Comparison of upper and lower airway responses of two sensitized rat strains to inhaled antigen

1992 ◽  
Vol 73 (4) ◽  
pp. 1608-1613 ◽  
Author(s):  
L. J. Xu ◽  
S. Sapienza ◽  
T. Du ◽  
S. Waserman ◽  
J. G. Martin
Keyword(s):  
Upper Airway ◽  
Brown Norway ◽  
Lower Airway ◽  
Sprague Dawley ◽  
Pulmonary Resistance ◽  
Upper Airways ◽  
Tracheal Pressure ◽  
Airway Response ◽  
Airway Responses ◽  
Inbred Rat

The purpose of the study was to investigate the relationships between upper airways responses and pulmonary responses of two strains of highly inbred rats to inhaled antigen. To do this we measured the upper and lower airways resistance for 60 min after challenge of Brown-Norway rats (BN; n = 13) and an inbred rat strain (MF; n = 11), derived from Sprague-Dawley, with aerosolized ovalbumin (OA). Rats were actively sensitized with OA (1 mg sc) using Bordetella pertussis as an adjuvant. Two weeks later the animals were anesthetized and challenged. Tracheal pressure, esophageal pressure, and airflow were measured, from which total pulmonary resistance was partitioned into upper airway and lower pulmonary resistance (RL). The peak upper airway response to inhaled OA was similar in BN (1.89 +/- 0.66 cmH2O.ml-1.s; n = 7) and MF (2.85 +/- 0.68 cmH2O.ml-1.s; n = 6). The lower airway response to OA challenge was substantially greater in BN, and RL changed from 0.07 +/- 0.01 to 0.34 +/- 0.13 (n = 6; P < 0.05). The MF did not have any significant increase in RL after challenge; the baseline RL was 0.12 +/- 0.02 and only reached a peak value of 0.15 +/- 0.05 (n = 5; P = NS). Lower airway responsiveness of BN (n = 10) to serotonin, an important mediator early allergic airway responses, was similar to MF (n = 7).(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Strain dependence of the airway response to dry-gas hyperpnea challenge in the rat

1999 ◽  
Vol 86 (1) ◽  
pp. 152-158 ◽  
Author(s):  
X. X. Yang ◽  
W. S. Powell ◽  
L. J. Xu ◽  
J. G. Martin
Keyword(s):  
Tidal Volume ◽  
Receptor Antagonist ◽  
Spontaneous Breathing ◽  
Brown Norway ◽  
Pulmonary Resistance ◽  
Strain Dependence ◽  
Fischer 344 ◽  
Airway Response ◽  
Airway Responses ◽  
Strain Dependent

The aim of the study was to investigate strain dependence and mechanisms of airway responses to dry-gas hyperpnea challenge in the rat. We studied responses in a strain that is hyperresponsive to methacholine, Fischer 344 (F-344); in two normoresponsive strains, Lewis and ACI; and in an atopic but normoresponsive strain, Brown Norway (BN). We examined the effects of a neurokinin (NK) 1-receptor (CP-99994), an NK2-receptor (SR-48968), and a leukotriene D4(LTD4)-receptor antagonist (pranlukast) on responses to hyperpnea challenge in BN rats. The animals were ventilated with a tidal volume of 8 ml/kg and a frequency of 150 breaths/min with either a dry or humidified mixture of 5% CO2-95% O2 for 5 min for hyperpnea challenge, whereas responses to challenge were measured during spontaneous breathing. Pulmonary resistance increased after dry-gas challenge in BN and ACI but not in F-344 and Lewis rats. CP-99994, SR-48968, and pranlukast significantly attenuated the increase in pulmonary resistance after dry-gas challenge. There were no significant differences in responsiveness to airway challenge with LTD4 among the BN, F-344 and ACI rats. We conclude that responses to dry-gas hyperpnea challenge are strain dependent in rats and are mediated by NKs and LTD4.

