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PubMed1995

Pulmonary responses to amiodarone in hamsters: comparison of intratracheal and oral administrations.

Amiodarone (AD) has been shown to produce a transient pulmonary fibrosis in hamsters after intratracheal (i.t.) instillation. The goal of this study was to examine bronchoalveolar lavage (BAL) parameters during the development of fibrosis after i.t. AD in hamsters and to examine the responses to oral AD in hamsters for comparison to responses to i.t. AD in an effort to explore the roles of inflammation, phospholipidosis, and lung drug burden in AD-induced pulmonary disease. Two i.t. instillations on Days 0 and 7 of AD in hamsters produced fibrosis as characterized by elevated lung hydroxyproline content and variable increases in lavage macrophage, neutrophil, and eosinophil number through Day 28. Intratracheal AD also increased the permeability of the alveolar-capillary barrier as evidenced by an increase in BAL fluid albumin only on Day 8. Pulmonary phospholipidosis was not induced by i.t. AD and only small amounts of AD and its metabolite desethyl-AD (dAD) were detected in lung tissue through Day 10 after instillation on Days 0 and 7. The repeated oral administration of AD did not result in pulmonary fibrosis during the 35-day course of this study. Oral AD did cause a sustained increase in BAL fluid neutrophil number; other BAL cells were only slightly affected. Oral AD did not increase BAL fluid albumin content but a prominent BAL cell phospholipidosis was noted. Measurement of AD and dAD in lung tissue demonstrated a substantial accumulation of drug and metabolite after oral treatment with AD. The results of this study indicate that lung drug burden, pulmonary phospholipidosis, and lung neutrophil influx are not crucial factors in the development of AD-induced pulmonary fibrosis in hamsters. This study supports the possible involvement of physical damage to the lung and/or pulmonary eosinophilia in the generation of AD-induced pulmonary fibrosis in hamsters.

Administration, Oral↗
PubMed2001

Intratracheal priming with ovalbumin- and ovalbumin 323-339 peptide-pulsed dendritic cells induces airway hyperresponsiveness, lung eosinophilia, goblet cell hyperplasia, and inflammation.

Dendritic cells (DC) are the primary APC responsible for the capture of allergens in the airways and the shuttling of processed allergens to the draining lymph nodes where Ag presentation and T cell activation take place. The mechanism of this Ag handling and presentation in asthma is poorly understood. In addition, the feasibility of asthma induction by DC priming has not been directly tested. In this report an asthma model using intratracheally (i.t.) injected splenic DC was used to address these issues. DC pulsed with a model Ag OVA or the major MHC class II-restricted OVA T epitope peptide OVA(323-339) and instilled i.t. primed mice to exhibit asthma-like diseases. With OVA as the Ag, mice exhibit airway hyperresponsiveness (AHR), lung eosinophilia and inflammation, and pulmonary goblet cell hyperplasia. In OVA(323-339)-immunized mice, AHR and goblet cell hyperplasia were noted, with little eosinophilia and parenchymal inflammation. The latter finding provides evidence for dissociating AHR from eosinophilia. In both cases mediastinal node hypertrophy occurred, and high levels of Th2 cytokines were produced by the lung and mediastinal lymph node cells (LNC). Interestingly, mediastinal LNC also produced high levels of Th1 cytokines. Lung cells produced much less Th1 cytokines than these LNC. These results demonstrate that DC when introduced i.t. are potent in inducing asthma-like diseases by recruiting lymphocytes to the lung-draining lymph nodes and by stimulating Th2 responses and also suggest that the lung environment strongly biases T cell responses to Th2.

Animals↗
PubMed1996

Expression of inducible nitric oxide synthase and its involvement in pulmonary granulomatous inflammation in rats.

