Subclinical pulmonary edema in endurance athletes

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.

Download Full-text

Effects of Ischemic Acute Kidney Injury on Lung Water Balance: Nephrogenic Pulmonary Edema?

Pulmonary Medicine ◽

10.1155/2011/414253 ◽

2011 ◽

Vol 2011 ◽

pp. 1-6 ◽

Cited By ~ 5

Author(s):

Rajit K. Basu ◽

Derek Wheeler

Keyword(s):

Acute Kidney Injury ◽

Pulmonary Edema ◽

Disease Process ◽

Kidney Injury ◽

Fluid Accumulation ◽

Lung Water ◽

Edema Formation ◽

Bulk Fluid ◽

Capillary Membrane ◽

Alveolar Capillary

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.

Download Full-text

Effects of altitude and exercise on pulmonary capillary integrity: evidence for subclinical high-altitude pulmonary edema

Journal of Applied Physiology ◽

10.1152/japplphysiol.01048.2005 ◽

2006 ◽

Vol 100 (3) ◽

pp. 972-980 ◽

Cited By ~ 43

Author(s):

Marlowe W. Eldridge ◽

Ruedi K. Braun ◽

Ken Y. Yoneda ◽

William F. Walby

Keyword(s):

Pulmonary Edema ◽

High Altitude ◽

Strenuous Exercise ◽

Intense Exercise ◽

Healthy Humans ◽

Hypoxic Conditions ◽

Pulmonary Capillary ◽

Ergometer Exercise ◽

High Altitude Pulmonary Edema ◽

Pulmonary Microcirculation

Strenuous exercise may be a significant contributing factor for development of high-altitude pulmonary edema, particularly at low or moderate altitudes. Thus we investigated the effects of heavy cycle ergometer exercise (90% maximal effort) under hypoxic conditions in which the combined effects of a marked increase in pulmonary blood flow and nonuniform hypoxic pulmonary vasoconstriction could add significantly to augment the mechanical stress on the pulmonary microcirculation. We postulated that intense exercise at altitude would result in an augmented permeability edema. We recruited eight endurance athletes and examined their bronchoalveolar lavage fluid (BALF) for red blood cells (RBCs), protein, inflammatory cells, and soluble mediators at 2 and 26 h after intense exercise under normoxic and hypoxic conditions. After heavy exercise, under all conditions, the athletes developed a permeability edema with high BALF RBC and protein concentrations in the absence of inflammation. We found that exercise at altitude (3,810 m) caused significantly greater leakage of RBCs [9.2 (SD 3.1) × 104 cells/ml] into the alveolar space than that seen with normoxic exercise [5.4 (SD 1.2) × 104 cells/ml]. At altitude, the 26-h postexercise BALF revealed significantly higher RBC and protein concentrations, suggesting an ongoing capillary leak. Interestingly, the BALF profiles following exercise at altitude are similar to that of early high-altitude pulmonary edema. These findings suggest that pulmonary capillary disruption occurs with intense exercise in healthy humans and that hypoxia augments the mechanical stresses on the pulmonary microcirculation.

Download Full-text

Qidonghuoxue Decoction Ameliorates Pulmonary Edema in Acute Lung Injury Mice through the Upregulation of Epithelial Sodium Channel and Aquaporin-1

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2020/2492304 ◽

2020 ◽

Vol 2020 ◽

pp. 1-8

Author(s):

Chunfang Ma ◽

Lei Dong ◽

Minjing Li ◽

Wanru Cai

Keyword(s):

Pulmonary Edema ◽

Lung Tissue ◽

Biochemical Parameters ◽

Molecular Mechanisms ◽

Low Dose ◽

Control Group ◽

High Dose ◽

Aquaporin 1 ◽

Capillary Membrane ◽

Alveolar Capillary

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.

Download Full-text

Structural and functional disorders of the respiratory system in laboratory animals when intoxicated by pyrolysis products of chlorine-containing polymer materials

Medical academic journal ◽

10.17816/maj35170 ◽

2020 ◽

Vol 20 (3) ◽

pp. 13-22

Author(s):

P. K. Potapov ◽

Yu. V. Dimitriev ◽

P. G. Tolkach

Keyword(s):

Carbon Monoxide ◽

Pulmonary Edema ◽

Hydrogen Chloride ◽

Respiratory System ◽

Polymer Materials ◽

Laboratory Animals ◽

Functional Disorders ◽

Pyrolysis Products ◽

Capillary Membrane ◽

Alveolar Capillary

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.

Download Full-text