Effects of elastase-induced emphysema on airway responsiveness to methacholine in rats

1989 ◽  
Vol 66 (2) ◽  
pp. 606-612 ◽  
Author(s):  
S. Bellofiore ◽  
D. H. Eidelman ◽  
P. T. Macklem ◽  
J. G. Martin
Keyword(s):  
Lung Volume ◽  
Brown Norway ◽  
Pulmonary Mechanics ◽  
Maximum Increase ◽  
Before And After ◽  
Airway Response ◽  
Residual Capacity ◽  
Airway Responses ◽  
Norway Rats ◽  
Concentration Response Curve

We examined the effects of elastase-induced emphysema on lung volumes, pulmonary mechanics, and airway responses to inhaled methacholine (MCh) of nine male Brown Norway rats. Measurements were made before and weekly for 4 wk after elastase in five rats. In four rats measurements were made before and at 3 wk after elastase; in these same animals the effects of changes in end-expiratory lung volume on the airway responses to MCh were evaluated before and after elastase. Airway responses were determined from peak pulmonary resistance (RL) calculated after 30-s aerosolizations of saline and doubling concentrations of MCh from 1 to 64 mg/ml. Porcine pancreatic elastase (1 IU/g) was administered intratracheally. Before elastase RL rose from 0.20 +/- 0.02 cmH2O.ml-1.s (mean +/- SE; n = 9) to 0.57 +/- 0.06 after MCh (64 mg/ml). A plateau was observed in the concentration-response curve. Static compliance and the maximum increase in RL (delta RL64) were significantly correlated (r = 0.799, P less than 0.01). Three weeks after elastase the maximal airway response to MCh was enhanced and no plateau was observed; delta RL64 was 0.78 +/- 0.07 cmH2O.ml-1.s, significantly higher than control delta RL64 (0.36 +/- 0.7, P less than 0.05). Before elastase, increase of end-expiratory lung volume to functional residual capacity + 1.56 ml (+/- 0.08 ml) significantly reduced RL at 64 mg MCh/ml from 0.62 +/- 0.05 cmH2O.ml-1.s to 0.50 +/- 0.03, P less than 0.05.(ABSTRACT TRUNCATED AT 250 WORDS)

Late response of the upper airway of the rat to inhaled antigen

1990 ◽  
Vol 69 (4) ◽  
pp. 1360-1365 ◽  
Author(s):  
L. J. Xu ◽  
D. H. Eidelman ◽  
J. H. Bates ◽  
J. G. Martin
Keyword(s):  
Time Course ◽  
Airway Resistance ◽  
Upper Airway ◽  
Brown Norway ◽  
Control Group ◽  
Late Response ◽  
Lung Elastance ◽  
Upper Airway Resistance ◽  
Airway Responses ◽  
Peak Value

We studied the magnitude and time course of changes in upper airway resistance (Ruaw) of actively sensitized Brown-Norway rats after aerosol challenge with ovalbumin (OA). Two weeks after sensitization, eight rats were challenged by inhalation of aerosolized OA through the nose. The airway responses of these rats 5-10 h after OA challenge were compared with those of seven animals challenged with saline. Seven of eight test rats had increased Ruaw, and six displayed discrete late responses (LR). Ruaw during expiration was highly alinear so analysis was confined to Ruaw during inspiration (Ruaw,I). The Ruaw,I averaged over 5 h was 1.262 +/- 0.09 (SE) cmH2O.ml-1.s, 2.6 times the value for saline-challenged animals (0.476 +/- 0.143 cmH2O.ml-1.s), and it reached a peak value of 3.454 +/- 0.45 cmH2O.ml-1.s. The time to the peak of the LR was 446 +/- 37.3 min. The duration of the LR in the upper airway was 146 +/- 34.9 min. At the time corresponding to the peak value of Ruaw,I, the lung elastance in the test rats was double the value preceding the peak. Lung elastance was unchanged in the control group. We conclude that inhalation of antigen through the upper airway of the sensitized rat results in a substantial increase in upper airway resistance and a distinct LR. The predominant site of the change in respiratory system resistance is in the upper airway.

