Effects of 100% oxygen breathing on the capillary filtration coefficient in rabbit lungs

Matalon, Sadis; Cesar, Michael A.

doi:10.1016/0026-2862(85)90007-x

Cited by 11 publications

(3 citation statements)

References 23 publications

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“…Thus our results (Tables 2 and 3) show that continuous exposure to 100% 0, causes progressive injury to the alveolar epithelium, resulting in increased permeability to solute. This damage is first detected after 48 h in 100% OL, when functional injury to microvascular permeability has first been reported [5], but before the onset of pulmonary edema or the compromise in gas exchange. Permeability to solute remains high at 24 h after exposure but returns to control levels in rabbits that were alive 7 days after being returned to room air [6].…”

Section: Discussionmentioning

confidence: 96%

Sublethal Hyperoxic Injury to the Alveolar Epithelium and the Pulmonary Surfactant System

Matalon

Holm

Loewen

et al. 1988

Experimental Lung Research

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We quantified the effects of continuous exposure to 100% O2 on the development of sublethal injury to the pulmonary alveolar epithelium of rabbits. There was a progressive increase in alveolar permeability to solute after 48 h in O2, which coincided with the onset of damage to the pulmonary microvasculature. Rabbits that were exposed to 100% O2 for 64 h and returned to room air for 24 h had, in addition to increased permeability to solute, decreased phospholipid levels, decreased total lung capacity, pulmonary edema, high minimum surface tensions in their bronchoalveolar lavage, and moderate hypoxemia. Intratracheal instillation of calf lung surfactant (CLSE) significantly ameliorated the progression of hyperoxic injury by increasing alveolar phospholipid levels and thus preventing the inhibition of lung surfactant activity by plasma proteins and other high molecular weight components of alveolar edema. We concluded that the alveolar epithelium and the pulmonary microvasculature show similar sensitivity to hyperoxia and that clinical manifestations of hyperoxic lung injury may be due, at least in part, to surfactant dysfunction.

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Section: Discussionmentioning

confidence: 96%

Sublethal Hyperoxic Injury to the Alveolar Epithelium and the Pulmonary Surfactant System

Matalon

Holm

Loewen

et al. 1988

Experimental Lung Research

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“…Further observations that alveolar epithelial Na +2 transport can be supported by glycolysis in the presence of mitochondrial inhibitors, including rotenone, has actually led others to conjecture that the pulmonary endothelium is the site of barrier failure in mitochondrial insufficiency [43]. In light of these studies, the implication is that the pulmonary endothelium is also a predominant site of the hyperoxia-induced increase in K f observed in the rabbit lung [25]. Nonetheless, our conclusion that complex I bypass affords significant protection against rotenone-induced barrier dysfunction in lung remains valid regardless of whether the endothelium, epithelium or both provide the main target.…”

Section: Discussionmentioning

confidence: 99%

“…While the functional impact of the effect on complex I activity was not specifically investigated, there was no discernible pulmonary edema resulting from the hyperoxic exposure, as reflected in lung wet-to-dry weight ratios [2]. On the other hand, in rabbits exposed to 100% O 2 for 48 hours, while there was also little change in lung water or arterial blood gases in the intact animal, the pulmonary endothelial filtration coefficient (K f ) increased, portending compromised endothelial barrier integrity [25]. Thus, we asked whether there could be a link between mitochondrial complex I activity blockade, mitochondrial function reflected as diminished ATP generation and pulmonary endothelial barrier function.…”

Section: Introductionmentioning

confidence: 99%

Depleted energy charge and increased pulmonary endothelial permeability induced by mitochondrial complex I inhibition are mitigated by coenzyme Q1 in the isolated perfused rat lung

Bongard

Yan

Hoffmann

et al. 2013

Free Radical Biology and Medicine

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Mitochondrial dysfunction is associated with various forms of lung injury and disease that also involve alterations in pulmonary endothelial permeability, but the relationship, if any, between the two is not well understood. This question was addressed by perfusing the isolated intact rat lung with a buffered physiological saline solution in the absence or presence of the mitochondrial complex I inhibitor rotenone (20 uM). As compared to control, rotenone depressed whole lung tissue ATP from 5.66 ± 0.46 (SEM) to 2.34 ± 0.15 (SEM) μmol·gram−1 dry lung, with concomitant increases in the ADP:ATP and AMP:ATP ratios. Rotenone also increased lung perfusate lactate (from 12.36 ± 1.64 (SEM) to 38.62 ± 3.14 μmol·15 min−1 perfusion·gm−1 dry lung) and the lactate:pyruvate ratio, but had no detectable impact on lung tissue GSH:GSSG redox status. The amphipathic quinone, coenzyme Q1 (CoQ1; 50 μM) mitigated the impact of rotenone on the adenine nucleotide balance, wherein mitigation was blocked by NAD(P)H:quinone oxidoreductase 1 (NQO1) or mitochondrial complex III inhibitors. In separate studies, rotenone increased the pulmonary vascular endothelial filtration coefficient (Kf) from 0.043 ± 0.010 (SEM) to 0.156 ± 0.037 (SEM) ml·min−1·cm H2O−1·gm−1 dry lung weight, and CoQ1 protected against the effect of rotenone on Kf. A second complex I inhibitor, piericidin A, qualitatively reproduced the impact of rotenone on Kf and the lactate/pyruvate ratio. Taken together, the observations imply that pulmonary endothelial barrier integrity depends on mitochondrial bioenergetics as reflected in lung tissue ATP levels and that compensatory activation of whole lung glycolysis cannot protect against pulmonary endothelial hyperpermeability in response to mitochondrial blockade. The study further suggests that low molecular weight amphipathic quinones may have therapeutic utility in protecting lung barrier function in mitochondrial insufficiency.

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Surfactant System in Lung Injury

Haslam¹

1996

ARDS Acute Respiratory Distress in Adults

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Effects of 100% oxygen breathing on the capillary filtration coefficient in rabbit lungs

Cited by 11 publications

References 23 publications

Sublethal Hyperoxic Injury to the Alveolar Epithelium and the Pulmonary Surfactant System

Sublethal Hyperoxic Injury to the Alveolar Epithelium and the Pulmonary Surfactant System

Depleted energy charge and increased pulmonary endothelial permeability induced by mitochondrial complex I inhibition are mitigated by coenzyme Q1 in the isolated perfused rat lung

Surfactant System in Lung Injury

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