Effects of 100% O2 breathing on permeability of alveolar epithelium to solute

1981 ◽  
Vol 50 (4) ◽  
pp. 859-863 ◽  
Author(s):  
S. Matalon ◽  
E. A. Egan

We measured the effects of 100% O2 exposure at 1 atm for 48 (n = 5) and 63 h (n = 6) on the solute permeability of the alveolar epithelium of rabbits. We instilled 10-15 ml of saline containing trace amounts of 131I-albumin (r approximately 35 A), 125I-cytochrome c (r approximately 17 A), and [57Co]cyanocobalamin (r approximately 6.5 A) into an atelectatic segment of the right lower lobe. Egress of these tracers was determined from their change in concentration in the alveolar saline and their detection in arterial blood. All tracers left the alveolar space and appeared in the arterial blood on the 63-h O2 group, cytochrome c and cyanocobalamin in the 48-h O2 group, and only cyanocobalamin in the control (air breathing). The O2-exposed animals had PaO2 values higher than 500 Torr, normal PaCO2 and pH, and wet-to-dry lung weight ratios not different from control. We concluded that increasing the length of O2 exposure increases the solute permeability of the alveolar epithelium and this precedes the appearance of pulmonary edema.

1985 ◽  
Vol 58 (4) ◽  
pp. 1092-1098 ◽  
Author(s):  
M. D. Walkenstein ◽  
B. T. Peterson ◽  
J. E. Gerber ◽  
R. W. Hyde

Histological studies provide evidence that the bronchial veins are a site of leakage in histamine-induced pulmonary edema, but the physiological importance of this finding is not known. To determine if a lung perfused by only the bronchial arteries could develop pulmonary edema, we infused histamine for 2 h in anesthetized sheep with no pulmonary arterial blood flow to the right lung. In control sheep the postmortem extravascular lung water volume (EVLW) in both the right (occluded) and left (perfused) lung was 3.7 +/- 0.4 ml X g dry lung wt-1. Following histamine infusion, EVLW increased to 4.4 +/- 0.7 ml X g dry lung wt-1 in the right (occluded) lung (P less than 0.01) and to 5.3 +/- 1.0 ml X g dry wt-1 in the left (perfused) lung (P less than 0.01). Biopsies from the right (occluded) lungs scored for the presence of edema showed a significantly higher score in the lungs that received histamine (P less than 0.02). Some leakage from the pulmonary circulation of the right lung, perfused via anastomoses from the bronchial circulation, cannot be excluded but should be modest considering the low pressures in the pulmonary circulation following occlusion of the right pulmonary artery. These data show that perfusion via the pulmonary arteries is not a requirement for the production of histamine-induced pulmonary edema.


1977 ◽  
Vol 233 (1) ◽  
pp. H80-H86 ◽  
Author(s):  
E. A. Egan ◽  
R. M. Nelson ◽  
I. H. Gessner

Ten anesthetized dogs, 48 h postintravenous 131I-albumin injection, had a segment of lung airspace isolated by a balloon-tipped catheter lodged in a bronchus. An isotonic saline solution containing trace amounts of Blue Dextran, 125I-albumin, and 57Co-cyanocobalamin was instilled into the lung segment. During control periods, lung saline was absorbed at a rate of 0.133% per minute as measured by indicator dilution of Blue Dextran. Only 57Co-cyanocobalamin crossed the epithelium. Acute hemodynamic pulmonary edema was produced by aortic constriction plus saline overload. In pulmonary edema the fluid volume in the airspace increased at the rate of 0.96% per minute, and there was a significant influx of 131I-albumin into the lung saline from the blood in all animals. However, neither 125I-albumin nor Blue Dextran diffused from the airspace into blood during edema; both were merely diluted by fluid influx. The rate of diffusion of 57Co-cyanocobalamin increased fivefold during edema. A small number of discrete breaks in the lung epithelium allowing bulk flow of interstitial fluid is proposed to account for the one-way movement of albumin in hemodynamic alveolar edema.


2021 ◽  
Vol 23 (Supplement_G) ◽  
Author(s):  
Paolo Spontoni ◽  
Laura Stazzoni ◽  
Cristina Giannini ◽  
Giulia Costa ◽  
Marco Angelillis ◽  
...  

