter to 556 +/- 177 micrograms/g tissue at 16 weeks after administration. The concentrations of Ca, Mn and Ni decreased more rapidly than the other elements, suggesting that Ca, Mn and Ni were dissociated from the alumino-silicate matrix of the fly ash particles in the lungs. In the kidneys, the concentration of Ni significantly increased at 2, 8 and 16 weeks after administration; the concentration of Ni showed an increase of 0.4 +/- 0.2 micrograms/g over the control mouse at 16 weeks after administration. In the livers, increased concentrations of Ca and Mn were observed at 2, 4 and 16 weeks. On the other hand, no changes in the concentrations of these elements were observed in the spleen.

Animals↗
PubMed1995

Sephadex induced granulomatous reaction in rats.

Granuloma formation in the rat lung after single or repeated i.v. injections, intratracheal instillation and intradermal implantation of Sephadex beads was studied over a time period from 3 h to 3 mo. Macrophages were identified with the mAB ED1, vascular smooth muscle cells with an mAB against alpha SMC-actin, endothelial cells with a polyclonal AB against factor VIII and cyclic activity with an mAB against PCNA. The morphology and the time course of the development of the granulomas is identical in the different experimental conditions. The macrophages form the bulk of the cellular infiltrates, giant cells appear after 24 h. Cyclic activity is early and marked in the interstitially located macrophages, it is delayed and slight around the beads, suggesting a biphasic pattern. The macrophage reaction is markedly enhanced after a second i.v. injection, indicating the development of a hypersensitivity state. Numerous eosinophils are located in the interstitium, but only few are in direct contact with the beads. Their number doesn't increase after a second i.v. injection. Intradermal implantations show only macrophages and lymphocytes. A special feature is the disappearance of the arterial wall around the beads resulting in extrusion without haemorrhages or thromboses.

Animals↗
PubMed2003

Diesel exhaust particle-induced alterations of pulmonary phase I and phase II enzymes of rats.

Although diesel exhaust particles (DEP) are known to produce pulmonary disorders, the xenobiotic metabolic pathways associated with DEP detoxification and bioactivation remain unclear. In this study, the effect of acute exposure of DEP on phase I and phase II enzymes of rat lung was investigated. Intratracheal administration of DEP produced an induction of cytochrome P-450 (CYP) 1A1 enzyme protein and activity at 1 d postexposure, with the enzyme level returning to control at 5 d postexposure. On the other hand, carbon black (CB), a particle control, did not show any induction of CYP1A1 protein or enzyme activity. However, both DEP and CB significantly decreased CYP2B1 protein and enzyme activity at 1 d postexposure. The decrease in CYP2B1 enzyme protein and activity by DEP or CB treatment was observed up to 7 d postexposure. DEP and CB treatments also significantly attenuated glutathione S-transferase (GST)-pi protein at 1 d postexposure. Both DEP and CB at 35 mg/kg significantly decreased the activities of GST and catalase at 1 and 7 d postexposure. DEP, but not CB, significantly induced quinone reductase (QR) activity at 7 d postexposure. This study suggests that DEP may induce CYP1A1 and QR enzymes via a chemical effect, while the carbonaceous core may be involved in the attenuation of CYP2B1, GST, and catalase proteins and enzyme activities.

Animals↗
PubMed2002

Microscopic changes induced by the intratracheal inoculation of amniotic fluid and meconium in the lung of neonatal rats.

