Lung water balance

Snashall, P. D.; Hughes, J. M. B.

doi:10.1007/bfb0035264

Cited by 19 publications

(4 citation statements)

References 115 publications

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“…Excluding blood, the lung is ϳ80% water by weight. Between 30% and 50% of this water is extracellular, consisting of interstitial fluid and lymph (37). Interstitial pulmonary edema, measured as extravascular lung water (EVLW) and caused by an increase in the filtration of fluid from the pulmonary capillaries into the interstitial space between the alveolar epithelium and capillary endothelium, may interfere with gas exchange across the alveolar-capillary membrane.…”

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confidence: 99%

Human lung density is not altered following normoxic and hypoxic moderate-intensity exercise: implications for transient edema

Hodges¹,

Sheel²,

Mayo³

et al. 2007

Journal of Applied Physiology

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The purpose of this study was to examine the effects of exercise on extravascular lung water as it may relate to pulmonary gas exchange. Ten male humans underwent measures of maximal oxygen uptake (Vo2 max) in two conditions: normoxia (N) and normobaric hypoxia of 15% O2 (H). Lung density was measured by quantified MRI before and 48.0 +/- 7.4 and 100.7 +/- 15.1 min following 60 min of cycling exercise in N (intensity = 61.6 +/- 9.5% Vo2 max) and 55.5 +/- 9.8 and 104.3 +/- 9.1 min following 60 min cycling exercise in H (intensity = 65.4 +/- 7.1% hypoxic Vo2 max), where Vo2 max = 65.0 +/- 7.5 ml x kg(-1) x min(-1) (N) and 54.1 +/- 7.0 ml x kg(-1) x min(-1) (H). Two subjects demonstrated mild exercise-induced arterial hypoxemia (EIAH) [minimum arterial oxygen saturation (SaO2 min) = 94.5% and 93.8%], and seven subjects demonstrated moderate EIAH (SaO2 min = 91.4 +/- 1.1%) as measured noninvasively during the Vo2 max test in N. Mean lung densities, measured once preexercise and twice postexercise, were 0.177 +/- 0.019, 0.181 +/- 0.019, and 0.173 +/- 0.019 g/ml (N) and 0.178 +/- 0.021, 0.174 +/- 0.022, and 0.176 +/- 0.019 g/ml (H), respectively. No significant differences (P > 0.05) were found in lung density following exercise in either condition or between conditions. Transient interstitial pulmonary edema did not occur following sustained steady-state cycling exercise in N or H, indicating that transient edema does not result from pulmonary capillary leakage during sustained submaximal exercise.

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mentioning

confidence: 99%

Human lung density is not altered following normoxic and hypoxic moderate-intensity exercise: implications for transient edema

Hodges¹,

Sheel²,

Mayo³

et al. 2007

Journal of Applied Physiology

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“…The lung is ∼80% water by weight, and between 30% and 50% of the aqueous content is extracellular, consisting of interstitial fluid and lymph, respectively (14).…”

Section: Causes Of Eiahmentioning

confidence: 99%

Study Of Exercise-Induced Hypoxemia In Athletes: Role Of Interstitial Pulmonary Edema

Sharma

Lu²,

Coneys³

et al. 2011

C72. Cardiopulmonary Stressors: Exercise, Hypoxia and Altitude: New Insights

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Exercise-induced arterial hypoxemia (EIAH), defined as a significant decrease in oxygen saturation (<95%) during maximal and sub-maximal exercise, is a phenomenon observed in moderately and highly trained athletes. The consequences of EIAH on exercise performance relate to its negative influence on maximal O 2 uptake (VO 2 max) and impairment of oxygen delivery. The causes of EIAH are yet to be completely elucidated. Proposed mechanisms include ventilation/perfusion inequality, relative alveolar hypoventilation, right-to-left shunt, and diffusion limitation. We hypothesized that development of interstitial pulmonary edema during maximal exercise triggers the physiological mechanisms leading to EIAH. Eleven subjects, who had previously developed EIAH during a similar testing protocol, performed an incremental cycling or running protocol to exhaustion, and pre-and post-exercise lungs scanned using computed tomography. Scans were analyzed both qualitatively and quantitatively for the development of pulmonary edema. We employed two different procedures for lung density assessment, specifically, lung sampling technique (Method A) and whole lung measurements (Method B). The lung density measurements were as follows: 0.088±0.008 g/cm 3 pre-exercise, 0.090±0.008 g/cm 3 post-exercise (p=0.27) with Method A, and 0.190±0.018 g/cm 3 pre-exercise, 0.178±0.010 g/cm 3 post-exercise (p=0.94) with Method B. These results do not support the presence of interstitial pulmonary edema in individuals known to develop EIAH. Development of interstitial pulmonary edema cannot be conclusively identified as a significant cause of EIAH in moderately and highly trained athletes.

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“…Where Qf is net water flow out of the vascular compartment, Kf is the membrane filtration coefficient, P mv is the hydrostatic pressure in the microvasculature, Pp mv is the interstitial hydrostatic pressure, a is the microvascular membrane coefficient for plasma proteins, nmv is the osmotic pressure in the microvasculature, and Tlpmv is the interstitial osmotic pressure. 109 Thus, net water flow is governed by the differences in hydrostatic and osmotic pressures.…”

Section: Pulmonary Capillary Leakagementioning

confidence: 99%

“…Estimates of the hydrostatic pressures of the pulmonary capillaries and the interstitial space are 10 mm Hg and -3 mm Hg respectively, while the corresponding osmotic pressures are estimated as 25 mm Hg and 19 mm Hg. 2 ' 60 It is likely that under normal resting circumstances, Qf is positive 109 indicating some filtration of fluid out of the pulmonary capillaries at an estimated rate of 20 ml-hr" 1 in normal conditions. 126 An added complication in the practical use of the Starling equation is the discrepancy in pressures between the apices and bases of the lungs.…”

Section: Pulmonary Capillary Leakagementioning

confidence: 99%

Pulmonary Oedema following Exercise in Humans

2006

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Pulmonary physiologists have documented many transient changes in the lung and the respiratory system during and following exercise, including the incomplete oxygen saturation of arterial blood in some subjects, possibly due to transient pulmonary oedema. The large increase in pulmonary arterial pressure during exercise, leading to either increased pulmonary capillary leakage and/or pulmonary capillary stress failure, is likely to be responsible for any increase in extravascular lung water during exercise. The purpose of this article is to summarise the studies to date that have specifically examined lung water following exercise. A limited number of studies have been completed with the specific purpose of identifying pulmonary oedema following exercise or a similar intervention. Of these, approximately 50% have observed a positive change and the remaining have provided results that are either inconclusive or show no change in extravascular lung water. While it is difficult to draw a firm conclusion from these studies, we believe that pulmonary oedema does occur in some humans following exercise. As such, this is a phenomenon of significance to pulmonary and exercise physiologists. This possibility warrants further study in the area with more precise measurement tools than has previously been undertaken.

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Lung water balance

Cited by 19 publications

References 115 publications

Human lung density is not altered following normoxic and hypoxic moderate-intensity exercise: implications for transient edema

Human lung density is not altered following normoxic and hypoxic moderate-intensity exercise: implications for transient edema

Study Of Exercise-Induced Hypoxemia In Athletes: Role Of Interstitial Pulmonary Edema

Pulmonary Oedema following Exercise in Humans

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