Pulmonary interstitial edema in the pig after heavy exercise

Schaffartzik, Walter; Arcos, José P; Tsukimoto, K.; Mathieu-Costello, Odile; Wagner, Peter D.

doi:10.1152/jappl.1993.75.6.2535

Cited by 62 publications

(48 citation statements)

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“…In the present study, fluid flux returned to normal by min 2 of recovery, which is in agreement with experiments in the lung lymphatic system (Coates et al 1984;Newman et al 1988Newman et al , 1993Schaffartzik et al 1993). In human athletes, post-exercise clearance of accumulated pulmonary fluid to pre-exercise levels is achieved within 2 h (Hanel et al 2003).…”

Section: Discussionsupporting

confidence: 90%

Transvascular fluid flux from the pulmonary vasculature at rest and during exercise in horses

Vengušt

Staempfli

Viel

et al. 2006

The Journal of Physiology

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Exercise causes changes in pulmonary haemodynamics through redistribution of blood flow, increase in the pulmonary surface area, and increase in pulmonary vascular pressures. These changes contribute to the increase in fluid exchange across the alveolar-capillary barrier. To determine the extent of the fluid exchange across the alveolar-capillary barrier at rest and during exercise, six horses were exercised on a high-speed treadmill until fatigue. Arterial and mixed venous blood were sampled at rest and during exercise and recovery. Blood volume changes across the lung (∆BV; measured in percentage) were calculated from changes in plasma protein and haemoglobin concentration, and haematocrit. Cardiac output (Q) was calculated using the Fick equation. Fluid flux (J V−A ; measured in l min -1 ) across the alveolar-capillary barrier was then quantified based on Q and ∆BV. At rest, no fluid movement occurred across the pulmonary vasculature (0.6 ± 0.6 l min -1 ). During exercise, the amount of fluid moved from the pulmonary circulation was 8.3 ± 1.3 l min -1 at 1 min, 6.4 ± 2.9 l min -1 at 2 min, 10.1 ± 1.0 l min -1 at 3 min, 12.9 ± 2.5 l min -1 at 4 and 9.6 ± 1.5 l min -1 at fatigue (all P < 0.0001). Erythrocyte volume decreased by 6% (P < 0.01) across the lungs, which decreased the colloid osmotic gradient in the pulmonary vasculature. Decrease colloid osmotic gradient along with increased hydrostatic forces in the pulmonary vasculature would enhance displacement of fluid into the pulmonary interstitium. In conclusion, exercise caused large increases in transpulmonary fluid fluxes in horses. Here, we present a simple method to calculate transpulmonary fluid fluxes in different species, which can be used to elucidate mechanisms of lung fluid balance in vivo.

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Section: Discussionsupporting

confidence: 90%

Transvascular fluid flux from the pulmonary vasculature at rest and during exercise in horses

Vengušt

Staempfli

Viel

et al. 2006

The Journal of Physiology

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“…Various mechanisms of the increase in V /Q inequality have been proposed, including 1) a reduced common dead space-to-tidal volume ratio and therefore reduced admixture of the expired air, unmasking existing V /Q heterogeneity present at rest (27); 2) nonuniform pulmonary vasoconstriction and increased pulmonary arterial pressure (4); 3) interstitial edema (22,23); or 4) ventilatory time-constant inequality (27). None of these mechanisms have been investigated in exercising birds; however, the rather nonelastic structure of the avian lung may reduce the importance of those mechanisms relying on pressure changes in the pulmonary tissue and/or microenvironment.…”

Section: Ventilation-perfusion Inequality In Exercising Birdsmentioning

confidence: 99%

Ventilation-perfusion inequality during normoxic and hypoxic exercise in the emu

Schmitt

Powell

Hopkins

2002

Journal of Applied Physiology

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Many avian species exhibit an extraordinary ability to exercise under hypoxic condition compared with mammals, and more efficient pulmonary O(2) transport has been hypothesized to contribute to this avian advantage. We studied six emus (Dromaius novaehollandaie, 4-6 mo old, 25-40 kg) at rest and during treadmill exercise in normoxia and hypoxia (inspired O(2) fraction approximately 0.13). The multiple inert gas elimination technique was used to measure ventilation-perfusion (V/Q) distribution of the lung and calculate cardiac output and parabronchial ventilation. In both normoxia and hypoxia, exercise increased arterial Po(2) and decreased arterial Pco(2), reflecting hyperventilation, whereas pH remained unchanged. The V/Q distribution was unimodal, with a log standard deviation of perfusion distribution = 0.60 +/- 0.06 at rest; this did not change significantly with either exercise or hypoxia. Intrapulmonary shunt was <1% of the cardiac output in all conditions. CO(2) elimination was enhanced by hypoxia and exercise, but O(2) exchange was not affected by exercise in normoxia or hypoxia. The stability of V/Q matching under conditions of hypoxia and exercise may be advantageous for birds flying at altitude.

