Respiratory water loss

Ferrus, Lydia; Guénard, H.; Vardon, Guy; Varène, P

doi:10.1016/0034-5687(80)90067-5

Cited by 99 publications

(66 citation statements)

References 9 publications

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“…Previous studies of this heat exchange process have focused on measurements of air temperature or indirect estimates of bronchial surface temperature at steadystate conditions (Eschenbacher and Sheppard 1985;Ferrus et al 1980;Ingenito et al 1987;Primiano et al 1988). Several models have been developed to characterize the conditioning of the inspired air by the bronchial tree (Daviscas et al 1990;Eisner 1989;George et al 1990;Hanna and Scherer 1986;Ingenito et al 1986;Ramm et al 1989;Tsu et al 1988).…”

Section: Discussionmentioning

confidence: 99%

“…The total heat flux from the lung J (J s )1 ) can also be measured experimentally. As the expired gas is fully saturated (Eschenbacher and Sheppard 1985;Ferrus et al 1980;Primiano et al 1988), its temperature characterizes water vapor content and therefore enthalpy. J includes conductive (first term) and evaporative (second term) heat losses, and we presume that J can be expressed as a product of the lung overall heat transfer coefficient (HTC) and driving temperature difference:…”

Section: Development Of the Numerical Modelmentioning

confidence: 99%

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Effects of the ventilation pattern and pulmonary blood flow on lung heat transfer

Serikov¹,

Fleming

Talalov

et al. 2004

European Journal of Applied Physiology

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To investigate the relative role of pulmonary perfusion compared to ventilation on lung heat exchange, we determined the effects of blood flow, tidal volume and frequency of ventilation on the rate of lung heat transfer. In anesthetized dogs and isolated, perfused lungs, we investigated the dependence of the overall lung heat transfer coefficient (HTC) and lung thermal capacitance upon ventilation and pulmonary blood flow. The relationship between the HTC and pulmonary blood flow was strongly dependent on ventilation parameters. A distributed model of non-steady-state heat exchange adequately described these observations and demonstrated that changes in pulmonary blood flow may be considered as changes in the effective conductivity of the bronchial walls as 0.4 (0.1) J s(-1)m(-1) K(-1) per (l/min(-1)) of pulmonary blood flow. Our model describes the complex relationship between HTC, ventilation pattern, and effective thermal conductivity of the bronchial walls, all of which present limitations for the use of lung heat transfer to determine pulmonary blood flow.

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Section: Discussionmentioning

confidence: 99%

Section: Development Of the Numerical Modelmentioning

confidence: 99%

Effects of the ventilation pattern and pulmonary blood flow on lung heat transfer

Serikov¹,

Fleming

Talalov

et al. 2004

European Journal of Applied Physiology

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“…Pilot studies have demonstrated that the thermal challenge of these conditions is not sufficient to affect airway calibre in a 5-min test [14]. Validation studies with this apparatus [16], have shown the calculated moisture loss for a range of minute ventilations agrees with published values using the gold standard-freeze out method [10]. Measurements were made after 1-min breathing into the apparatus.…”

Section: Subjectsmentioning

confidence: 97%

“…However, in this study measurements were made with subjects breathing ambient room air and evaporative heat loss was not assessed. This is relevant because in resting conditions, the majority of heat exchange takes place in the upper airway and evaporative heat loss is a major component of total heat loss from the respiratory tract [10]. In intubated patients, measurements of tracheal temperature do not accurately predict total respiratory heat losses, but measurement of absolute humidity appears to be a better predictor [11].…”

mentioning

confidence: 99%

Respiratory heat and moisture loss is associated with eosinophilic inflammation in asthma

Noble¹,

McCafferty²,

Greening³

et al. 2007

European Respiratory Journal

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Increased mucosal vascularity is a hallmark of airway inflammation in asthma. It was hypothesised that this would lead to a detectable increase in respiratory heat and moisture loss (RHML), which would reflect the degree of airway inflammation present.A total of 23 subjects with asthma and 18 healthy controls had RHML measured in a crosssectional study. The measurements were made using a device that combines temperature and humidity measurement during inspiration and expiration and allows precise control over inspirate conditions and ventilatory pattern. The subjects with asthma underwent parallel measurements of exhaled nitric oxide, sputum eosinophil percentage and exhaled breath condensate pH.Mean¡SD RHML was elevated in patients with asthma ( This novel correlation between thermal and cellular measurements in asthma suggests that both of these noninvasive indices are sensitive to the degree of underlying chronic airway inflammation.

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“…Expired air was conducted through a heated pneumotachograph and airflow was electronically integrated to give tidal volume. Expired air was assumed to be fully saturated at the expired temperature and the respiratory heat exchange (RHE) was calculated according to saturation temperature relationships (Ferrus, 1980). During the ISH challenge calculation of the respiratory heat exchange was performed every 20 s. Patients were asked to adjust tidal volume in order to achieve a heat loss of 1.5, 3 and 6 kcal in 4 min respectively.…”

Section: Methodsmentioning

confidence: 99%

Effects of a PAF‐antagonist (BN 52063) on bronchoconstriction and platelet activation during exercise induced asthma.

Wilkens

Uffmann

et al. 1990

Brit J Clinical Pharma

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1. The effects of a specific PAF acether antagonist (BN 52063) on the response to isocapnic hyperventilation with dry cold air (ISH study) and exercise (EIA study) were assessed in a single dose and short term treatment study in 10 patients with exercise induced asthma. 2. ISH challenge was performed twice within 1 h after administration of either placebo, 240 mg BN 52063 p.o. or inhalation of 2.4 mg BN 52063. Hyperventilation increased Raw from 0.30 +/‐ 0.02 to 0.89 kPa s l‐1 (P less than 0.001) after the first challenge and from 0.28 +/‐ 0.04 to 0.84 +/‐ 0.06 kPa s l‐1 (P less than 0.001) after the second challenge. Oral pretreatment with BN 52063 did not result in a reduction of bronchoconstriction during both challenges. A significant increase of Raw was noted immediately after inhalation of BN 52063. An inhibition of PAF induced platelet aggregation (by a factor of 2) occurred after oral administration of BN 52063 after both ISH challenges (P less than 0.05). No significant inhibition of PAF induced platelet aggregation was seen after inhalation of BN 52063. At concentrations up to 30 microM in vitro, BN 52063 inhibited PAF induced platelet aggregation in a dose dependent manner. The IC50 of BN 52063 against the aggregating effect of 1 microM PAF was 7.0 +/‐ 2.1 microM. 3. In the EIA study the patients were challenged on the third day of treatment with either placebo or 240 mg BN 52063 p.o. or 5 mg BN 52063 by inhalation. Peak expiratory flow rates (PEFR) fell by 155 +/‐ 37 1 min‐1 after exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

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Respiratory water loss

Cited by 99 publications

References 9 publications

Effects of the ventilation pattern and pulmonary blood flow on lung heat transfer

Effects of the ventilation pattern and pulmonary blood flow on lung heat transfer

Respiratory heat and moisture loss is associated with eosinophilic inflammation in asthma

Effects of a PAF‐antagonist (BN 52063) on bronchoconstriction and platelet activation during exercise induced asthma.

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