Abstract Aims PlatypneaOrthodeoxiasyndrome (POS) is a rare clinical condition characterized by dyspnoea and arterial desaturation, typically occurring in orthostatism and vanishing in a supine position. The real pathophysiologic triggers are still not completely understood. Methods and results In January 2021, a 76-year-old female patient was admitted to our department for the management of a large mass in the right lung (69 × 54 × 76 cm). Pre-operative Computed Tomography (CT)-scan showed a lesion of the right lower lobe, with suspected infiltration of posterior costal pleura and bronchoscopy revealed distal occlusion of intermedious bronchus. Surgical treatment was planned: extrapleural lower bilobectomy with the removal of the VI rib to reduce intracavity space was performed, using postero-lateral thoracotomy approach. On the third post-operative day, an acute neurologic deficit with left-sided paralysis, associated with desaturation and hypotension, occurred during a new attempt to mobilize the patient. Nonetheless the patient showed complete resolution of symptoms in supine position. A new similar episode of severe desaturation (SO2 80%) was observed in the 7th post-operative day. Arterial blood gas test showed PO2 37 mmHg; PCO2 27 mmHg; SO2 80.3%, pH 7.61, tHb 12.4 g/dl; O2Hb 78.4%. CT pulmonary angiography excluded a suspicious of pulmonary embolism. A right to left atrial shunt was suspected. Contrast-enhanced transcranial Doppler ultrasound showed microembolic signals in the basal cerebral arteries. Transoesophageal echocardiography was performed, confirming an interatrial septum with an exuberant hyperdynamic movement and showing an abundant passage of contrast from the right atrium to the left, even without the Valsalva manoeuvre, compatible with an important patent foramen ovale (PFO). Patient was referred to the cardiac Catheterization Laboratory for percutaneous closure of PFO. The device was successfully placed via right femoral venous catheter access and on transesophageal echocardiogram guidance. The procedure was performed without any complications. The implanted device was noted to be in a stable position with trivial residual inter-atrial shunting immediately after the procedure. The day after implantation, positional discomfort improved remarkably and the patient was able to stand-up with no symptoms, maintaining normal saturation (SaO2 100%). The patient was discharged and sent home on the third post-implantation day. The 4 month follow-up examination showed a good andstable condition. Conclusions Platypnoea Orthodeoxia Syndrome after lobectomy is a rare cause of postoperative dyspnoea/hypoxia.It is the result of right-to-left shunt via interatrial communication. Mediastinal relocation, stretching of the atrial septum are among the functional elements necessary for the clinical manifestations. It is essential to have a high index of suspicion to detect POS in patient with dyspnoea given the subtle and positional nature of the symptoms. Physicians should always consider POS in patients with unexplained dyspnoea; hence the treatment modalities could alleviate symptoms and be potentially curative.


2017 ◽  
Vol 2 (1) ◽  

Intralobar sequestration accounts for 75% of pulmonary sequestrations. It is characterized by the presence of nonfunctional parenchymal lung tissue, receiving systemic arterial blood supply. We conducted a retrospective medical records review of all patients evaluated and treated in our pulmonary department of military hospital of Tunisia with diagnosis of PS from January 2007 through December 2015. Among them, we report 5 cases of intralobar pulmonary sequestrations operated. There are three women and two men; the mean age is 27.6 years. The sequestration was intralobar in all cases. Clinical presentations were chest pain and productive cough in three cases. Chest X-ray showed left basal opacity in three cases, bilateral basal reticulonodular opacities in one case and round hydric opacity in the right lower lobe in one other case. Computed tomography was performed and revealed an aberrant systemic artery born from the lateral side of aorta supplying a left lower lobe sequestration in four cases and a right lower lobe mass in only one case. The confirmation was operative in all cases and histologic only in three cases. All patients were treated by lobectomy. Only one case presented with a pulmonary sequestration combined with tuberculosis and he was treated firstly by antituberculous chemotherapy. The results were excellent with a favorable clinical course and the mortality was nil.