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“…1). While an offsetting factor in this regard may be suggested to be the pre-exercise osmotic absorption of fluid from the pulmonary tissues in our hypertonic saline experiments, it should be noted that according to the pulmonary edema hypothesis, hypoxemia is expected to intensify with increasing exercise duration as pulmonary edema worsens over time (Schaffartzik et al 1993;West et al 1993). This was also not the case in either treatment in the present study (Fig.…”

Section: Discussionmentioning

confidence: 82%

“…According to the pulmonary injury evoked airway inflammatory mediator release hypothesis (Pre´faut et al 1997(Pre´faut et al , 2000, an exaggeration of the arterial hypoxemia would be expected with increasing exercise duration as structural changes in the blood-gas barrier (Schaffartzik et al 1993;West et al 1993) intensify over time. Despite considerable appeal of this hypothesis (Pre´faut et al 1997(Pre´faut et al , 2000, the findings of Wetter et al (2001Wetter et al ( , 2002 in exercising human subjects did not lend credence to it.…”

Section: Discussionmentioning

confidence: 99%

“…In this context, whereas hyperhydration in the equine studies (Sosa-Leon et al 2002;Manohar et al 2003) was induced gradually over several hours following nasogastric administration of salt/fluids-which may have allowed H 2 O equilibration across various compartments-hypervolemia in the human athletes was induced rather acutely upon rapid osmotic absorption of water from tissues into the vascular compartment following intravenous (IV) administration of 10% pentastarch (Zavorsky et al 2003). In this study (Zavorsky et al 2003), pre-exercise significant osmotic removal of fluid from the pulmonary tissues caused upon IV pentastarch administration, may have limited the exercise-induced increase in thickness of the blood-gas barrier [note: interstitial pulmonary edema has been demonstrated in healthy exercising pigs (Schaffartzik et al 1993) and horses (West et al 1993)], thereby affecting the pulmonary gas exchange and resulting in the observed improvement in arterial oxygen tension (Zavorsky et al 2003). However, this is unlikely when hypervolemia is induced over several hours following nasogastric administration of NaCl (Manohar et al 2003).…”

Section: Introductionmentioning

confidence: 91%

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Acute hypervolemia does not improve arterial oxygenation in maximally exercising thoroughbred horses

2004

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Recently, it was reported that acute hypervolemia improves arterial oxygen tension in human athletes known to experience exercise-induced arterial hypoxemia. Since exercise-induced arterial hypoxemia is routinely observed in racehorses and is known to limit performance, we examined whether pre-exercise induction of acute hypervolemia would similarly benefit arterial oxygenation in maximally exercising thoroughbred horses. Two sets of experiments, namely, placebo [intravenous (IV) physiological saline] and acute hypervolemia (IV 7.2% NaCl, causing an 18.2% expansion of plasma volume) studies were carried out in random order on 13 healthy, exercise-trained thoroughbred horses, 7 days apart. An incremental exercise protocol leading to 120 s of galloping at 14 m s(-1) on a 3.5% uphill incline was used. Galloping at this workload elicited maximal heart rate and induced pulmonary hemorrhage in all horses in both treatments. In the placebo study, arterial oxygen tension decreased to 76.1 (2) mmHg (P<0.0001) at 30 s of maximal exertion, but further significant changes did not occur as exercise duration increased to 120 s [arterial oxygen tension 72.4 (2) mmHg]. A significant arterial hypoxemia also developed in galloping horses in the acute hypervolemia study [arterial oxygen tension at 30 and 120 s was 76.7 (1.7) and 71.9 (1.6) mmHg, respectively], but significant differences between treatments could not be demonstrated. In both treatments, a similar desaturation of arterial hemoglobin was also observed at 30 s of maximal exercise, which intensified with increasing exercise duration as hyperthermia, acidosis and hypercapnia intensified. Thus, acute expansion of plasma volume did not benefit arterial oxygenation in maximally exercising thoroughbred horses.

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Pulmonary interstitial edema in the pig after heavy exercise

Cited by 62 publications

References 0 publications

Transvascular fluid flux from the pulmonary vasculature at rest and during exercise in horses

Transvascular fluid flux from the pulmonary vasculature at rest and during exercise in horses

Ventilation-perfusion inequality during normoxic and hypoxic exercise in the emu

Acute hypervolemia does not improve arterial oxygenation in maximally exercising thoroughbred horses

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