Developmental changes in upper airway dynamics

2004 ◽  
Vol 97 (1) ◽  
pp. 98-108 ◽  
Author(s):  
Carole L. Marcus ◽  
Lucila B. Fernandes Do Prado ◽  
Janita Lutz ◽  
Eliot S. Katz ◽  
Cheryl A. Black ◽  
...  
Keyword(s):  
Upper Airway ◽  
Older Children ◽  
Normal Children ◽  
Compensatory Response ◽  
Pharyngeal Airway ◽  
Ventilatory Drive ◽  
Airway Response ◽  
Airway Responses ◽  
Airway Dynamics ◽  
Normal Adults

Normal children have a less collapsible upper airway in response to subatmospheric pressure administration (PNEG) during sleep than normal adults do, and this upper airway response appears to be modulated by the central ventilatory drive. Children have a greater ventilatory drive than adults. We, therefore, hypothesized that children have increased neuromotor activation of their pharyngeal airway during sleep compared with adults. As infants have few obstructive apneas during sleep, we hypothesized that infants would have an upper airway that was resistant to collapse. We, therefore, compared the upper airway pressure-flow (V̇) relationship during sleep between normal infants, prepubertal children, and adults. We evaluated the upper airway response to 1) intermittent, acute PNEG (infants, children, and adults), and 2) hypercapnia (children and adults). We found that adults had a more collapsible upper airway during sleep than either infants or children. The children exhibited a vigorous response to both PNEG and hypercapnia during sleep ( P < 0.01), whereas adults had no significant change. Infants had an airway that was resistant to collapse and showed a very rapid response to PNEG. We conclude that the upper airway is resistant to collapse during sleep in infants and children. Normal children have preservation of upper airway responses to PNEG and hypercapnia during sleep, whereas responses are diminished in adults. Infants appear to have a different pattern of upper airway activation than older children. We speculate that the pharyngeal airway responses present in normal children are a compensatory response for a relatively narrow upper airway.

scholarly journals The Effect of Particulate Matter Exposure on the Inflammatory Airway Response of Street Runners and Sedentary People

Atmosphere ◽  
2019 ◽  
Vol 11 (1) ◽  
pp. 43 ◽  
Author(s):  
Lucas G. Pagani ◽  
Juliana M.B. Santos ◽  
Roberta Foster ◽  
Marcelo Rossi ◽  
Luiz A. Luna Junior ◽  
...  
Keyword(s):  
Particulate Matter ◽  
Inflammatory Responses ◽  
Sedentary Lifestyle ◽  
Upper Airway ◽  
Polluted Environment ◽  
Fractional Exhaled Nitric Oxide ◽  
Upper Airways ◽  
Tnf Α ◽  
Airway Response ◽  
Particulate Matter Exposure

Physical exercise promotes many health benefits. However, its effects are not well known in a polluted environment. Thus, this study aimed to compare upper airway inflammatory responses between street runners and sedentary individuals. Twenty-eight volunteers were recruited: runners (n = 14) and sedentary individuals (n = 14), who lived and worked in the same metropolitan area of São Paulo, Brazil. Particulate matter (PM) levels were monitored ten weeks before winter (low PM levels) and ten weeks after the beginning of winter (high PM levels) [PM10 (p < 0.0001) and PM2.5 (p < 0.0001)]. The cytokines (TNF-α, IL-6, IL-10, and IL-17A) levels in the nasal lavage and fractional exhaled nitric oxide (FeNO) were taken at the beginning of the winter (baseline) and ten weeks afterwards (after ten weeks of high PM exposure). IL-6 concentration increased in both runners (p = 0.037) and sedentary individuals (p = 0.027) after high PM exposure compared to the baseline. IL-10 concentration increased in sedentary individuals (p = 0.037) while IL-17A levels were increased in runners (p = 0.001) after high PM exposure compared to the baseline. FeNO levels decreased in runners (p = 0.025) after high PM exposure compared to the baseline. Outdoor endurance training acts as an inducer of a differentiated immune response in the upper airways of runners compared to individuals with a sedentary lifestyle from the same community after elevated PM exposure.

