Dynamics in the content of the cytokines in the bronchoalveolar lavage fluid in rats after acute inhalation intoxication by clorine and pyrolysis products, containing hydrogen chloride

2021 ◽  
Vol 23 (1) ◽  
pp. 135-142
Author(s):  
Petr K. Potapov ◽  
Pavel G. Gennad`evich ◽  
Nadezhda Yu. Rogovskaya ◽  
Vladimir N. Babakov ◽  
Vadim A. Basharin

It is known that inhalation exposure to chlorine and hydrogen chloride leads to damage to the respiratory system up to the development of acute pulmonary edema in victims. No data on the mechanisms of development of pulmonary edema upon exposure to hydrogen chloride have been found in the available literature. The study was carried out on white outbred male rats, which were divided into 3 groups: Group I control; Group II animals were intoxicated with chlorine at a dose of 1.5 median lethal concentration (30 min); Group III animals were intoxicated with hydrogen chloride at a dose of 1.5 median lethal concentration (30 min). Immediately after exposure to the studied toxicants, as well as after 1, 3 and 6 h, the lung coefficient and the content of cytokines (interleukins-1, 6, 10 and interferon-) in the bronchoalveolar lavage fluid were determined in animals. It was revealed that an increase in the lung coefficient (p 0.05) in animals in groups II and III was accompanied by a significant increase (1.5 times) in the content of the studied cytokines in the bronchial-alveolar lavage fluid compared with animals in group I. III an increase (p 0.05) in the content of cytokines is recorded later only 3 hours after exposure, while it is significantly lower than in animals of group II at all studied periods. Thus, intoxication with hydrogen chloride leads to a slower development of pulmonary edema and an increase in the content of both pro (interleukins-1, 6) and anti-inflammatory cytokines (interleukin-10, interferon-) in the bronchial-alveolar lavage fluid compared to animals, exposed to chlorine intoxication.

2003 ◽  
Vol 94 (5) ◽  
pp. 1836-1840 ◽  
Author(s):  
Masayuki Hanaoka ◽  
Yunden Droma ◽  
Atsuhiko Naramoto ◽  
Takayuki Honda ◽  
Toshio Kobayashi ◽  
...  

To examine the role of VEGF in the pathogenesis of high-altitude pulmonary edema (HAPE), we measured the concentrations of VEGF in venous serum and bronchoalveolar lavage fluid in patients with HAPE and in healthy volunteers. The VEGF in venous serum of the patients was normal at admission and significantly increased at recovery. Similarly, the VEGF in bronchoalveolar lavage fluid of the patients was increased at recovery compared with admission, but values at both admission and recovery were significantly lower than those of the controls. The present finding suggests that VEGF probably is destroyed in the lung of HAPE, and it appears less likely to have a critical part in the pathogenesis of HAPE but has rather an important role in the repair process for the impaired cell layer.


1988 ◽  
Vol 137 (4) ◽  
pp. 783-789 ◽  
Author(s):  
Akitoshi Ishizaka ◽  
Kenton E. Stephens ◽  
Henry D. Tazelaar ◽  
Elaine W. Hall ◽  
Peter O'Hanley ◽  
...  

1997 ◽  
Vol 27 (4) ◽  
pp. 396-405 ◽  
Author(s):  
L. M. TERAN ◽  
M. G. CAMPOS ◽  
B. T. BEGISHVILLI ◽  
J.-M. SCHRODER ◽  
R. DJUKANOVIC ◽  
...  

2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Asbjørn G. Petersen ◽  
Peter C. Lind ◽  
Anne-Sophie B. Jensen ◽  
Mark A. Eggertsen ◽  
Asger Granfeldt ◽  
...  

Abstract Background Senicapoc is a potent and selective blocker of KCa3.1, a calcium-activated potassium channel of intermediate conductance. In the present study, we investigated whether there is a beneficial effect of senicapoc in a large animal model of acute respiratory distress syndrome (ARDS). The primary end point was the PaO2/FiO2 ratio. Methods ARDS was induced in female pigs (42–49 kg) by repeated lung lavages followed by injurious mechanical ventilation. Animals were then randomly assigned to vehicle (n = 9) or intravenous senicapoc (10 mg, n = 9) and received lung-protective ventilation for 6 h. Results Final senicapoc plasma concentrations were 67 ± 18 nM (n = 9). Senicapoc failed to change the primary endpoint PaO2/FiO2 ratio (senicapoc, 133 ± 23 mmHg; vehicle, 149 ± 68 mmHg). Lung compliance remained similar in the two groups. Senicapoc reduced the level of white blood cells and neutrophils, while the proinflammatory cytokines TNFα, IL-1β, and IL-6 in the bronchoalveolar lavage fluid were unaltered 6 h after induction of the lung injury. Senicapoc-treatment reduced the level of neutrophils in the alveolar space but with no difference between groups in the cumulative lung injury score. Histological analysis of pulmonary hemorrhage indicated a positive effect of senicapoc on alveolar–capillary barrier function, but this was not supported by measurements of albumin content and total protein in the bronchoalveolar lavage fluid. Conclusions In summary, senicapoc failed to improve the primary endpoint PaO2/FiO2 ratio, but reduced pulmonary hemorrhage and the influx of neutrophils into the lung. These findings open the perspective that blocking KCa3.1 channels is a potential treatment to reduce alveolar neutrophil accumulation and improve long-term outcome in ARDS.


Lung Cancer ◽  
2003 ◽  
Vol 41 ◽  
pp. S286
Author(s):  
Guzin Gursoy ◽  
Sibel Alpar ◽  
Nazire Ucar ◽  
Tulay Bakirci ◽  
Ahmet Aydin ◽  
...  

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