1987 ◽  
Vol 62 (6) ◽  
pp. 2460-2466 ◽  
Author(s):  
B. E. Goodman ◽  
K. J. Kim ◽  
E. D. Crandall

We have previously presented evidence that cultured alveolar epithelial cell monolayers actively transport sodium from medium to substratum, a process that can be inhibited by sodium transport blockers and stimulated by beta-agonists. In this study, the isolated perfused rat lung was utilized in order to investigate the presence of active sodium transport by intact adult mammalian alveolar epithelium. Radioactive tracers (22Na and [14C]sucrose) were instilled into the airways of isolated Ringer-perfused rat lungs whose weight was continuously monitored. The appearance of isotopes in the recirculated perfusate was measured, and fluxes and apparent permeability-surface area products were determined. A pharmacological agent (amiloride, ouabain, or terbutaline) was added to the perfusate during each experiment after a suitable control period. Amiloride and ouabain resulted in decreased 22Na fluxes and a faster rate of lung weight gain. Terbutaline resulted in increased 22Na flux and a more rapid rate of lung weight loss. [14C]sucrose fluxes were unchanged by the presence of these pharmacological agents. These data are most consistent with the presence of a regulable active component of sodium transport across intact mammalian alveolar epithelium that leads to removal of sodium from the alveolar space, with anions and water following passively. Regulation of the rate of sodium and fluid removal from the alveolar space may play an important role in the prevention and/or resolution of alveolar pulmonary edema.


1987 ◽  
Vol 62 (4) ◽  
pp. 1690-1697 ◽  
Author(s):  
F. W. Cheney ◽  
M. J. Bishop ◽  
E. Y. Chi ◽  
B. L. Eisenstein

We studied the effects of regional alveolar hypoxia on permeability pulmonary edema formation. Anesthetized dogs had a bronchial divider placed so that the left lower lobe (LLL) could be ventilated with a hypoxic gas mixture (HGM) while the right lung was continuously ventilated with 100% O2. Bilateral permeability edema was induced with 0.05 ml/kg oleic acid and after 4 h of LLL ventilation with an HGM (n = 9) LLL gross weight was 161 +/- 13 (SE) g compared with 204 +/- 13 (SE) g (P less than 0.05) in the right lower lobe (RLL). Bloodless lobar water and dry weight were also significantly lower in the LLL as compared with the RLL of the study animals. In seven control animals in which the LLL fractional inspired concentration of O2 (FIO2) was 1.0 during permeability edema, there were no differences in gravimetric variables between LLL and RLL. In eight additional animals, pulmonary capillary pressure (Pc), measured by simultaneous occlusion of left pulmonary artery and vein, was not significantly different between LLL FIO2 of 1.0 and 0.05 either before or after pulmonary edema. We conclude that, in the presence of permeability pulmonary edema, regional alveolar hypoxia causes reduction in edema formation. The decreased edema formation during alveolar hypoxia is not due to a reduction in Pc.


1979 ◽  
Vol 47 (3) ◽  
pp. 556-560 ◽  
Author(s):  
B. C. Lee ◽  
H. van der Zee ◽  
A. B. Malik

The effect of unilateral pulmonary microembolization on regional lung extravascular fluid accumulation was determined in dogs. Embolization was produced by injecting 100-micrometer-diam glass beads (0.25 g/kg) into the right pulmonary artery. After embolization of one lung, pulmonary arterial pressure (Ppa) and pulmonary vascular resistance increased (P less than 0.05) from base-line values of 11.7 +/- 1.3 to 17.9 +/- 1.3 Torr and of 3.4 +/- 0.5 to 5.5 +/- 0.5 Torr/(1/min). Blood flow to embolized lung measured with labeled microspheres decreased from 104.2 +/- 24.9 to 35.2 +/- 9.2 ml/min.g bloodless lung after embolization, whereas flow to the normal lung increased from 43.1 +/- 5.6 to 71.2 +/- 19.2 ml/min.g bloodless lung. Extravascular lung water-to-bloodless dry lung weight ratio (W/D) of 4.97 +/- 0.32 was greater (P less than 0.001) in the embolized lung than the value of 3.34 +/- 0.15 in nonembolized lung. In six dogs pretreated with 500 U/kg of heparin, a similar degree of duration of embolization and similar hemodynamic changes did not result in significant differences in W/D (3.88 +/- 0.18 in right lung vs. 3.02 +/- 0.53 in the left lung), and the right lung ratio was less (P less than 0.05) than the value in the heparinized dogs, suggesting that humoral mechanisms contribute to the genesis of pulmonary edema after regional embolization. Therefore, unilateral embolization leads to a greater increase in extravascular content in the embolized lung than in the nonembolized lung. Because Ppa was in the normal range after embolization, regional pulmonary edema may be due partly to the local release of factors that increase lung vascular permeability.