Two types of pulmonary granulomatosis were produced in rats by intratracheal instillation of zymosan or silica. In both models, immunostaining with anti-rat monoclonal antibody for inducible nitric oxide synthase (iNOS), ANOS11, showed that the intensity of iNOS immunoreactivity in the inflammatory lesions peaked at 3 days and declined thereafter. Immunohistochemical double staining and in situ hybridization demonstrated the expression of iNOS in neutrophils, monocyte-derived macrophages, and bronchiolar epithelial cells in the pulmonary lesions. Electron spin resonance spectroscopy revealed the production of an excessive amount of nitric oxide (NO) in the pulmonary lesions. Immunostaining with a polyclonal antibody against nitrotyrosine indicated the formation of nitrotyrosine residues in the granulomatous lesions, particularly in the periphery of the lesions, providing indirect evidence for the generation of peroxynitrite anion in the zymosan- or silica-instilled lungs. Administration of N omega-nitro-L-arginine methyl ester or S-methylisothiourea sulfate, which significantly suppressed NO production, resulted in marked reduction of monocyte/macrophage infiltration as well as in inhibition of induction of monocyte chemoattractant protein-1 in the lesions. These data indicate that NO and its more reactive product peroxynitrite anion may be important mediators of granuloma formation in the lung.

Animals↗
PubMed1997

In vivo accumulation of iron on crocidolite is associated with decrements in oxidant generation by the fiber.

In vivo exposures to fibrous silicates are characterized by the formation of asbestos bodies. These structures consist of the original fiber with a coating of inexact composition, but it will include iron and protein. We tested the hypothesis that this iron, accumulated on asbestos bodies, participates in electron transport and oxidant generation. Thirty-day-old, male guinea pigs were intratracheally instilled with 1.0 mg crocidolite. Six months later, the animals were anesthetized, euthanized, and the fibers were isolated from the lungs. Energy-dispersive x-ray analysis and x-ray photoelectron spectroscopy confirmed an accumulation of metal onto the fiber after in vivo exposure. Stains for iron demonstrated a heterogeneous distribution of the metal on the silicate, while the uptake of a commercially available polyclonal antibody to ferritin localized to beaded enlargements along the coated fibers. Chelatable [Fe3+] associated with the fiber increased after in vivo exposure. However, oxidant generation by asbestos bodies was decreased relative to uncoated fibers despite the elevation in the concentration of metal associated with the crocidolite. We conclude that iron is accumulated onto fibers in the lungs of guinea pigs. Some portion of this accumulation of iron is in the form of ferritin, and this metal is not chemically reactive in oxidant production. Asbestos bodies may represent a successful attempt by the host to sequester the metal adsorbed to the surface of a fiber and diminish the oxidative challenge introduced by a fibrous silicate. Subsequently, the generation of free radicals by the fibrous silicate is diminished.

Animals↗
PubMed1993

Pulmonary clearance and toxicity of intratracheally instilled cupric oxide in rats.

Pulmonary clearance and toxicity of cupric oxide (CuO) dusts, which are probably formed in refining and smelting factories, were investigated. Groups of three rats received intratracheal (i.t.) instillation of CuO at a dose of 20 micrograms Cu/rat in time-course experiments (up to 7 days post-instillation). Other groups of three rats received i.t. instillation of CuO at doses of 2.5, 5, 10, 30, 50 and 100 micrograms Cu/rat and were killed at 2 days post-instillation in dose-effect experiments. Intratracheally instilled CuO particles were cleared from the lung with a half-time of 37 h. Copper binding metallothionein (MT) was induced in a dose-dependent manner and detected at 12 h to 3 days post-instillation. Rapid clearance of CuO from the lung and induction of MT at 12 h post-instillation suggest that CuO particles were solubilized and then cleared from the lung. The acute pulmonary toxicity of CuO was evaluated by cytological (numbers of macrophages and polymorphonuclear leukocytes), biochemical and elemental inflammatory indices (lactate dehydrogenase and beta-glucuronidase activities and protein, sulfur, phosphorus and calcium contents) in the bronchoalveolar lavage (BAL) fluid. These inflammatory indices peaked at 12 h to 3 days post-instillation, and increased with dose over the dose range, except for phosphorus content. Dose-effect relationships in BAL inflammatory indicators of CuO-injected (i.t.) groups were compared to those of CuSO4-injected (i.t.) groups. The results of the comparison indicated that there was no significant difference in acute inflammatory potency between CuSO4 (soluble form of Cu) and CuO (insoluble form of Cu) in the rat lung.

Air Pollutants, Occupational↗
PubMed1999

Human meconium has high phospholipase A2 activity and induces cellular injury and apoptosis in piglet lungs.

