Acetazolamide attenuates transvascular fluid flux in equine lungs during intense exercise
Notice bibliographique
Résumé
Key points During high intensity exercise approximately 4% of the cardiac output leaves the pulmonary circulation into the interstitium. This fluid flux has been attributed to an increase in pulmonary transmural hydrostatic (Starling) forces. Fluid efflux from erythrocytes may account for a considerable fraction of fluid exiting the pulmonary circulation. Transcapillary erythrocyte volume changes are largely determined by the Jacobs–Stewart cycle, a series of intracellular and extracellular diffusion and chemical reaction events of carbon dioxide, water, bicarbonate, hydrogen ions and chloride that are initiated when blood is exposed to a gradient such as when blood enters and traverses systemic and pulmonary capillaries. We tested the hypothesis that the Jacobs–Stewart cycle contributes to pulmonary transvascular fluid fluxes during exercise by inhibiting red cell carbonic anhydrase, the activity of which is critical to rapid completion of the Jacobs–Stewart cycle during capillary transit. Our results indicate that during exercise in horses, transvascular fluid fluxes in the lung appear to be dependent on the Jacobs–Stewart cycle and much less dependent upon transmural hydrostatic (Starling) forces. It also appears that pulmonary circulation transvascular fluid fluxes are mediated by chloride and water egress from erythrocytes directly into the interstitium without transit through plasma, which is likely the result of functional apposition of the erythrocyte and vascular endothelial membranes occurring during capillary transit. Abstract During intense exercise in horses the transvascular fluid flux in the pulmonary circulation ( J v‐a ) represents 4% of cardiac output ( ). This fluid flux has been attributed to an increase in pulmonary transmural hydrostatic forces, increases in perfused microvascular surface area, and reversible alterations in capillary permeability under conditions of high flow and pressure. Erythrocyte fluid efflux, however, accounts for a significant fraction of J v‐a . In the lung the Jacobs–Stewart cycle occurs with diffusion of CO 2 into alveolar space with possible accompanying chloride (Cl − ) and water movement from the erythrocyte directly into the pulmonary interstitium. We hypothesised that inhibition of carbonic anhydrase in erythrocytes inhibits the Jacobs–Stewart cycle and attenuates J v‐a . Five horses were exercised on a treadmill until fatigue without (control) and with acetazolamide treatment (30 mg kg −1 30 min before exercise). Erythrocyte fluid efflux, plasma fluid flux across the lung and J v‐a were calculated using haemoglobin, haematocrit, plasma protein and Q. Fluid fluxes were used to calculate erythrocyte, plasma and whole blood Cl − fluxes across the lung. Cardiac output was not different between control and acetazolamide treatment. During exercise erythrocyte fluid efflux and J v‐a increased in control (9.3 ± 3.3 and 11.0 ± 4.4 l min −1 , respectively) and was higher than after acetazolamide treatment (3.8 ± 1.6 and 1.2 ± 1.2 l min −1 , respectively) ( P < 0.05). Plasma fluid flux did not change from rest in control and decreased after acetazolamide treatment (−4.5 ± 1.5 l min −1 ) ( P < 0.05). Erythrocyte Cl − flux increased during exercise in control and after acetazolamide treatment ( P < 0.05). During exercise plasma Cl − flux across the lung did not change in control; however, it increased with acetazolamide treatment ( P = 0.0001). During exercise whole blood Cl − flux increased across the lung in control ( P < 0.05) but not after acetazolamide treatment. The results indicate that J v‐a in the lung is dependent on the Jacobs–Stewart cycle and mostly independent of transmural hydrostatic forces. It also appears that J v‐a is mediated by Cl − and water egress from erythrocytes directly into the interstitium without transit through plasma.
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Prédiction distillée sur la base complète
Imitation des enseignantsNi prévalence calibrée, ni vérité terrain. Validation humaine à venir. Apprise à partir de 10 348 étiquettes directes de Codex et de 10 348 étiquettes directes de Gemma. Le mode candidate est l'union des têtes enseignantes seuillées; le consensus est leur intersection. Ces sorties portent le statut machine_predicted_unvalidated et ne sont ni des étiquettes humaines ni des étiquettes directes de modèles de pointe.
Scores Codex et Gemma par catégorie
| Catégorie | Codex | Gemma |
|---|---|---|
| Métarecherche | 0,000 | 0,000 |
| Méta-épidémiologie (sens strict) | 0,000 | 0,000 |
| Méta-épidémiologie (sens large) | 0,000 | 0,000 |
| Bibliométrie | 0,000 | 0,000 |
| Études des sciences et des technologies | 0,000 | 0,000 |
| Communication savante | 0,000 | 0,000 |
| Science ouverte | 0,000 | 0,000 |
| Intégrité de la recherche | 0,000 | 0,000 |
| Charge utile insuffisante (le modèle a refusé de juger) | 0,000 | 0,000 |
Scores machine (provisoires)
Les deux têtes enseignantes du modèle étudiant, lues sur ce travail. Un score ordonne la base pour la relecture; il n'affirme jamais une catégorie, et le statut de validation accompagne chaque rangée tel quel.
Scores de référence d'un modèle non mature (critères de maturité non atteints, 7 itérations). Un score ordonne; il n'affirme jamais une catégorie.
score_only:v0-immature-baseline · tel quel depuis la passe de notation : score_only signifie que le nombre peut ordonner les travaux, et qu'aucune étiquette de catégorie n'en découleClassification
machine, non validéePrédiction automatique; un appel candidat d’une seule tête enseignante, pas un consensus.
Le détail, modèle par modèle et score par score, se trouve en fin de page sous « Comment cette classification a été obtenue ».