Nonlinear fluid systems identified by random noise input.

E Delavault; G Saumon; R Georges

doi:10.1152/jappl.1982.53.6.1643

Home/Archive/PubMed

PubMed · 7153161

Nonlinear fluid systems identified by random noise input.

E Delavault·G Saumon·R Georges

View original source ↗Export metadata ↓

Abstract

The usual impedance measurement by Fourier analysis leads to undetectable errors when applied to nonlinear fluid systems where a nonlinear pressure drop p = K X V2 adds to the linear pressure-flow relationship, but processing series of impedance data with various input levels allows the measurement of such systems. This new method has been tested on simulations, nonlinear resistances, and intubation tubings. It gives accurate estimates of the nonlinear coefficient K together with the true linear impedance of the measured system. This way, the usual respiratory impedance measurement may be applied to intubated patients, as the respiratory impedance of the subject can be separated from the nonlinear behavior of the endotracheal tube or cannula.

Explore related subjects

Airway Resistance Biomechanical Phenomena Fourier Analysis Intubation, Intratracheal Models, Biological Pulmonary Ventilation Regression Analysis Rheology Journal Article

Keep this discovery

Explore connections, maps & timelines

BibTeX RIS

E Delavault, G Saumon, R Georges. 1982. Nonlinear fluid systems identified by random noise input.. https://doi.org/10.1152/jappl.1982.53.6.1643

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed1995

[Physiopathology of COPD (steady-state)].

Chronic obstructive pulmonary disease (COPD) have several pathophysiological characteristics in common, the main one being an increased airways resistance (raw). It is the result of bronchial abnormalities and reduced parenchymal elasticity, and is influenced by lung volume. Raw decreases with increasing lung volume, and increases with decreasing lung volume. Such expiratory events are generally compensated on the inspiratory side. Inspiration is shortened to prolong expiration, and breathing takes place at higher lung volume to take benefit of the higher lung recoil. This inspiratory load is associated to an increased inspiratory drive, and contributes to put inspiratory muscles at disadvantage. However, with time, adaptative changes take place that restore their force at a shorter length. Chronic fatigue, often suspected in this setting, is therefore not currently demonstrated. Bronchial and parenchymal abnormalities lead to ventilation-perfusion mismatch, that contribute to hypoxemia and hypercapnia through deadspace and shunt effects. Hypercapnia can also correspond in part to protective mechanisms, if the energy requirements for its maintenance are too high.

Airway Resistance↗

PubMed1995

Alterations in bronchoalveolar lavage and plasma endothelin-1 levels early after lung transplantation.

A temporary increase in pulmonary vascular resistance is observed during the first 24 hr following lung allotransplantation. We hypothesized that such early vascular changes are secondary to endothelial injury by ischemia-reperfusion, and that this may be mediated by an increased pulmonary endothelin-1 production/release. To test this hypothesis, radioimmunoassay was used to analyze endothelin-1 levels in bronchoalveolar lavage and plasma taken before surgery and at 1 hr, 4 hr, 24 hr, and 1 week after transplantation. The study was carried out on 2 groups of mongrel dogs. One group was subjected to left single-lung allotransplantation and the other to autotransplantation. Endothelin-1 levels in the bronchoalveolar lavage samples from the lung allografts were significantly increased at 1 (0.70 +/- 0.18 pg/ml) and 4 (1.84 +/- 0.65 pg/ml) hr after transplantation compared with the preoperative value (0.14 +/- 0.05 pg/ml), and declined at 24 (0.85 +/- 0.84 pg/ml) hr after transplantation. Similarly, plasma endothelin-1 levels in the allografts were significantly increased at 1 (2.0 +/- 0.80 pg/ml) and 4 (2.0 +/- 0.71 pg/ml) hr after transplant when compared with preoperative levels (0.54 +/- 0.09 pg/ml). Plasma endothelin-1 levels, however, remained significantly high after 24 hr (1.4 +/- 0.4 pg/ml; P < 0.007) and decreased after 1 week after transplant (0.89 +/- 0.32 pg/ml). On the other hand, endothelin-1 levels in bronchoalveolar lavage from the autograft group remained relatively unchanged; however, plasma levels showed a significant increase at 4 hr (6.6 +/- 1.8 pg/ml) after transplantation compared with preoperative levels (2.8 +/- 0.38 pg/ml). Elevation of endothelin-1 levels early after lung transplantation may play an important role in early high pulmonary vascular resistance and temporary graft dysfunction.

Airway Resistance↗

PubMed1995

Neurogenic goblet cell secretion and bronchoconstriction in guinea pigs sensitised to trimellitic anhydride.

Trimellitic anhydride is a cause of occupational asthma in humans. We have previously found that tracheal instillation of trimellitic anhydride conjugated to guinea pig serum albumin induces acute bronchoconstriction and airway plasma exudation in sensitised animals, responses mediated primarily via histamine release. In the present study, neural mechanisms mediating bronchoconstriction and goblet cell secretion were determined in trimellitic anhydride-sensitised guinea pigs using the ganglionic blocker hexamethonium to eliminate efferent reflex mechanisms, pretreatment with capsaicin to eliminate afferent mechanisms, or cimetidine and mepyramine to eliminate histamine-mediated mechanisms. The magnitude of secretion of intracellular mucus from tracheal goblet cells was quantified morphometrically as a mucus score which is inversely related to the degree of discharge. Guinea pigs were injected intradermally either with 0.1 ml 0.3% trimellitic anhydride in corn oil or with corn oil alone as control. Fourteen to eighteen days later all sensitised animals had developed specific immunoglobulin (Ig) G1 antibodies whereas the controls had not. Tracheal instillation of conjugated trimellitic anhydride in anaesthetised animals significantly increased airway lung resistance (RL) 24-fold in sensitised guinea pigs (34.3 +/- 7.9 cm H2O.ml-1.s) compared with controls (1.4 +/- 0.1 cm H2O.ml-1.s). Mucus score was significantly reduced by 51% (indicating goblet cell secretion) in sensitised guinea pigs (183 +/- 22 mucus score units) compared with controls (372 +/- 41 mucus score units). The antihistamines significantly inhibited conjugated trimellitic anhydride-induced bronchoconstriction by 89%, but did not significantly affect goblet cell discharge. Hexamethonium alone did not significantly affect conjugated trimellitic anhydride-induced bronchoconstriction or goblet cell secretion.(ABSTRACT TRUNCATED AT 250 WORDS)

Airway Resistance↗