scholarly journals Developmental changes in airway and tissue mechanics in mice

2005 ◽  
Vol 99 (1) ◽  
pp. 108-113 ◽  
Author(s):  
Elizabeth M. Bozanich ◽  
Rachel A. Collins ◽  
Cindy Thamrin ◽  
Zoltán Hantos ◽  
Peter D. Sly ◽  
...  
Keyword(s):  
Airway Resistance ◽  
Structural Changes ◽  
Low Frequency ◽  
Postnatal Period ◽  
Tissue Mechanics ◽  
Forced Oscillation Technique ◽  
Impedance Data ◽  
Age Related ◽  
System Pressure ◽  
Tissue Elastance

Most studies using mice to model human lung diseases are carried out in adults, although there is emerging interest in the effects of allergen, bacterial, and viral exposure early in life. This study aims to characterize lung function in BALB/c mice from infancy (2 wk) through to adulthood (8 wk). The low-frequency forced oscillation technique was used to obtain impedance data, partitioned into components representing airway resistance, tissue damping, tissue elastance, and hysteresivity (tissue damping/tissue elastance). Measurements were made at end-expiratory pause (transrespiratory system pressure = 2 cmH2O) and during relaxed slow expiration from 20 to 0 cmH2O. Airway resistance decreased with age from 0.63 cmH2O·ml−1·s at 2 wk to 0.24 cmH2O·ml−1·s at 8 wk ( P < 0.001). Both tissue damping and tissue elastance decreased with age ( P < 0.001) from 2 to 5 wk, then plateaued through to 8 wk ( P < 0.001). This pattern was seen both in measurements taken at end-expiratory pause and during expiration. There were no age-related changes seen in hysteresivity when measured at end-expiratory pause, but the pattern of volume dependence did differ with the age of the mice. These changes in respiratory mechanics parallel the reported structural changes of the murine lung from the postnatal period into adulthood.

Variability in preterm lamb lung mechanics after intra-amniotic endotoxin is associated with changes in surfactant pool size and morphometry

2004 ◽  
Vol 287 (5) ◽  
pp. L992-L998 ◽  
Author(s):  
J. Jane Pillow ◽  
Alan H. Jobe ◽  
Rachel A. Collins ◽  
Zoltán Hantos ◽  
Machiko Ikegami ◽  
...  
Keyword(s):  
Low Frequency ◽  
Tissue Mechanics ◽  
Pool Size ◽  
Lung Mechanics ◽  
Forced Oscillation Technique ◽  
Respiratory Impedance ◽  
Tissue Impedance ◽  
Lung Structure ◽  
Alveolar Surfactant ◽  
Tissue Elastance

Antenatal exposure to intra-amniotic (IA) endotoxin initiates a complex series of events, including an inflammatory cascade, increased surfactant production, and alterations to lung structure. Using the low frequency forced oscillation technique as a sensitive tool for measurement of respiratory impedance, we aimed to determine which factors contributed most to measured changes in lung mechanics. Respiratory impedance data obtained from sedated preterm lambs exposed to either IA injection with saline or 20 mg of endotoxin 1, 2, 4, and 15 days before delivery at 125 days gestation were studied, and association with indexes of standard lung morphometry, inflammatory response, and alveolar surfactant-saturated phosphatidylcholine (Sat PC) pool size was demonstrated. Reduction in tissue impedance with increasing interval between exposure and delivery was evident as early as 4 days after IA endotoxin injection, coinciding with resolution of inflammatory reaction, increased alveolar surfactant pools, and contribution of alveolar ducts to the parenchymal fraction, and a later decrease in the tissue component of the parenchymal fraction. Decreases in tissue damping (resistance) were more marked than decreases in tissue elastance. Log alveolar Sat PC accounted for most variability in tissue damping (88.9%) and tissue elastance (73.4%), whereas tissue fraction contributed 2 and 6.4%, respectively. The alveolar Sat PC pool size was the sole factor contributing to change in tissue hysteresivity. No changes were observed in airway resistance. Despite the complex cascade of events initiated by antenatal endotoxin exposure, variability in lung tissue mechanics is associated primarily with changes in alveolar Sat PC pool and lung morphology.

