The Alveolar-Capillary Membrane and Pulmonary Edema

1972 ◽  
Vol 286 (22) ◽  
pp. 1200-1204 ◽  
Author(s):  
Jan P. Szidon ◽  
Giuseppe G. Pietra ◽  
Alfred P. Fishman
2011 ◽  
Vol 2011 ◽  
pp. 1-6 ◽  
Author(s):  
Rajit K. Basu ◽  
Derek Wheeler

Pulmonary edema worsens the morbidity and increases the mortality of critically ill patients. Mechanistically, edema formation in the lung is a result of net flow across the alveolar capillary membrane, dependent on the relationship of hydrostatic and oncotic pressures. Traditionally, the contribution of acute kidney injury (AKI) to the formation of pulmonary edema has been attributed to bulk fluid accumulation, increasing capillary hydrostatic pressure and the gradient favoring net flow into the alveolar spaces. Recent research has revealed more subtle, and distant, effects of AKI. In this review we discuss the concept of nephrogenic pulmonary edema. Pro-inflammatory gene upregulation, chemokine over-expression, altered biochemical channel function, and apoptotic dysregulation manifest in the lung are now understood as “extra-renal” and pulmonary effects of AKI. AKI should be counted as a disease process that alters the endothelial integrity of the alveolar capillary barrier and has the potential to overpower the ability of the lung to regulate fluid balance. Nephrogenic pulmonary edema, therefore, is the net effect of fluid accumulation in the lung as a result of both the macroscopic and microscopic effects of AKI.


2015 ◽  
Vol 77 (2) ◽  
Author(s):  
M. Bussotti ◽  
S. Di Marco ◽  
G. Marchese ◽  
P.G. Agostoni

Strenuous exercise may cause progressive and proportional haemodynamic overload damage to the alveolar membrane, even in athletes. Despite the high incidence of arterial desaturation reported in endurance athletes has been attributed, into other factors, also to the damage of the alveolar-capillary membrane this evidence is equivocal. Some studies demonstrated flood of the interstitial space and consequent increase in pulmonary water content, but most of them were able to show this through indirect signs of interstitial oedema. The present review illustrates the literature’s data in favour or against pulmonary interstitial edema due to intense exercise in athletes.


2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Chunfang Ma ◽  
Lei Dong ◽  
Minjing Li ◽  
Wanru Cai

QDHX decoction is an effective traditional Chinese medicine that has been used to treat ALI, a disease characterized by pulmonary edema and inflammation. In this study, the aim is to elucidate the molecular mechanisms of QDHX decoction on improving the alveolar-capillary membrane permeability and alleviating inflammatory response. The BALB/c mice were divided into five groups including the control group, ALI group, ALI + low-dose QDHX decoction, ALI + high-dose QDHX decoction, and ALI + dexamethasone. When the animals were sacrificed, the pathology and wet/dry of lung tissue were tested and confirmed Ali model, the LDH and nucleated cells in BALF, and TNF-α and IL-1β in serum; α-ENaC and AQP-1 in lung tissue were examined. In the results, QDHX decoction downregulated the cytokine such as TNF-α and IL-1β, reduced the nucleated cells, and some biochemical parameters of the BALF. It also ameliorated the ENaC-α and AQP-1 expression induced by LPS in primary epithelial cells. These findings may provide new insights into the application of QDHX decoction for the prevention and treatment of LPS-related ALI.


2020 ◽  
Vol 20 (3) ◽  
pp. 13-22
Author(s):  
P. K. Potapov ◽  
Yu. V. Dimitriev ◽  
P. G. Tolkach