Aspiration of meconium produces an inflammatory reaction resulting in necrotic changes in lung tissue. To further investigate the mechanisms of the meconium-induced early pulmonary injury, twenty 10-12-d-old piglets were studied for lung tissue ultrastructural and apoptotic changes and phospholipase A2 activity. Twelve piglets received an intratracheal bolus (3 mL/kg) of a 20-mg/mL (thin, n = 6) or 65-mg/mL (thick, n = 6) mixture of human meconium, and control piglets (n = 5) received the same amount of intratracheal saline. Three ventilated piglets with no aspiration were also studied. Pulmonary hemodynamics and systemic oxygenation were followed for 6 h after meconium or saline insufflation. In the control groups, the pulmonary tissue showed open alveolar spaces and intact vascular walls, whereas meconium administration resulted in severe pneumonitis, with alveolar spaces filled with inflammatory exudate. Meconium instillation additionally resulted in edematous changes in the vascular walls and alveolar epithelium, whereas type II pneumocytes were intact. The amount of apoptotic cells was increased, especially in the respiratory epithelium, and the catalytic activity of phospholipase A2 in lung tissue samples was significantly elevated after thick meconium instillation. This activity rise proved to be mainly because of human group I phospholipase A2, introduced by meconium. Our data thus show that aspiration of meconium leads to severe lung tissue inflammation with early ultrastructural changes in the pulmonary alveolar walls and is associated with apoptotic cell death in the epithelium, already during the first hours after the insult. These results further suggest that high phospholipase A2 activity, mainly introduced into the lungs within the meconium, may have an important role in the initiation of these alterations in neonatal lungs.

Animals↗
PubMed1992

Protective effect of pulmonary surfactant on elastase-induced emphysema in mice.

The aim of this study was to obtain some evidence of a protective role for pulmonary surfactant in the pathogenesis of emphysema. Firstly, we developed a quick and easy method to treat mice with a series of intratracheal instillations. Subsequently, three groups of mice were treated as follows: two groups received intratracheal instillations with pancreatic elastase (1.8 mg.kg-1 BW) followed after 3, 48 and 96 h in one group (El/Surf group) by intratracheal administration of surfactant (100 mg phospholipid.kg-1 BW), and in the other group by instillations with saline (El/s group). The third group of control mice was treated with saline followed by three doses of surfactant (s/Surf group). After eight weeks, the mice were killed and emphysema was measured by calculating the mean linear intercepts (Lm) of airspaces. The Lm values in the different groups were statistically tested for differences by the Mann-Whitney test. Instillation of pancreatic elastase (El/s group) resulted in an evenly distributed increase in Lm compared with the control group. Administration of surfactant in elastase-treated mice (El/Surf group) resulted in a statistically significant inhibition of airspace enlargement. Although the Lm in the El/Surf group was still higher than in the control group, analysis of histograms of Lm values per field of examination revealed that the Lm distribution in the former group was similar to that of the s/Surf group. The El/s group, on the contrary, showed the presence of many fields with enlarged air spaces. Repeated instillations with saline and/or surfactant had no effect on the Lm.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Inhalation↗
PubMed1999

Increased 8-hydroxyguanine in DNA and its repair activity in hamster and rat lung after intratracheal instillation of crocidolite asbestos.

Asbestos and man-made-mineral fibers are known to increase one type of oxidative DNA damage, 8-hydroxyguanine (8-OH-(Gua), in vitro. In this study, we analyzed the 8-OH-Gua level in DNA and its repair activity after a single intratracheal instillation of fibers (crocidolite or glass) or saline to Syrian hamsters or Wistar rats. The 8-OH-Gua level was measured with a high-performance liquid chromatography-electrochemical detector (HPLC-ECD) system. The 8-OH-Gua repair enzyme activity was determined with an endonuclease nicking assay using a 32P-labeled or fluorescently labeled 22mer DNA that contains 8-OH-Gua at a specific position. A significant increase in the 8-OH-Gua level in the lung DNA was observed 1 day after the exposure to crocidolite, as compared to the saline control. The repair activity was increased significantly at 7 days. On the other hand, after exposure to glass fibers, little or no increase of these carcinogenicity indicators was detected. These assays of 8-OH-Gua and its repair activity in short-term animal experiments will be useful for evaluating the carcinogenicity of fibers. This is the first report of the increase of 8-OH-Gua and its repair activity in the animal lung after the instillation of asbestos fibers.