Protective Effects of Volatile Agents against Methacholine-induced Bronchoconstriction in Rats

2001 ◽  
Vol 94 (2) ◽  
pp. 348-353 ◽  
Author(s):  
Walid Habre ◽  
Ferenc Peták ◽  
Peter D. Sly ◽  
Zoltán Hantos ◽  
Denis R. Morel
Keyword(s):  
Airway Resistance ◽  
Model Fitting ◽  
Low Frequency ◽  
Tissue Mechanics ◽  
Control Group ◽  
Protective Effects ◽  
Airway Constriction ◽  
Impedance Data ◽  
Significant Difference ◽  
Volatile Agents

Background The protective properties of common volatile agents against generalized lung constriction have previously been addressed only via estimations of parameters that combine airway and tissue mechanics. Their effectiveness in preventing airway constriction have not been compared systematically. Therefore, the authors investigated the abilities of halothane, isoflurane, sevoflurane, and desflurane to provide protection against airway constriction induced by methacholine. Methods Low-frequency pulmonary impedance data were collected in open-chest rats under baseline conditions and during three consecutive intravenous infusions of methacholine (32 microg x kg(-1) x min(-1)) while the animals were anesthetized with intravenous pentobarbital (control group). Methacholine challenges were performed in four other groups of rats, first during intravenous anesthesia and then repeated during the inhalation of halothane, isoflurane, sevoflurane, or desflurane at concentrations of 1 and 2 minimum alveolar concentration (MAC). Airway resistance and inertance, parenchymal damping, and elastance were estimated from the impedance data by model fitting. Results The methacholine-induced increases in airway resistance during intravenous pentobarbital anesthesia (204 +/- 53%) were markedly and significantly (P &lt; 0.005) reduced by 1-MAC doses of halothane (80 +/- 48%), isoflurane (112 +/- 59%), sevoflurane (68 +/- 34%), and desflurane (96 +/- 34%), with no significant difference between the gases applied. Increasing the concentration to 2 MAC did not lead to any significant further protection against the increase in airway resistance. Conclusions These data demonstrate that isoflurane, sevoflurane, and desflurane are as effective as the widely accepted halothane in protecting against methacholine-induced airway constriction.

Airway and tissue mechanics in a murine model of asthma: alveolar capsule vs. forced oscillations

2002 ◽  
Vol 93 (1) ◽  
pp. 263-270 ◽  
Author(s):  
Shinichiro Tomioka ◽  
Jason H. T. Bates ◽  
Charles G. Irvin
Keyword(s):  
Airway Resistance ◽  
Forced Oscillation ◽  
Tissue Mechanics ◽  
Forced Oscillations ◽  
Control Group ◽  
Bronchial Responsiveness ◽  
Lung Elastance ◽  
Functional Consequences ◽  
Lung Periphery ◽  
Tissue Elastance

To better address the functional consequences of inflammation on bronchial responsiveness, we studied two groups of BALB/c mice: a nonimmunized control group ( n = 8) and a group immunized and challenged with inhaled ovalbumin ( n = 8). An alveolar capsule (AC) measured airway resistance (RawAC) and lung elastance (El). A forced oscillation (FO) technique independently estimated airway resistance (RawFO) and a parameter H ti related to tissue elastance. Ovalbumin-immunized and -challenged mice had increased numbers of eosinophils in bronchoalveolar lavage and increased responsiveness to methacholine (MCh). Corresponding parameters from the AC and FO techniques were correlated: RawAC vs. RawFO( r = 0.76) and El vs. H ti ( r = 0.88, P< 0.0001 in all cases). AC and FO techniques showed significant increases in tissue elastance in response to MCh but no significant increases in airway resistance. These results demonstrated that the AC and FO techniques yield essentially equivalent results in mice, even when the lung is inhomogeneous, and that the bronchoconstrictive responses to MCh and inflammation in mice are predominantly located in the lung periphery.