Relevance.The widespread use of chlorine-containing polymer materials in the modern world is due to their various advantages over natural analogues. Given the continuing large number of fires, there is still a high risk of exposure to pyrolysis products of chlorine-containing polymer materials, primarily hydrogen chloride and carbon monoxide on the victims. The complexity of determining the toxic effect of pyrolysis products of chlorine-containing polymers makes it necessary to conduct toxicological experimental studies. Intention.The goal is to evaluate the structural and functional disorders of the respiratory system in laboratory animals when intoxicated by pyrolysis products of chlorine-containing polymer materials. Methodology.In an experimental study, pyrolysis of chlorine-containing polymer materials was performed. Thestudy was performed on 96 male rats, in which vital function indicators, pulmonary coefficient, parameters of oxygenation and acid-base state of arterial blood were determined, and histological examination of tracheal and lung tissues was performed. Results and Discussion.It was found that the pyrolysis of chlorinated paraffin (CP-70) with a mass of 7 g and sawdust with a mass of 3 g produces thermal degradation products containing hydrogen chloride at a concentration of 7325 ppm and carbon monoxide at a concentration of 1000 ppm. Exposure to pyrolysis products in laboratory animals resulted in a pronounced irritant effect during intoxication and in the early post-intoxication period. Microscopic examination of lung tissue 48 hours after exposure showed histological signs of interstitial phase of toxic pulmonary edema. We found a decrease in vital functions (heart rate, respiratory rate, rectal temperature) 24, 48 and 72 hours after exposure. Exposure to pyrolysis products led to a violation of gas exchange through the alveolar-capillary membrane, which was confirmed by a decrease in the index of oxygenation and saturation. Violation of the integrity of the alveolar-capillary membrane contributed to the penetration of fluid into the interstitial and alveolar space and the development of toxic pulmonary edema. An increase in the pulmonary coefficient (p 0.05) was observed, after 24 and 48 hours, respectively. Conclusion.As a result of the study, toxic pulmonary edema was simulated in laboratory animals by inhalation of pyrolysis products of chlorine-containing polymer materials, and structural and functional disorders of the respiratory system were determined. It was found that intoxication with pyrolysis products of chlorine-containing materials led to the development of inflammatory changes in the trachea and the manifestation of interstitial pulmonary edema. These changes were accompanied by the development of bradycardia, bradypnea, a decrease in body temperature, as well as an increase (p 0.05) in the pulmonary coefficient, and the development of decompensated respiratory acidosis. The obtained results indicate that the formation of a toxic effect when exposed to pyrolysis products is due to the combined action of hydrogen chloride and carbon monoxide.


2010 ◽  
Vol 24 (S1) ◽  
Author(s):  
Courtney M. Wheatley ◽  
Nicholas A. Cassuto ◽  
William T. Foxx‐Lupo ◽  
Eric C. Wong ◽  
Nicholas A. Delamere ◽  
...  

2015 ◽  
Vol 185 (4) ◽  
pp. 913-919 ◽  
Author(s):  
Shawn K. Ahlfeld ◽  
Yong Gao ◽  
Simon J. Conway ◽  
Robert S. Tepper

2011 ◽  
pp. 135-140
Author(s):  
James R. Munis

The pathway of oxygen through the body consists of the diffusion of oxygen across the alveolar-capillary membrane and then the peripheral tissue membranes, followed by the convective transport of oxygen in the blood. Any transport process will have its choke points and limitations. In the case of oxygen, the constraints can take 1 of 2 forms, perfusion limitation or diffusion limitation.


2011 ◽  
pp. 94-100
Author(s):  
James R. Munis

We often confuse the ‘Fick principle’ with ‘Fick's law of diffusion.’ They are not the same. Ironically, Fick borrowed heavily from already known physical laws when he first described both his law of diffusion and his principle. Borrowing from Ohm's law of electricity, Fick applied concepts of diffusion and transfer across a resistance to formulate a law of diffusion that could be applied to gas or solute transfer across a membrane. Whether we are talking about transfer across the alveolar-capillary membrane or across a dialysis membrane, the concept is the same. The concept is similar to electricity—you have a transfer rate, resistance, and a gradient. Now let's consider the Fick principle. On the basis of another physical law he understood that, in the steady state, the difference between the amount of oxygen going into a tissue bed minus that leaving the tissue bed must be equal to the oxygen consumed. With a little reworking, this became the Fick principle: Cardiac output = O2 consumption / (arterial O2 - venous O2).


1964 ◽  
Vol 19 (2) ◽  
pp. 243-245 ◽  
Author(s):  
Alf Holmgren ◽  
Malcolm B. McIlroy

We measured arterial blood Po2, Pco2 and pH at rest and during a standard exercise test on a bicycle ergometer in ten normal subjects. In five we measured esophageal and five arterial blood temperature during the exercise and corrected the arterial blood values to the temperature at the time the samples were collected. We found an average rise in temperature of 1 C (range 0.2–1.6 C) during exercise lasting about 30 min at loads up to an average of 1,200 kg-m/min. At the highest load the average correction for PaOO2 was 5.6 mm Hg, for PaCOCO2 1.6 mm Hg and for pH 0.014 units. Our corrected values showed a fall in PaCOCO2 and pH and a rise in PaOO2 during severe exercise. These findings are compatible with the development of a metabolic acidosis during severe exercise and indicate that our subjects were not limited by diffusion across the alveolar-capillary membrane. metabolic acidosis; alveolar capillary membrane diffusion; hyperventilation; PaOO2 and PaCOCO2 in severe exercise Submitted on June 17, 1963


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