Animals↗
PubMed2000

Increased elastase and myeloperoxidase activity associated with neutrophil recruitment by IL-17 in airways in vivo.

BACKGROUND: A recent study demonstrated that intratracheal administration of the T-lymphocyte cytokine IL-17 recruits neutrophils into airways in vivo by C-X-C chemokine release. It is not known whether IL-17 may also activate airway neutrophils. OBJECTIVE: Our purpose was to evaluate whether IL-17 activates neutrophils in airways in vivo and, if so, whether the proinflammatory cytokine IL-1beta modulates this action of IL-17. METHODS: Intratracheal administration of human (h) IL-17 or rat (r) IL-1beta or hIL-17 plus rIL-1beta in anesthetized, spontaneously breathing rats was followed by bronchoalveolar lavage (BAL) 6 hours later. The BAL fluid was characterized in terms of neutrophil count, of the activity for myeloperoxidase (MPO), and in some cases of the activity for elastase (ELA). Isolated rat neutrophils were stimulated with hIL-17 in vitro, followed by characterization of MPO activity in the cell medium. RESULTS: hIL-17 (1 microg) increased the ELA and the MPO activity, as well as the neutrophil count in BAL fluid, whereas the proinflammatory cytokine rIL-1beta (2.5 ng) did not. Pretreatment with rIL-1beta enhanced IL-17induced ELA and MPO activity, without increasing the neutrophil count. The BAL ELA activity was inhibited by a specific inhibitor of neutrophil serine proteases. Stimulation with hIL-17 in vitro did not increase MPO activity in isolated neutrophils. CONCLUSION: IL-17 can activate neutrophils in association with their recruitment into the airways in vivo and this effect is probably achieved through induced release of mediators from other airway cells.

Animals↗
PubMed1999

Bioavailability of a small unilamellar low-clearance liposomal amikacin formulation after extravascular administration.

Amikacin in small, low-clearance liposomes (MiKasome) has prolonged plasma and tissue residence and in vivo activity against extracellular infections, including Klebsiella pneumonia and Pseudomonas endocarditis. Small liposomes may cross endothelial barriers, and enter the systemic circulation after extravascular administration. We compared the systemic bioavailability (F) of low-clearance liposomal amikacin in rats following intravenous (i.v.), intraperitoneal (i.p.), intramuscular (i.m.) and subcutaneous (s.c.) injection (20 mg/kg) and intratracheal (i.t.) instillation (10 mg/kg). Drug-containing liposomes were extensively absorbed after i.p. (F = 87-146%) and i.t. (F = 64%) administration, with maximum amikacin plasma concentrations of 171 micrograms/ml at 9 h and 80 micrograms/ml at 18 h, respectively. Absorption was slower and less extensive following s.c. (plasma Tmax: 20.3 micrograms/ml at 48 h) and i.m. (plasma Tmax: 49.6 micrograms/ml at 19 h) injection, but a significant fraction (12-27%) of the liposomes was absorbed. The plasma AUCs of liposomal amikacin exceeded the AUC of conventional i.v. amikacin by at least 25-fold for all routes. Amikacin AUCs in regional lymph nodes exceeded plasma AUCs by 4-fold after s.c. and i.m. injection of liposomal amikacin. AUCs in tissues surrounding the injection sites were 20- and 191-fold higher than plasma AUCs after i.m. and s.c. injection, respectively. Thus, small low-clearance liposomes produced sustained levels of liposome-encapsulated amikacin in plasma, local tissues and lymph nodes after extravascular administration, suggesting applications in perioperative prophylaxis, pneumonias and intralesional therapy as well as sustained systemic delivery of encapsulated drugs.

Amikacin↗
PubMed1998

Blood monocyte migration to acute lung inflammation involves both CD11/CD18 and very late activation antigen-4-dependent and independent pathways.