Meconium aspiration syndrome is a major contributor to neonatal respiratory distress in infants and it has been sporadically recognized in neonatal animals. This investigation was designed to study the short and long term effects of meconium and amniotic fluid in the lungs of neonatal rats. Seven-day-old rats (n = 123) divided in three groups were intratracheally inoculated with saline solution, amniotic fluid or meconium. Rats were euthanatized on 1, 3, 7, 14, 28, 56 and 112 postinoculation days (PID) and the lungs were examined by light microscopy. Saline solution did not induce any change while amniotic fluid elicited only a mild foreign body response which disappeared by PID 14. In contrast, meconium induced an exudative alveolitis characterized by recruitment of neutrophilsn in the bronchoalveolar spaces. Meconium also induced atelectasis, hyperinflation and thickening of alveolar septa all of which had disappeared by PID 14. Starting at PID 7, neutrophils were progressively replaced by macrophages, giant cells, and some fibroblasts. There were sporadic foci of mineralization starting at PID 14 and lasting up to PID 112. Some mineralized foci became lined with cuboidal epithelial cells at PID 28. Meconium was slowly degraded but still evident by PID 112. It was concluded that inoculation of meconium in neonatal rats induces acute microscopic changes typical of meconium aspiration syndrome. The long term lesions induced by meconium consisted of persistent multifocal histiocytic alveolitis and bronchiolitis reaction with occasional foci of calcification.

Amniotic Fluid↗
PubMed1999

[Continuous flow apnoeic ventilation via intratracheal oxygen insufflation].

BACKGROUND: In patients with disturbed gas-exchange (e.g. COPD) intratracheal oxygen insufflation (ITO2) improves oxygenation and reduces the minute ventilation. We use a bronchoscopic technique of intratracheal catheter placement in unintubated patients. In a patient with a pink-puffer emphysema after endoscopical insertion of the catheter ITO2 induced a "continuous flow apnoeic ventilation" (CFAV). CASE REPORT: A patient (female, 58 years) with a pink-puffer emphysema was admitted to the ICU with acute on chronic respiratory failure due to acute laryngitis. Because of laryngitis associated upper airway obstruction a non-invasive mechanical ventilation could not be performed. The ensuing high flow ITO2 (10 l/min) induced a CFAV characterized by no chest wall movement and adequate ventilation as reflected by stable, elevated PaCO2 (between 118 and 125 mm Hg), which could be maintained for 4 hours. After an ensuing short-term invasive mechanical ventilation and the administration of high dose glucocorticoids the patient was successfully extubated and the clinical status improved continuously. CONCLUSION: In a patient with an acute on chronic respiratory failure due to end-stage emphysema ITO2 induced CFAV and stabilized the clinical status. Especially in patients with end-stage emphysema, who are likely to be difficult to be weaned from the respirator ITO2 may be a feasible technique in order to bridge an emergency situation.

Emphysema↗
PubMed2001

Trimellitic anhydride-induced eosinophilia in a mouse model of occupational asthma.

Trimellitic anhydride (TMA) is a low-molecular-weight chemical known to cause occupational asthma. The present study was designed to determine if TMA elicited eosinophil infiltration into lungs of sensitized mice similar to previous studies with the protein allergen ovalbumin (OA). BALB/c mice were sensitized intradermally with 0.1 ml of 3% TMA or 0.3% OA in corn oil followed by intratracheal instillation with TMA conjugated to mouse serum albumin (TMA-MSA; 30 or 400 microg) or OA (30 microg). Nonsensitized mice received corn oil vehicle intradermally and MSA (30 microg) intratracheally. The allergic response was elicited 3 weeks later by intratracheal instillation of 30 or 400 microg TMA-MSA, OA, or control MSA. Cellular infiltration into bronchoalveolar lavage fluid (BAL) was determined 72 h later. Eosinophil peroxidase (EPO) and myeloperoxidase (MPO) activity in lung homogenates was used as an estimate of numbers of eosinophils and neutrophils, respectively, in lung tissue. In TMA-sensitized mice, TMA-MSA challenge significantly increased numbers of eosinophils in BAL and EPO in lung, indicating an increase in number of eosinophils in the airway and tissue. In nonsensitized mice, TMA-MSA challenge also caused a small but significant increase in eosinophils in BAL compared to MSA control. Total IgE in both plasma and BAL was significantly higher in TMA-sensitized compared to nonsensitized mice. The eosinophil infiltration in TMA-sensitized mice was similar in magnitude to the response in OA-sensitized mice. These studies are the first to demonstrate TMA-induced eosinophilia in mouse lung and to provide a model for comparing mechanisms and mediators responsible for the substantial eosinophilia induced by TMA and OA.

Allergens↗