Effects of acute hyperoxic exposure on solute fluxes across the blood-gas barrier in rat lungs

Zheng, Lulin; Du, Rui; Goodman, Barbara E.

doi:10.1152/jappl.1997.82.1.240

Cited by 8 publications

(10 citation statements)

References 13 publications

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“…The first finding was that basal alveolar fluid clearance did not change for 56 h. Similar results were observed in the studies where basal alveolar fluid clearance was sustained (6,21); and terbutaline, a selective b2-adrenergic agonist, increased alveolar fluid clearance in rats exposed to >95% oxygen for 40 and 60 h (6,7). In contrast to this study, rats exposed to 100% oxygen for 60 or 64 h had a decreased basal rate in alveolar fluid clearance, active sodium transport and Na + -K + ATPase activity (20,22).…”

Section: Discussionsupporting

confidence: 80%

Beta1-Adrenergic Agonist Is a Potent Stimulator of Alveolar Fluid Clearance in Hyperoxic Rat Lungs

Sakuma

Hida

Nambu

et al. 2001

Japanese Journal of Pharmacology

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ABSTRACT-Because it was still uncertain whether a stimulation of b 1-adrenoceptors accelerated alveolar fluid clearance in hyperoxic lung injury, the effect of denopamine, a selective b1-adrenergic agonist, on alveolar fluid clearance was determined in rats exposed to 93% oxygen for 48 and 56 h. Alveolar fluid clearance was measured by the progressive increase in the concentration of Evans blue labeled albumin instilled into the alveolar spaces over 1 h at 37°C in isolated rat lungs. The principle results were as follows: 1) Although lung water volume increased in rats exposed to hyperoxia for 48 and 56 h, basal alveolar fluid clearance did not change for up to 56 h; 2) Denopamine increased alveolar fluid clearance in rats exposed to hyperoxia as well as in rats without exposure to hyperoxia; 3) Denopamine primarily increased amilorideinsensitive alveolar fluid clearance in rats exposed to hyperoxia; 4) The potency of denopmaine was similar to that of terbutaline, a selective b 2-adrenergic agonist. In summary, denopamine is a potent stimulator of alveolar fluid clearance in rats exposed to hyperoxia. Keywords: Pulmonary edema, Lung injury, Sodium transport, Alveolar epitheliumThe stimulation of b 2-adrenoceptors accelerates transepithelial sodium transport out of the alveolar spaces through apical sodium channels and basolateral Na + -K + ATPase on type II alveolar epithelial cells (1). Alveolar fluid clearance occurs in accordance with sodium transport and results in the resolution of pulmonary edema (2, 3). Terbutaline, epinephrine and salmeterol are potent stimulators of b2-adrenoceptors on type II alveolar epithelial cells in rat lungs (4 -9). Amiloride, a sodium channel inhibitor, inhibits the increase in alveolar fluid clearance in the presence of b2-adrenergic agonists (10, 11). However, inconsistent with rat lungs, b2-adrenergic agonists did not increase alveolar fluid clearance in rabbit and guinea pig lungs (12, 13). Interestingly, isoproterenol increased alveolar fluid clearance via b 1-adrenoceptors in guinea pig lungs (13), whereas isoproterenol increased alveolar fluid clearance via b 2-adrenoceptors in rat lungs (14). Recently, we reported that denopamine, a selective b1-adrenergic agonist, increased alveolar fluid clearance in normal rat and guinea pig lungs (15).The exposure to hyperoxia (>95%) induces lung injury and results in high mortality in rats (16,17). Recently, it was reported that isoproterenol increased alveolar fluid clearance by stimulating b 2-adrenoceptors in severely injured rat lungs exposed to hyperoxia for 64 h (18). The stimulating effect by terbutaline on alveolar fluid clearance was also reported in moderately injured rat lungs exposed to 100% oxygen for 40 h (6). However, it was uncertain whether a selective b1-adrenergic agonist increased alveolar fluid clearance in rats exposed to hyperoxia. Therefore, the first objective was to determine whether alveolar fluid clearance changed in rats with hyperoxic lung injury. Alveolar fluid clearance was measured in rats exposed to...