In acute lung inflammation, blood neutrophils and monocytes migrate into the lung parenchyma and bronchoalveolar space. The infiltration of the inflamed lung by monocytes is poorly understood because of difficulties in quantifying these cells in the presence of resident macrophages. Radiolabeled monocytes were used to study monocyte migration into the inflamed rat lung. Monocytes and neutrophils were purified from blood, labeled with 51Cr and (111)In, respectively, and injected i.v. into rats given an intratracheal injection of LPS. The accumulation of 51Cr-labeled monocytes increased > 10-fold in the lung parenchyma and 170-fold in the bronchoalveolar lavage (BAL) 18 h after LPS. (111)In-labeled neutrophils increased > 30-fold in the lung tissue and 500-fold in the BAL. Treatment of rats with a blocking anti-CD18 mAb inhibited monocyte accumulation in the lung and BAL by about 30%, whereas blocking very late activation Ag-4 (VLA-4) had no effect. Combined blockade of VLA-4 and CD18 inhibited approximately 30% of the migration to the lung parenchyma, but decreased the BAL by 80%. Monocyte migration to cutaneous inflammation was completely abolished by the combined mAb treatment. Neutrophil accumulation in the lung and BAL was not decreased by blocking either CD18 or VLA-4 and was only partially reduced by blocking CD18 plus VLA-4. Thus, monocyte migration to the LPS inflamed lung is substantially CD11/CD18 and VLA-4 independent, but accumulation in BAL is mediated by CD18 and VLA-4. Monocytes as well as neutrophils may use a previously unrecognized endothelial adhesion and migration pathway in the lung.

Acute Disease↗
PubMed2001

CD40/CD40 ligand interactions are critical for elicitation of autoimmune-mediated fibrosis in the lung.

Pulmonary interstitial fibrosis (PIF), associated with persistent inflammation and increased collagen deposition in the interstitium, is often considered an autoimmune disease. Hapten immune PIF (HIPIF), a model for PIF, is elicited in the lung by a single intratracheal (i.t.) challenge in mice sensitized with hapten (2,4,6-trinitrobenzene sulfonic acid, TNBS). In this study, we characterized the role of CD40/CD40 ligand (CD40L) interactions in the elicitation of secondary cell-mediated immune responses that lead to development of fibrosis in the lung using an adoptive transfer model of HIPIF. The expression of CD40 was detected on bronchoalveolar lavage (BAL) cells 1-3 days after i.t. challenge with hapten in the HIPIF lung, but not lungs from the control mice. The CD40(bright) BAL cells morphologically resembled infiltrating monocytes. Furthermore, blocking CD40/CD40L interactions with blocking Ab decreased BAL production of Th1-mediators (IL-12 and TNF-alpha). Moreover, either blocking CD40/CD40L interactions with the Ab or using IL-12 knockout recipient mice prevented the increased collagen deposition (accumulation of hydroxyproline) in the lungs during HIPIF induction. We conclude that second signals (CD40/CD40L interactions) are required for elicitation of secondary immune responses that lead to PIF in vivo. The results support the notion that CD40/CD40L interactions are involved in the pathogenesis of an ongoing autoimmune disease.

Animals↗
PubMed2006

Toll/IL-1R domain-containing adaptor protein (TIRAP) is a critical mediator of antibacterial defense in the lung against Klebsiella pneumoniae but not Pseudomonas aeruginosa.

Bacterial pneumonia is a leading cause of mortality and is associated with extensive neutrophil accumulation. Major pathogens associated with this disease include nonflagellated Klebsiella pneumoniae (Kp) and flagellated Pseudomonas aeruginosa (Pa). TLRs are essential for innate immune defense. TIRAP (Toll/IL-1R domain-containing adaptor protein) is an adaptor in TLR1, TLR2, TLR4, and TLR6 signaling, whereas MyD88 is an adaptor for all TLRs. However, the importance of TIRAP in pulmonary defense against Kp or Pa has not been examined. To demonstrate the role of TIRAP, TIRAP-deficient and wild-type littermates were intratracheally inoculated with Kp or Pa. We found that TIRAP(-/-) mice had substantial mortality, higher bacterial burden in the lungs, and enhanced dissemination following Kp challenge. Furthermore, Kp-induced neutrophil sequestration, histopathology, and MIP-2, TNF-alpha, IL-6, and LIX (lipopolysaccharide-induced CXC chemokine) production were attenuated in the lungs of TIRAP(-/-) mice. In contrast, TIRAP is not required for Pa-induced mortality, pulmonary bacterial burden, bacterial dissemination, neutrophil accumulation, or histopathology, yet it is necessary for MIP-2, TNF-alpha, and IL-6 production, but not LIX production. However, both Kp- and Pa-induced neutrophil influxes are MyD88 dependent. To determine the mechanisms associated with Pa-induced neutrophil accumulation, we inoculated mice with a flagellin C mutant of Pa (PaDeltafliC) or purified flagellin, a TLR5 agonist. PaDeltafliC-induced neutrophil sequestration and LIX expression are dependent on TIRAP, whereas flagellin-induced neutrophil influx and LIX expression are independent of TIRAP. These novel findings illustrate a pathogen-specific role for TIRAP in pulmonary defense and suggest that TLR5 plays an essential role for Pa-induced neutrophil influx via LIX production.