Protective mechanical ventilation does not exacerbate lung function impairment or lung inflammation following influenza A infection

2009 ◽  
Vol 107 (5) ◽  
pp. 1472-1478 ◽  
Author(s):  
Graeme R. Zosky ◽  
Vincenzo Cannizzaro ◽  
Zoltan Hantos ◽  
Peter D. Sly
Keyword(s):  
Mechanical Ventilation ◽  
Lung Injury ◽  
Influenza A ◽  
Airway Resistance ◽  
Inflammatory Cells ◽  
Lung Mechanics ◽  
Forced Oscillation Technique ◽  
Protective Ventilation Strategy ◽  
Protective Mechanical Ventilation ◽  
Tissue Elastance

The degree to which mechanical ventilation induces ventilator-associated lung injury is dependent on the initial acute lung injury (ALI). Viral-induced ALI is poorly studied, and this study aimed to determine whether ALI induced by a clinically relevant infection is exacerbated by protective mechanical ventilation. Adult female BALB/c mice were inoculated with 104.5 plaque-forming units of influenza A/Mem/1/71 in 50 μl of medium or medium alone. This study used a protective ventilation strategy, whereby mice were anesthetized, tracheostomized, and mechanically ventilated for 2 h. Lung mechanics were measured periodically throughout the ventilation period using a modification of the forced oscillation technique to obtain measures of airway resistance and coefficients of tissue damping and tissue elastance. Thoracic gas volume was measured and used to obtain specific airway resistance, tissue damping, and tissue elastance. At the end of the ventilation period, a bronchoalveolar lavage sample was collected to measure inflammatory cells, macrophage inflammatory protein-2, IL-6, TNF-α, and protein leak. Influenza infection caused significant increases in inflammatory cells, protein leak, and deterioration in lung mechanics that were not exacerbated by mechanical ventilation, in contrast to previous studies using bacterial and mouse-specific viral infection. This study highlighted the importance of type and severity of lung injury in determining outcome following mechanical ventilation.

scholarly journals Acute hemorrhagic shock decreases airway resistance in anesthetized rat

2011 ◽  
Vol 111 (2) ◽  
pp. 458-464 ◽  
Author(s):  
Sam Bayat ◽  
Gergely Albu ◽  
Skander Layachi ◽  
Flore Portier ◽  
Marc Fathi ◽  
...  
Keyword(s):  
Blood Flow ◽  
Hemorrhagic Shock ◽  
Airway Resistance ◽  
Tissue Mechanics ◽  
Pulmonary Vasculature ◽  
Aortic Blood Flow ◽  
Forced Oscillation Technique ◽  
Acute Hemorrhage ◽  
Aortic Blood ◽  
Respiratory Tissue

We studied the relation between changes in pulmonary and systemic hemodynamics to those in the airway resistance, respiratory tissue mechanics, and thoracic gas volume (TGV) following acute hemorrhage and blood reinfusion in rats. Forced oscillation technique was used to measure airway resistance (Raw), respiratory tissue damping, and elastance at baseline and after stepwise 1-ml blood withdrawals up to 5 ml total, followed by stepwise reinfusion up to full restoration. Mean systemic (Pam) and pulmonary arterial pressures and suprarenal aortic blood flow were measured at each step. In supplemental animals, plethysmographic TGV, Pam, and respiratory mechanics measurements were performed. Blood volume loss (BVL) led to proportional decreases in Raw (66.5 ± 8.8 vs. 44.8 ± 9.0 cmH2O·s·l−1 with 5 ml, P < 0.001), Pam, and aortic blood flow. In contrast, tissue damping increased significantly (1,070 ± 91 vs. 1,235 ± 105 cmH2O/l, P = 0.009 with 5 ml BVL), whereas tissue elastance did not change significantly. TGV significantly increased with acute BVL (3.7 ± 0.2 vs. 4.2 ± 0.2 ml, P = 0.01). Stepwise reinfusions produced opposite changes in the above parameters, with Raw reaching a higher value than baseline ( P = 0.001) upon full volume restoration. Both adrenalin ( P = 0.015) and noradrenalin levels were elevated ( P = 0.010) after 5-ml blood withdrawal. Our data suggest that the decreases in Raw following BVL may be attributed to the following: 1) an increased TGV enhancing airway parenchymal tethering forces; and 2) an increase in circulating catecholamines. The apparent beneficial effect of a reduction in Raw in acute hemorrhagic shock is counteracted by an increase in dead space and the appearance of peripheral mechanical heterogeneities due to de-recruitment of the pulmonary vasculature.

