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

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.

Author(s):  
P. G. Tolkach ◽  
V. A. Basharin ◽  
S. V. Chepur

In the study conducted on laboratory animals (rats) toxic pulmonary edema (TPE) was simulated by inhalation of pyrolysis products of chlorinated paraffin-70 (CP-70). The average-lethal dose of CP-70 burned at 280 ÷ 350 ° C for 3 minutes is 8.1 ± 0.9 g and provides a concentration of hydrogen chloride (HCl) in the chamber at the level of 7325 [5850; 8460] ppm. Under these conditions exposure for 30 minutes led to an increase in the pulmonary rate (LC) in laboratory animals 24 hours after poisoning. The diagnosis of TPE was confirmed histologically by the signs of interstitial and alveolar edema, as well as arterial hypoxemia (TI = 204.5 [180; 228]) indicating respiratory failure. The death of animals was recorded 3 days after application of the pyrolysis products of CP-70. The simulated experimental TPE model can be used to search for the means of pathogenetic therapy of pulmonary toxicants poisoning.


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

1960 ◽  
Vol 15 (3) ◽  
pp. 372-376 ◽  
Author(s):  
J. E. Cotes ◽  
D. P. Snidal ◽  
R. H. Shepard

In one of two subjects studied in detail, using 0.1% carbon monoxide in the test gas and a 10-second breath-holding period, the alveolar capillary blood volume (Vc) was found to increase by nearly 100% when the intra-alveolar pressure was made negative during breath holding. This was accompanied by a reduction in venous pressure in the forearm. In both subjects Vc was increased on exercise. The diffusing capacity of the alveolar capillary membrane (Dm) remained relatively constant in spite of large changes in Vc. The findings suggest that stationary blood is present in some alveolar capillaries at rest. The implications of this finding and a likely mechanism for the increase in Vc with negative pressure are discussed. xsSubmitted on September 14, 1959


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.


1963 ◽  
Vol 18 (1) ◽  
pp. 123-128 ◽  
Author(s):  
Benjamin Burrows ◽  
Albert H. Niden

Hemorrhagic shock induced a marked fall in the pulmonary diffusing capacity for carbon monoxide in the dog (Dl) and produced marked nonuniformity of Dl/Va ratios throughout the lung as assessed by the “equilibration technique”. Difficulties in calculating over-all Dl under these conditions are discussed. Induced anemia also produced a fall in Dl, but little change in the uniformity of Dl/Va ratios was noted. In isolated perfused dog lungs where blood flow, pulmonary vascular pressures, lung volume, and ventilation were maintained constant, Dl was found to be proportional to hematocrit, suggesting either: 1) that virtually all resistance to CO diffusion is in the erythrocyte or 2) that the apparent diffusing capacity of the alveolar-capillary membrane is dependent upon hematocrit, carbon monoxide transfer being reduced across portions of membrane which are some distance from a red blood cell. Submitted on January 12, 1962


Author(s):  
P. G. Tolkach ◽  
V. A. Basharin ◽  
S. V. Chepur

Relevance.Thermal decomposition of various polymeric materials occur in emergency situations associated with fires, with pulmonotoxicants releasing in the environment. During pyrolysis of polytetrafluoroethylene (Teflon), a highly toxic perfluoroisobutylene is produced.Intention.To create an experimental animal model of toxic pulmonary edema due to products of thermal decomposition of polytetrafluoroethylene.Methodology.Polytetrafluoroethylene underwent pyrolysys at 440–750 0С during 6 minutes. Toxic pulmonary edema was modeled on rats via inhalation of pyrolysis products of polytetrafluoroethylene. An amount of polytetrafluoroethylene burned under these conditions with resulting death of 50 % of rats during 1 day was (2.68 ± 0.60) g. The toxic pulmonary edema diagnosis was confirmed histologically and by lung/body ratio.Results.In the pyrolysis products of polytetrafluoroethylene, highly toxic perfluoroisobutylene was found via gas chromatography with mass spectrometric detection, with relative content of 85.9 %. Such an exposure during 15 min increased (p = 0.01) lung/body ratio in laboratory animals in 3 hours. The toxic pulmonary edema diagnosis was confirmed histologically  (signs of alveolar edema). Animals started to die 7 hours after the pyrolysis products inhalation.Conclusion.In the study on rats, toxic pulmonary edema was modeled via inhalation of pyrolysis products of polytetrafluoroethylene. This model can be used for searching etiotropic and pathogenetic therapy for poisoning with pulmonotoxicants.


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.


1977 ◽  
Vol 43 (5) ◽  
pp. 880-884 ◽  
Author(s):  
C. Mendoza ◽  
H. Peavy ◽  
B. Burns ◽  
G. Gurtner

Steady-state diffusing capacity of the lungs for carbon monoxide (DLCO) was measured in 13 anesthetized, paralyzed dogs ventilated at constant tidal volume and rate, using four different inspired CO levels (190, 600, 1,110, and 2,000 ppm). DLCO increased and reached a maximum as the inspired CO level was raised from 190 to 600 ppm. Further increases in inspired CO concentration were accompanied by a decrease in inspired CO concentration were accompanied by a decrease in DLCO. CO dead space and Pao2 remained constant at all inspired O2 levels. In some experiments a second set of measurements was made, the results of which were similar to those of the first set. The results cannot be explained by changes in CO back pressure, pulmonary capillary volume, or reaction rate of CO with hemoglobin, but can be explained if there is carrier-mediated CO transport in the alveolar capillary membrane.


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.


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