Animals↗
PubMed1996

Intratracheal pulmonary ventilation provides effective ventilation in a near-drowning model.

Overdistension of the lungs from high inspiratory pressure is increasingly recognized as a major contributor to lung injury and worsening respiratory failure in the child who requires prolonged mechanical ventilation. Many modes of ventilation (such as high-frequency ventilation) have been introduced in an attempt to decrease this lung injury. Recently, a new mode of tracheal ventilation, intratracheal pulmonary ventilation (ITPV), has been described. By using a catheter positioned at the carina with continuous gas flow, it is possible to achieve effective ventilation at very low pressures. The purpose of this study was to evaluate the usefulness of ITPV in a near-drowning model. Ten domestic Yorkshire swine underwent arterial, venous, and pulmonary arterial catheter as well as tracheotomy placement. All animals received 13 mL/kg of fresh water intratracheally to induce a pulmonary injury. Six pigs were ventilated for 4 hours using ITPV; the other four pigs received conventional mechanical ventilation (CMV). Circulatory and ventilatory pressures, hemodynamic variables, arterial blood gases, and end-tidal CO2 were measured before lung injury and every 30 minutes thereafter. Both proximal and distal peak and mean airway pressures were measured. The animals were ventilated as needed to maintain the arterial blood gases in the normal range. The authors found the expected changes in pulmonary compliance, oxygen requirement, and airway pressure after inducement of lung injury. The six animals treated with ITPV had significantly lower airway pressures than those of controls. Peak inspiratory pressures with ITPV were 8.2 +/- 1.9 cm H2O versus 17.8 +/- 3.7 with CMV (P < .001). Distal mean airway pressures using ITPV were 2.3 +/- 0.1 cm H2O versus 9.0 +/- 3.2 with CMV (P < .01). With respect to hemodynamic variables, there were no differences between experimental and control animals. In conclusion, ITPV can afford effective ventilation in a near-drowning model of lung injury at airway pressures significantly lower than those required with CMV. ITPV could be a very valuable addition to the currently available methods of mechanical ventilation.

Animals↗
PubMed2006

Acute and subacute pulmonary toxicity of low dose of ultrafine colloidal silica particles in mice after intratracheal instillation.

To study the acute and subacute lung toxicity of low dose of ultrafine colloidal silica particles (UFCSs), mice were intratracheally instilled with 0, 0.3, 3, 10, 30 or 100 microg of UFCSs. Cellular and biochemical parameters in bronchoalveolar lavage fluid (BALF), histological alteration and the body weight were determined at 3 days after instillation. Exposure to 30 or 100 microg of UFCSs produced moderate to severe pulmonary inflammation and tissue injury. To investigate the time response, mice were instilled with 30 microg of UFCSs and sacrificed at intervals from 1 to 30 days post-exposure. UFCSs induced moderate pulmonary inflammation and injury on BALF indices at acute period; however, these changes gradually regressed until recovery during the experiment. Concomitant histopathological and laminin immunohistochemical findings generally correlated to BALF data. TUNEL analyses in UFCSs-treated animals showed a significant increase of the apoptotic index in lung parenchyma at all observation times. 8-OHdG expression occurred in lung epithelial cells and activated macrophages, which correlated to lung lesions in UFCSs-treated mice. These findings suggest that instillation of a small dose of UFCSs causes transient acute moderate lung inflammation and tissue damage. Oxidative stress and apoptosis may underlie the lung tissue injury induction.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed1996

Efficacy of cardiopulmonary resuscitation using intratracheal insufflation.