Effects of heterogeneities on the partitioning of airway and tissue properties in normal mice

2007 ◽  
Vol 102 (3) ◽  
pp. 859-869 ◽  
Author(s):  
Satoru Ito ◽  
Kenneth R. Lutchen ◽  
Béla Suki
Keyword(s):  
Mechanical Properties ◽  
Tidal Volume ◽  
Chest Wall ◽  
Airway Resistance ◽  
Mechanical Parameters ◽  
Tissue Properties ◽  
Closed Chest ◽  
Impedance Data ◽  
Open Chest ◽  
Tissue Elastance

We measured the mechanical properties of the respiratory system of C57BL/6 mice using the optimal ventilation waveform method in closed- and open-chest conditions at different positive end-expiratory pressures. The tissue damping (G), tissue elastance (H), airway resistance (Raw), and hysteresivity were obtained by fitting the impedance data to three different models: a constant-phase model by Hantos et al. (Hantos Z, Daroczy B, Suki B, Nagy S, Fredberg JJ. J Appl Physiol 72: 168–178, 1992), a heterogeneous Raw model by Suki et al. (Suki B, Yuan H, Zhang Q, Lutchen KR. J Appl Physiol 82: 1349–1359, 1997), and a heterogeneous H model by Ito et al. (Ito S, Ingenito EP, Arold SP, Parameswaran H, Tgavalekos NT, Lutchen KR, Suki B. J Appl Physiol 97: 204–212, 2004). Both in the closed- and open-chest conditions, G and hysteresivity were the lowest and Raw the highest in the heterogeneous Raw model, and G and H were the largest in the heterogeneous H model. Values of G, Raw, and hysteresivity were significantly higher in the closed-chest than in the open-chest condition. However, H was not affected by the conditions. When the tidal volume of the optimal ventilation waveform was decreased from 8 to 4 ml/kg in the closed-chest condition, G and hysteresivity significantly increased, but there were smaller changes in H or Raw. In summary, values of the obtained mechanical properties varied among these models, primarily due to heterogeneity. Moreover, the mechanical parameters were significantly affected by the chest wall and tidal volume in mice. Contribution of the chest wall and heterogeneity to the mechanical properties should be carefully considered in physiological studies in which partitioning of airway and tissue properties are attempted.

Low-dose aspirin prevents age-related endothelial dysfunction in a mouse model of physiological aging

2008 ◽  
Vol 294 (4) ◽  
pp. H1562-H1570 ◽  
Author(s):  
Hélène Bulckaen ◽  
Gaétan Prévost ◽  
Eric Boulanger ◽  
Géraldine Robitaille ◽  
Valérie Roquet ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Dysfunction ◽  
Protective Effect ◽  
Structural Changes ◽  
Low Dose ◽  
Age Groups ◽  
Dose Aspirin ◽  
Age Related ◽  
Low Dose Aspirin ◽  
Old Mice

The age-related impairment of endothelium-dependent vasodilatation contributes to increased cardiovascular risk in the elderly. For primary and secondary prevention, aspirin can reduce the incidence of cardiovascular events in this patient population. The present work evaluated the effect of low-dose aspirin on age-related endothelial dysfunction in C57B/J6 aging mice and investigated its protective antioxidative effect. Age-related endothelial dysfunction was assessed by the response to acetylcholine of phenylephrine-induced precontracted aortic segments isolated from 12-, 36-, 60-, and 84-wk-old mice. The effect of low-dose aspirin was examined in mice presenting a decrease in endothelial-dependent relaxation (EDR). The effects of age and aspirin treatment on structural changes were determined in mouse aortic sections. The effect of aspirin on the oxidative stress markers malondialdehyde and 8-hydroxy-2′-deoxyguanosine (8-OhdG) was also quantified. Compared with that of 12-wk-old mice, the EDR was significantly reduced in 60- and 84-wk-old mice ( P < 0.05); 68-wk-old mice treated with aspirin displayed a higher EDR compared with control mice of the same age (83.9 ± 4 vs. 66.3 ± 5%; P < 0.05). Aspirin treatment decreased 8-OHdG levels ( P < 0.05), but no significant effect on intima/media thickness ratio was observed. The protective effect of aspirin was not observed when treatment was initiated in older mice (96 wk of age). It was found that low-dose aspirin is able to prevent age-related endothelial dysfunction in aging mice. However, the absence of this effect in the older age groups demonstrates that treatment should be initiated early on. The underlying mechanism may involve the protective effect of aspirin against oxidative stress.