scholarly journals Chromosome-substituted rat strains provide insights into the genetics of placentation

2011 ◽  
Vol 43 (15) ◽  
pp. 930-941 ◽  
Author(s):  
Toshihiro Konno ◽  
Lea A. Rempel ◽  
M. A. Karim Rumi ◽  
Amanda R. Graham ◽  
Kazuo Asanoma ◽  
...  
Keyword(s):  
Quantitative Trait ◽  
Strain Differences ◽  
Transcript Level ◽  
Trophoblast Invasion ◽  
Brown Norway ◽  
Sprague Dawley ◽  
Rat Strains ◽  
Junctional Zone ◽  
Transcript Levels ◽  
Inbred Rat

The rat possesses a hemochorial form of placentation. Pronounced intrauterine trophoblast cell invasion and vascular remodeling characterize this type of placentation. Strain-specific patterns of placentation are evident in the rat. Some rat strains exhibit deep intrauterine trophoblast invasion and an expanded junctional zone [Holtzman Sprague-Dawley (HSD), Dahl salt sensitive (DSS)], whereas placentation sites of other rat strains are characterized by shallow invasion and a restricted junctional zone [Brown Norway (BN)]. In this report, we identified a quantitative trait that was used to distinguish strain-specific features of rat placentation. Junctional zone prolactin family 5, subfamily a, member 1 ( Prl5a1) transcript levels were significantly greater in BN rats than in HSD or DSS rats. Prl5a1 transcript levels were used as a quantitative trait to screen placentation sites from chromosome-substituted rat strains (BN chromosomes introgressed into the DSS inbred strain; DSS-BN panel). Litter size, placental weights, and fetal weights were not significantly different among the chromosome-substituted strains. Regulation of the junctional zone Prl5a1 transcript-level quantitative trait was multifactoral. Chromosome-substituted strains possessing BN chromosomes 14 or 17 introgressed into the DSS inbred rat strain displayed Prl5a1 transcript levels that were significantly different from the DSS pattern and more closely resembled the BN pattern. The in situ placental distribution of Prl5a1 mRNA and the structure of the junctional zone of DSS-BN17 rats mimicked that observed for the BN rat. Prl5a1 gene expression was also assessed in BN vs. HSD trophoblast stem cells and following reciprocal BN and HSD embryo transfer. Strain differences intrinsic to trophoblast and maternal environment were identified. In summary, we have identified chromosomes 14 and 17 as possessing regulatory information controlling a quantitative trait associated with rat placentation.

Inhalation injury in the ICU

2016 ◽  
Author(s):  
Silvia Coppola ◽  
Franco Valenza
Keyword(s):  
Imaging Techniques ◽  
Carbon Monoxide Poisoning ◽  
Significant Risk ◽  
Upper Airway ◽  
Injured Patient ◽  
Inhalation Injury ◽  
Smoke Inhalation ◽  
Lower Airway ◽  
Upper Airways ◽  
Chemical Injury