1978 ◽  
Vol 44 (5) ◽  
pp. 759-762 ◽  
Author(s):  
R. K. Albert ◽  
S. Lakshminarayan ◽  
T. W. Huang ◽  
J. Butler

Edema transudation from extra-alveolar vessels was investigated in anesthetized, open-chested dogs. Fluid accumulation at different alveolar and extra-alveolar vascular pressures was assessed by continuous lung weighing and microscopy. The left (experimental) lung was distended with 6% CO2 and air while normal arterial blood gases were maintained by separately ventilating the right lung. Extra-alveolar vessels were isolated by compressing alveolar vessels with alveolar pressures high enough to stop blood flow. Weight increased steadily (edemogenesis) when pulmonary arterial and/or pulmonary venous pressure was 1 cmH2O below this pressure. Because some alveolar vessels at the lung base could have remained open and leaked, extra-alveolar vessels were also separated from alveolar vessels by glass bead embolization sufficient to stop perfusion. Lung weight gains followed selective pulmonary arterial or venous pressure elevations. Electron microscopy demonstrated edema in experimental lobes which was not present in control lobes with undistended extra-alveolar vessels at the same alveolar pressure. Thus pulmonary edema can be caused by fluid leaking from extra-alveolar vessels.


1978 ◽  
Vol 44 (3) ◽  
pp. 353-357 ◽  
Author(s):  
R. M. Nelson ◽  
B. R. McIntyre ◽  
E. A. Egan

The permeability of the alveolar epithelium following alloxan challenge was studied in dogs by determining transfer of radiolabeled solutes between alveolus and blood. Two days after injection of 131-Ialbumin into the blood, anesthetized dogs had the air space of part of one lung isolated by a balloon catheter lodged in a bronchus. We infused the atelectatis-isolated area with normal saline containing trace amounts of Blue Dextran, 125Ialbumin, and 57Co-cyanocobalamin; challenged six animals with intravenous alloxan, and six animals with alloxan added to the alveolar saline. During the pulmonary edema, 57Co-cyanocabalamin and 125I-albumin appeared in the blood and 131I-albumin entered the alveolar saline. The animals challenged by alveolar instillation showed a greater permeability change (P less than 0.05). The bidirectional transfer of macromolecules indicates that alloxan produces a change in the permeability of the alveolar epithelium, allowing diffusional exchange of macromolecules. Since alveolar flooding in hemodynamic edema does not show a similar change in the permeability of the epithelial lining, alveolar flooding in alloxan edema is not due solely to an effect on the endothelial membrane, but also to a direct effect on the epithelial membrane.


2019 ◽  
Vol 9 ◽  
pp. 41
Author(s):  
David Livingston ◽  
Matthew Grove ◽  
Rolf Grage ◽  
J. Mark McKinney

Systemic artery-to-pulmonary artery fistula (SA-PAF) is a rare phenomenon that can resemble a filling defect on computed tomography angiography (CTA). SA-PAF can be due to congenital or acquired etiologies and can alter the hemodynamics of the pulmonary circulation, with the most serious reported complication being hemoptysis, requiring embolization. We describe a case of an unusual SA-PAF between the right inferior phrenic artery and the right lower lobe pulmonary artery that mimicked an unprovoked pulmonary embolus (PE) on standard CTA in a patient with cardiomyopathy. This SA-PAF was interpreted on CTA as PE due to the presence of a filling defect, revealing that not all filling defects are PE. SA-PAF should always be considered when the clinical context or the imaging findings are atypical, specifically with an isolated filling defect visualized in the inferior lower lobe pulmonary artery. The false-positive PE was the result of mixing of systemic non-opacified blood with opacified pulmonary arterial blood.


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