The effects of constant-flow insufflation (CFI) of air in the trachea at the distal end of a modified endotracheal tube as the sole mode of ventilation during cardiopulmonary resuscitation (CPR) were studied in pigs. The ventilatory effect of CFI (15 +/- 2 L/min) generating a positive pressure of about 10 cm H2O with concomitant chest compression was studied first. In nine sedated, paralyzed animals disconnected from the ventilator, CFI alone did not significantly alter the decrease in PaO2 and the rise in PaCO2 observed during apnea. By contrast, the combination of precordial compression and CFI (CFI-CPR) maintained arterial blood gases over a 4-min period at the level obtained during mechanical ventilation. In the second part of the study, ventricular fibrillation was induced and CFI-CPR was compared with standard CPR using conventional mechanical ventilation during two successive 4-min periods, in random order. Ventilatory parameters were identical in the two situations, whereas hemodynamic parameters were similar or better with CFI-CPR than with standard CPR. Significant differences were observed between standard CPR and CFI-CPR for systolic aortic pressure (72 +/- 22 versus 82 +/- 27 mm Hg, respectively; p < 0.02) and for systolic (322 +/- 216 versus 431 +/- 237 ml/s; p < 0.01) and mean (116 +/- 106 versus 143 +/- 108 ml/s; p < 0.01) common carotid blood flows. The ease of use of CFI together with its beneficial hemodynamic effects suggests that CFI deserves to be investigated further as a mode of ventilation during CPR.

Animals↗
PubMed1995

Response of mouse lung to carbon deposition during injury and repair.

Increased respiratory disease and daily mortality rates are associated with higher levels of fine particulate air pollutants. We examined the possibility that deposition of even inert particles to previously injured lungs may accentuate pulmonary damage by investigating how the lung handles small carbon particles delivered during acute injury or during fibrotic repair. Mice received 2 mg carbon by intratracheal instillation into lungs already showing acute injury, 3 days after bleomycin (BL), or into lungs with fibrosis, 4 weeks after BL. At 3 days after BL, injury to the type I alveolar epithelium resulted in high protein levels in lavage fluid. Instilling carbon at this time induced a large increase in inflammatory cells, though many particles reached the interstitium, and a high proportion was retained up to 16 weeks later. However, fibrosis in these mice was equal to that found after BL alone. In the mice that received carbon 4 weeks after bleomycin, fibrotic repair had already occurred, and the epithelial surface was restored before particle instillation. After carbon, the subsequent inflammatory reaction cleared most particles, little reached the interstitium, and carbon retained at 16 weeks was not different from that in the carbon-only group. Instilling particles into fibrotic lung did not induce additional fibroblast growth or collagen production. The results indicate that instillation of fine particulates to the alveoli at a time of epithelial injury results in increased translocation to the interstitium. However, deposition of pure carbon into injured lungs does not further stimulate an ongoing fibrotic process, although it alters the patterns of particle deposition and retention in the lung.

Animals↗
PubMed1995

End-tidal oxygen concentration and pulse oximetry for monitoring oxygenation during intratracheal jet ventilation.

OBJECTIVE: In this study, we evaluated the usefulness of end-tidal oxygen monitoring during intratracheal jet ventilation (ITJV) for endolaryngeal laser surgery. METHODS: A total of 20 consecutive patients of both genders scheduled for endolaryngeal procedures under general anesthesia were studied. Inspiratory oxygen concentration and respiratory rate were varied, with patients serving as their own controls. Readings of pulse oximetry, airway oxygen, and carbon dioxide concentrations were recorded, and arterial blood samples for blood gas analysis were taken. RESULTS: At jet cycle rates of 20 cycles/min, end-tidal oxygen (ETO2) concentration indicated alveolar hypoxia 30 to 60 sec before hypoxemia was detected by pulse oximetry. Jet mixing of inspiratory and expiratory gas caused a larger difference between end-tidal and arterial gas concentrations than normally seen with conventional ventilation. Correlations between ETO2 concentrations, oxygen saturations, and arterial oxygen levels depended on respiratory rate and inspiratory oxygen concentration; correlations were stronger at low than at high inspiratory oxygen concentrations and stronger at low than at high respiratory rates. CONCLUSIONS: ETO2 concentration should be maintained well over 21% during ITJV to prevent alveolar and arterial hypoxia. Monitoring of respiratory oxygen concentrations at jet cycle rates of 20 cycles/min and less verifies safe oxygen levels during laser surgery, and confirms adequate alveolar oxygenation.

Adult↗