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Section: Discussionsupporting

confidence: 80%

Beta1-Adrenergic Agonist Is a Potent Stimulator of Alveolar Fluid Clearance in Hyperoxic Rat Lungs

Sakuma

Hida

Nambu

et al. 2001

Japanese Journal of Pharmacology

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“…We have confirmed that hyperoxia causes pulmonary edema in adult rats, as corroborated by the presence of pleural fluid in the thoracic cavity (volume: 9.1 Ϯ 0.6 ml) and a three-to fourfold increase in the alveolar ELF volume after 64 h of exposure to 100% O 2 . The lung permeability to small solutes (Na ϩ , mannitol) and large solutes (albumin) significantly increased after hyperoxia-induced lung injury, probably because of damage of lung capillaries (9,23,25,33,35). The different results that were obtained with the EBD-albumin and FITC-albumin assay probably represent a higher sensi- Fig.…”

Section: Discussionmentioning

confidence: 93%

Isoproterenol improves ability of lung to clear edema in rats exposed to hyperoxia

Saldías

Comellas

Ridge

et al. 1999

Journal of Applied Physiology

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Exposure of adult rats to 100% O(2) results in lung injury and decreases active sodium transport and lung edema clearance. It has been reported that beta-adrenergic agonists increase lung edema clearance in normal rat lungs by upregulating alveolar epithelial Na(+)-K(+)-ATPase function. This study was designed to examine whether isoproterenol (Iso) affects lung edema clearance in rats exposed to 100% O(2) for 64 h. Active Na(+) transport and lung edema clearance decreased by approximately 44% in rats exposed to acute hyperoxia. Iso (10(-6) M) increased the ability of the lung to clear edema in room-air-breathing rats (from 0.50 +/- 0.02 to 0.99 +/- 0. 05 ml/h) and in rats exposed to 100% O(2) (from 0.28 +/- 0.03 to 0. 86 +/- 0.09 ml/h; P < 0.001). Disruption of intracellular microtubular transport of ion-transporting proteins by colchicine (0. 25 mg/100 g body wt) inhibited the stimulatory effects of Iso in hyperoxia-injured rat lungs, whereas the isomer beta-lumicolchicine, which does not affect microtubular transport, did not inhibit active Na(+) transport stimulated by Iso. Accordingly, Iso restored the lung's ability to clear edema after hyperoxic lung injury, probably by stimulation of the recruitment of ion-transporting proteins (Na(+)-K(+)-ATPase) from intracellular pools to the plasma membrane in rat alveolar epithelium.

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“…Abernathy et al (1) have used radiolabeled dextran compared with albumin to evaluate macromolecule transport across the alveolar capillary membrane; however, their goal was not to measure a leak. Zheng et al (33) investigated effects of acute hyperoxia on solute transport in isolated rat lung by filling air spaces with solutions containing FITCdextran and other markers. However, to our knowledge, FITC-dextran has not yet been measured in the BAL to evaluate lung epithelial injury.…”

Section: Discussionmentioning

confidence: 99%

Fluorescein-labeled dextran concentration is increased in BAL fluid after ANTU-induced edema in rats

Guery¹,

Nelson

Viget³

et al. 1998

Journal of Applied Physiology

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Several methodologies have been developed to assess alveolocapillary membrane permeability in acute lung injury. The purpose of this study was to determine the reliability of FITC-dextran compared with radioactive tracers to assess lung permeability alterations. After intraperitoneal administration of alpha-naphthylthiourea (ANTU, 50 mg/kg) or DMSO-ANTU vehicle, the animals were euthanized and their lungs were studied in an isolated-lung preparation. FITC-dextran or radiolabeled tracers were added to the perfusate. At 2 h the bronchoalveolar lavage (BAL) fluid from the ANTU group showed a significantly greater amount of fluorescence in the supernatant after centrifugation of BAL fluid compared with the DMSO group. Consistent results were observed with the radioactive tracers: there was an increase in extravascular albumin space and extravascular lung water compared with the control group. No cleavage of the FITC from the dextran molecule was evident by chromatography comparing samples recovered from the BAL fluid to the pure FITC-dextran molecule. In conclusion, measurement of FITC-dextran in the supernatant of BAL fluid after intravascular administration is a reliable method of assessing lung permeability changes in vivo and ex vivo.

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Effects of acute hyperoxic exposure on solute fluxes across the blood-gas barrier in rat lungs

Cited by 8 publications

References 13 publications

Beta1-Adrenergic Agonist Is a Potent Stimulator of Alveolar Fluid Clearance in Hyperoxic Rat Lungs

Beta1-Adrenergic Agonist Is a Potent Stimulator of Alveolar Fluid Clearance in Hyperoxic Rat Lungs

Isoproterenol improves ability of lung to clear edema in rats exposed to hyperoxia

Fluorescein-labeled dextran concentration is increased in BAL fluid after ANTU-induced edema in rats

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