Nose-only water-pipe smoking effects on airway resistance, inflammation, and oxidative stress in mice

2013 ◽  
Vol 115 (9) ◽  
pp. 1316-1323 ◽  
Author(s):  
Abderrahim Nemmar ◽  
Haider Raza ◽  
Priya Yuvaraju ◽  
Sumaya Beegam ◽  
Annie John ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Airway Resistance ◽  
Reduced Glutathione ◽  
Mechanistic Explanation ◽  
The United States ◽  
Forced Oscillation Technique ◽  
Water Pipe ◽  
Respiratory Effects ◽  
And Oxidative Stress

Water-pipe smoking (WPS) is a common practice in the Middle East and is now gaining popularity in Europe and the United States. However, there is a limited number of studies on the respiratory effects of WPS. More specifically, the underlying pulmonary pathophysiological mechanisms related to WPS exposure are not understood. Presently, we assessed the respiratory effects of nose-only exposure to mainstream WPS generated by commercially available honey flavored “moasel ” tobacco. The duration of the session was 30 min/day and 5 days/wk for 1 mo. Control mice were exposed to air only. Here, we measured in BALB/c mice the airway resistance using forced-oscillation technique. Lung inflammation was assessed histopathologically and by biochemical analysis of bronchoalveolar lavage (BAL) fluid, and oxidative stress was evaluated biochemically by measuring lipid peroxidation, reduced glutathione and several antioxidant enzymes. Pulmonary inflammation assessment showed an increase in neutrophil and lymphocyte numbers. Likewise, airway resistance was significantly increased in the WPS group compared with controls. Tumor necrosis factor α and interleukin 6 concentrations were significantly increased in BAL fluid. Lipid peroxidation in lung tissue was significantly increased whereas the level and activity of antioxidants including reduced glutathione, glutathione S transferase, and superoxide dismutase were all significantly decreased following WPS exposure, indicating the occurrence of oxidative stress. Moreover, carboxyhemoglobin levels were significantly increased in the WPS group. We conclude that 1-mo nose-only exposure to WPS significantly increased airway resistance, inflammation, and oxidative stress. Our results provide a mechanistic explanation for the limited clinical studies that reported the detrimental respiratory effects of WPS.

scholarly journals Redefining lumbar spinal stenosis as a developmental syndrome: an MRI-based multivariate analysis of findings in 709 patients throughout the 16- to 82-year age spectrum

2018 ◽  
Vol 29 (6) ◽  
pp. 654-660 ◽  
Author(s):  
Sameer Kitab ◽  
Bryan S. Lee ◽  
Edward C. Benzel
Keyword(s):  
Multivariate Analysis ◽  
Spinal Stenosis ◽  
Lumbar Spinal Stenosis ◽  
Structural Changes ◽  
Age Cohorts ◽  
Age Related ◽  
Management Approaches ◽  
Definition Of ◽  
Lumbar Spinal ◽  
Lower Lumbar

OBJECTIVEUsing an imaging-based prospective comparative study of 709 eligible patients that was designed to assess lumbar spinal stenosis (LSS) in the ages between 16 and 82 years, the authors aimed to determine whether they could formulate radiological structural differences between the developmental and degenerative types of LSS.METHODSMRI structural changes were prospectively reviewed from 2 age cohorts of patients: those who presented clinically before the age of 60 years and those who presented at 60 years or older. Categorical degeneration variables at L1–S1 segments were compared. A multivariate comparative analysis of global radiographic degenerative variables and spinal dimensions was conducted in both cohorts. The age at presentation was correlated as a covariable.RESULTSA multivariate analysis demonstrated no significant between-groups differences in spinal canal dimensions and stenosis grades in any segments after age was adjusted for. There were no significant variances between the 2 cohorts in global degenerative variables, except at the L4–5 and L5–S1 segments, but with only small effect sizes. Age-related degeneration was found in the upper lumbar segments (L1–4) more than the lower lumbar segments (L4–S1). These findings challenge the notion that stenosis at L4–5 and L5–S1 is mainly associated with degenerative LSS.CONCLUSIONSIntegration of all the morphometric and qualitative characteristics of the 2 LSS cohorts provides evidence for a developmental background for LSS. Based on these findings the authors propose the concept of LSS as a developmental syndrome with superimposed degenerative changes. Further studies can be conducted to clarify the clinical definition of LSS and appropriate management approaches.

Sign in / Sign up

Export Citation Format

Share Document