Input impedance and peripheral inhomogeneity of dog lungs

Hantos, Zoltán; Daróczy, Bálint; Suki, Bélâ; Nagy, S.; Fredberg, J. J.

doi:10.1152/jappl.1992.72.1.168

Cited by 686 publications

(633 citation statements)

References 17 publications

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“…Mice were tracheostomized, and respiratory impedance was measured by using the forced oscillation technique (0.25-20 Hz) delivered by computerized flexiVent (SCIREQ, Montreal, Canada) (20). Estimated total lung compliance, airway resistance, airway elastance, tissue damping, and tissue elastance for mice at 2 cm H 2 O positive end expiratory pressure were obtained by fitting a model to each impedance spectrum (21). Hysteresivity was calculated as the ratio of tissue damping to tissue elastance.…”

Section: Methodsmentioning

confidence: 99%

Pneumonitis and Emphysema in sp-C Gene Targeted Mice

Glasser¹,

Detmer²,

Ikegami³

et al. 2003

Journal of Biological Chemistry

200

161

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Section: Methodsmentioning

confidence: 99%

Pneumonitis and Emphysema in sp-C Gene Targeted Mice

Glasser¹,

Detmer²,

Ikegami³

et al. 2003

Journal of Biological Chemistry

200

161

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show abstract

“…These perturbations were composed of 13 superimposed sine waves of varying amplitude and frequency, ranging from 1 to 20.5 Hz. The frequencies were set at mutually primed values to reduce harmonic distortion that can occur in nonlinear systems (10). Before beginning the protocol, we obtained dynamic calibration signals necessary to correct for the physical characteristics of the flexiVent in subsequent measurements of Zrs (13,32).…”

Section: Methodsmentioning

confidence: 99%

Transient mechanical benefits of a deep inflation in the injured mouse lung

Allen

Lundblad

Parsons

et al. 2002

Journal of Applied Physiology

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Allen, Gilman, Lennart K. A. Lundblad, Polly Parsons, and Jason H. T. Bates. Transient mechanical benefits of a deep inflation in the injured mouse lung. J Appl Physiol 93: 1709-1715. First published July 12, 2002 10.1152/japplphysiol.00473.2002The lasting effects of a recruitment maneuver (RM) in the injured lung are not well characterized. We speculated that the reduction in respiratory elastance (H) after a deep inflation (DI) is transient in nature and should be sustained longer at higher positive end-expiratory pressure (PEEP). Thirteen ventilated mice were given 2 DIs at various levels of PEEP before and after saline lavage. Forced oscillations were used to measure H periodically over 7 min after the DIs. Time constants ( ) were estimated for the post-DI recovery in H. Values for before lavage (80-115 s) were reduced after lavage (13-30 s) at all levels of PEEP (P ϭ 0.0001). PEEP did not significantly influence before or after lavage. The plateau level and total recovery in H after a DI were significantly influenced by PEEP and lavage (P Ͻ 0.0001). Our results suggest that for a DI to be beneficial in the injured mouse lung, it may have to be applied several times a minute. atelectasis; acute lung injury; recruitment; elastance; positive-pressure respiration PHYSICIANS HAVE KNOWN for a long time that atelectasis plays a pivotal role in the development of hypoxemia during mechanical ventilation, both in general anesthesia for routine surgery and in various instances of acute lung injury. Recent practice has now moved toward the use of lower tidal volumes (VT) in patients with acute lung injury and acute respiratory distress syndrome (ARDS) after two important studies demonstrated lower mortality outcomes by using this strategy (1, 1a). However, because of the progressive alveolar derecruitment that is often encountered with the use of lower VT (27), there has been a renewed interest in the use of recruitment maneuvers (RMs) as a means of reopening these regions of atelectasis. Many studies have demonstrated improvement in oxygenation, respiratory system compliance, and even lung volume after sustained or deep inflations (DIs) in many different scenarios (3-5, 17, 18, 26, 28), but some of these same studies were unable to show any lasting improvement when RMs were delivered during conventional positive pressure ventilation (4,18,25).These apparently conflicting results may be explained by the different experimental situations involved, as the effect of a RM is likely to depend on the size and duration of the inflation, the mode of ventilation in which the inflation is delivered, and the level of positive end-expiratory pressure (PEEP) employed. Furthermore, if the effects of a RM are transient, then its apparent benefits will depend on when they are measured. Different researchers have measured the effects of a RM at different time points after its administration (3,4,17,26,28), yet there has been little attempt to characterize the rate at which the benefits of a RM are lost in the period immediately after ...

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“…Lateral pressure at either end of this wave tube was measured using transducers (model 8507C‐2; Endevco) and load impedance on the wave tube was used to calculate Z rs . Z rs was partitioned into the airway compartment: airway resistance ( R aw ) and inertance ( I aw ) and tissue compartment: tissue damping (G) and tissue elastance (H) using a four parameter model with constant phase tissue impedance 44 . Fitted parameters were corrected for the impedance of the tracheal cannula and wave‐tube connectors.…”

Section: Methodsmentioning

confidence: 99%

Acute diesel exhaust particle exposure increases viral titre and inflammation associated with existing influenza infection, but does not exacerbate deficits in lung function

Larcombe

Foong

Boylen

et al. 2012

Influenza Resp Viruses

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Please cite this paper as: Larcombe et al. (2012) Acute diesel exhaust particle exposure increases viral titre and inflammation associated with existing influenza infection, but does not exacerbate deficits in lung function. Influenza and Other Respiratory Viruses DOI:10.1111/irv.12012. Background Exposure to diesel exhaust particles (DEP) is thought to exacerbate many pre‐existing respiratory diseases, including asthma, bronchitis and chronic obstructive pulmonary disease, however, there is a paucity of data on whether DEP exacerbates illness due to respiratory viral infection. Objectives To assess the physiological consequences of an acute DEP exposure during the peak of influenza‐induced illness. Methods We exposed adult female BALB/c mice to 100 μg DEP (or control) 3·75 days after infection with 104·5 plaque forming units of influenza A/Mem71 (or control). Six hours, 24 hours and 7 days after DEP exposure we measured thoracic gas volume and lung function at functional residual capacity. Bronchoalveolar lavage fluid was taken for analyses of cellular inflammation and cytokines, and whole lungs were taken for measurement of viral titre. Results Influenza infection resulted in significantly increased inflammation, cytokine influx and impairment to lung function. DEP exposure alone resulted in less inflammation and cytokine influx, and no impairment to lung function. Mice infected with influenza and exposed to DEP had higher viral titres and neutrophilia compared with infected mice, yet they did not have more impaired lung mechanics than mice infected with influenza alone. Conclusions A single dose of DEP is not sufficient to physiologically exacerbate pre‐existing respiratory disease caused by influenza infection in mice.

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Input impedance and peripheral inhomogeneity of dog lungs

Cited by 686 publications

References 17 publications

Pneumonitis and Emphysema in sp-C Gene Targeted Mice

Pneumonitis and Emphysema in sp-C Gene Targeted Mice

Transient mechanical benefits of a deep inflation in the injured mouse lung

Acute diesel exhaust particle exposure increases viral titre and inflammation associated with existing influenza infection, but does not exacerbate deficits in lung function

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