Inhalation injury represents one of the most serious associated injuries complicating the care of thermally-injured patient. It can result in severe respiratory failure and acute respiratory distress syndrome (ARDS) by three mechanisms—thermal or chemical injury, and impairment of systemic oxygen supply. Thermal injury can cause erythema, ulceration, and progressive, life-threatening oedema, particularly of the upper airways. Chemical injury is due to irritants or cytotoxic compounds, and depends on the material burned, the temperature of the fire, and the amount of oxygen present in the fire environment. It is responsible for irritation, ulceration, and oedema of the mucosal surface, and the initiation of a lung inflammatory reaction when small particles reach the alveoli. Moreover, the increased vascular permeability, and the reduced surfactant production carry a significant risk in the development of pneumonia and ARDS. Bronchospasm and upper airway oedema can occur rapidly, while lower airway oedema can be asymptomatic for up to 24 hours. Lung imaging techniques may not reveal injured areas for the first 24–48 hours. Fibre optic bronchoscopy is considered to be the most direct diagnostic method for the definitive diagnosis of inhalation injury. The patient management includes airways assessment, adequate fluid resuscitation, and mechanical ventilation when required. All victims of smoke inhalation should be always evaluated for cyanide and carbon monoxide poisoning.

scholarly journals Role of Aquaporin Water Channels in Airway Fluid Transport, Humidification, and Surface Liquid Hydration

2001 ◽  
Vol 117 (6) ◽  
pp. 573-582 ◽  
Author(s):  
Yuanlin Song ◽  
Sujatha Jayaraman ◽  
Baoxue Yang ◽  
Michael A. Matthay ◽  
A.S. Verkman
Keyword(s):  
Knockout Mice ◽  
Fluid Transport ◽  
Upper Airway ◽  
Lower Airway ◽  
Wild Type ◽  
Upper Airways ◽  
Airway Epithelia ◽  
Airway Humidification ◽  
Surface Liquid

Several aquaporin-type water channels are expressed in mammalian airways and lung: AQP1 in microvascular endothelia, AQP3 in upper airway epithelia, AQP4 in upper and lower airway epithelia, and AQP5 in alveolar epithelia. Novel quantitative methods were developed to compare airway fluid transport–related functions in wild-type mice and knockout mice deficient in these aquaporins. Lower airway humidification, measured from the moisture content of expired air during mechanical ventilation with dry air through a tracheotomy, was 54–56% efficient in wild-type mice, and reduced by only 3–4% in AQP1/AQP5 or AQP3/AQP4 double knockout mice. Upper airway humidification, measured from the moisture gained by dry air passed through the upper airways in mice breathing through a tracheotomy, decreased from 91 to 50% with increasing ventilation from 20 to 220 ml/min, and reduced by 3–5% in AQP3/AQP4 knockout mice. The depth and salt concentration of the airway surface liquid in trachea was measured in vivo using fluorescent probes and confocal and ratio imaging microscopy. Airway surface liquid depth was 45 ± 5 μm and [Na+] was 115 ± 4 mM in wild-type mice, and not significantly different in AQP3/AQP4 knockout mice. Osmotic water permeability in upper airways, measured by an in vivo instillation/sample method, was reduced by ∼40% by AQP3/AQP4 deletion. In doing these measurements, we discovered a novel amiloride-sensitive isosmolar fluid absorption process in upper airways (13% in 5 min) that was not affected by aquaporin deletion. These results establish the fluid transporting properties of mouse airways, and indicate that aquaporins play at most a minor role in airway humidification, ASL hydration, and isosmolar fluid absorption.

scholarly journals Bronchoconstriction induced by increasing airway temperature in ovalbumin-sensitized rats: role of tachykinins

2013 ◽  
Vol 115 (5) ◽  
pp. 688-696 ◽  
Author(s):  
Chun-Chun Hsu ◽  
Ruei-Lung Lin ◽  
You Shuei Lin ◽  
Lu-Yuan Lee
Keyword(s):  
Room Temperature ◽  
Airway Resistance ◽  
Allergic Inflammation ◽  
Brown Norway ◽  
Pulmonary Resistance ◽  
Temperature Dependent ◽  
C Fiber ◽  
Airway Response ◽  
Norway Rats

This study was carried out to determine the effect of allergic inflammation on the airway response to increasing airway temperature. Our results showed the following: 1) In Brown-Norway rats actively sensitized by ovalbumin (Ova), isocapnic hyperventilation with humidified warm air (HWA) for 2 min raised tracheal temperature (Ttr) from 33.4 ± 0.6°C to 40.6 ± 0.1°C, which induced an immediate and sustained (>10 min) increase in total pulmonary resistance (Rl) from 0.128 ± 0.004 to 0.212 ± 0.013 cmH2O·ml−1·s ( n = 6, P < 0.01). In sharp contrast, the HWA challenge caused the same increase in Ttrbut did not generate any increase in Rl in control rats. 2) The increase in Rl in sensitized rats was reproducible when the same HWA challenge was repeated 60–90 min later. 3) This bronchoconstrictive effect was temperature dependent: a slightly smaller increase in peak Ttr(39.6 ± 0.2°C) generated a significant but smaller increase in Rl in sensitized rats. 4) The HWA-induced bronchoconstriction was not generated by the humidity delivered by the HWA challenge alone, because the same water content delivered by saline aerosol at room temperature had no effect. 5) The HWA-evoked increase in Rl in sensitized rats was not blocked by atropine but was completely prevented by pretreatment either with a combination of neurokinin (NK)-1 and NK-2 antagonists or with formoterol, a β2agonist, before the HWA challenge. This study showed that increasing airway temperature evoked a pronounced and reversible increase in airway resistance in sensitized rats and that tachykinins released from the vagal bronchopulmonary C-fiber endings were primarily responsible.

scholarly journals Conserved Mechanisms in the Formation of the Airways and Alveoli of the Lung

2021 ◽  
Vol 9 ◽  
Author(s):  
David Warburton
Keyword(s):  
Airway Epithelium ◽  
Alveolar Epithelium ◽  
Upper Airway ◽  
Intrinsic Property ◽  
Branching Morphogenesis ◽  
Radial Symmetry ◽  
Respiratory Epithelium ◽  
Lower Airway ◽  
Upper Airways ◽  
Alveolar Duct

Branching is an intrinsic property of respiratory epithelium that can be induced and modified by signals emerging from the mesenchyme. However, during stereotypic branching morphogenesis of the airway, the relatively thick upper respiratory epithelium extrudes through a mesenchymal orifice to form a new branch, whereas during alveologenesis the relatively thin lower respiratory epithelium extrudes to form sacs or bubbles. Thus, both branching morphogenesis of the upper airway and alveolarization in the lower airway seem to rely on the same fundamental physical process: epithelial extrusion through an orifice. Here I propose that it is the orientation and relative stiffness of the orifice boundary that determines the stereotypy of upper airway branching as well as the orientation of individual alveolar components of the gas exchange surface. The previously accepted dogma of the process of alveologenesis, largely based on 2D microscopy, is that alveoli arise by erection of finger-like interalveolar septae to form septal clefts that subdivide pre-existing saccules, a process for which the contractile properties of specialized alveolar myofibroblasts are necessary. Here I suggest that airway tip splitting and stereotypical side domain branching are actually conserved processes, but modified somewhat by evolution to achieve both airway tip splitting and side branching of the upper airway epithelium, as well as alveologenesis. Viewed in 3D it is clear that alveolar “septal tips” are in fact ring or purse string structures containing elastin and collagen that only appear as finger like projections in cross section. Therefore, I propose that airway branch orifices as well as alveolar mouth rings serve to delineate and stabilize the budding of both airway and alveolar epithelium, from the tips and sides of upper airways as well as from the sides and tips of alveolar ducts. Certainly, in the case of alveoli arising laterally and with radial symmetry from the sides of alveolar ducts, the mouth of each alveolus remains within the plane of the side of the ductal lumen. This suggests that the thin epithelium lining these lateral alveolar duct buds may extrude or “pop out” from the duct lumen through rings rather like soap or gum bubbles, whereas the thicker upper airway epithelium extrudes through a ring like toothpaste from a tube to form a new branch.

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