scholarly journals Corrigendum to “Evaluation of Lung and Bronchoalveolar Lavage Fluid Oxidative Stress Indices for Assessing the Preventing Effects of Safranal on Respiratory Distress in Diabetic Rats”

2020 ◽  
Vol 2020 ◽  
pp. 1-1
Author(s):  
The Scientific World Journal
Keyword(s):  
Oxidative Stress ◽  
Respiratory Distress ◽  
Bronchoalveolar Lavage ◽  
Bronchoalveolar Lavage Fluid ◽  
Lavage Fluid ◽  
Diabetic Rats ◽  
Stress Indices

scholarly journals Evaluation of Lung and Bronchoalveolar Lavage Fluid Oxidative Stress Indices for Assessing the Preventing Effects of Safranal on Respiratory Distress in Diabetic Rats

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Saeed Samarghandian ◽  
Reza Afshari ◽  
Aghdas Sadati
Keyword(s):  
Oxidative Damage ◽  
Bronchoalveolar Lavage ◽  
Bronchoalveolar Lavage Fluid ◽  
Reduced Glutathione ◽  
Lavage Fluid ◽  
Diabetic Rats ◽  
Lung Homogenate ◽  
Crocus Sativus ◽  
Stress Indices ◽  
Diabetes Induction

We investigated the effects of antioxidant activity of safranal, a constituent ofCrocus sativusL., against lung oxidative damage in diabetic rats. The rats were divided into the following groups of 8 animals each: control, diabetic, and three diabetic + safranal-treated (0.25, 0.50, and 0.75 mg/kg/day) groups. Streptozotocin (STZ) was injected intraperitoneally (i.p.) at a single dose of 60 mg/kg for diabetes induction. Safranal was administered (i.p.) from 3 days after STZ administration to the end of the study. At the end of the 4-week period, malondialdehyde (MDA), nitric oxide (NO) and reduced glutathione (GSH) contents, activity of superoxide dismutase (SOD), and catalase (CAT) were measured in the bronchoalveolar lavage fluid (BALF) and lung tissue. Safranal in the diabetic groups inhibited the level of MDA and NO in BALF supernatant and lung homogenate. The median effective dose (ED50) values were 0.42, 0.58, and 0.48, 0.71 mg/kg, respectively. Safranal in the diabetic groups increased the level of GSH and the activity of CAT and SOD in BALF supernatant and lung homogenate. The ED50values were 0.25, 0.33, 0.26 in BALF and 0.33, 0.35, 0.46 mg/kg in lung, respectively. Thus, safranal may be effective to prevent lung distress by amelioration oxidative damage in STZ diabetic rats.

scholarly journals Treatment with senicapoc in a porcine model of acute respiratory distress syndrome

2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Asbjørn G. Petersen ◽  
Peter C. Lind ◽  
Anne-Sophie B. Jensen ◽  
Mark A. Eggertsen ◽  
Asger Granfeldt ◽  
...  
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Lung Injury ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Bronchoalveolar Lavage ◽  
Primary Endpoint ◽  
Bronchoalveolar Lavage Fluid ◽  
Distress Syndrome ◽  
Pulmonary Hemorrhage ◽  
Lavage Fluid

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.

scholarly journals Oxidative Stress and Increased Type-IV Collagenase Levels in Bronchoalveolar Lavage Fluid from Newborn Babies

2001 ◽  
Vol 50 (1) ◽  
pp. 29-33 ◽  
Author(s):  
Bettina C Schock ◽  
David G Sweet ◽  
Madeleine Ennis ◽  
Jane A Warner ◽  
Ian S Young ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Bronchoalveolar Lavage ◽  
Bronchoalveolar Lavage Fluid ◽  
Lavage Fluid ◽  
Type Iv Collagenase ◽  
Type Iv

Initial recruitment of neutrophils to alveolar structures in acute lung injury

1991 ◽  
Vol 70 (4) ◽  
pp. 1575-1585 ◽  
Author(s):  
G. C. Kindt ◽  
J. E. Gadek ◽  
J. E. Weiland
Keyword(s):  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Bronchoalveolar Lavage ◽  
Bacterial Pneumonia ◽  
Bronchoalveolar Lavage Fluid ◽  
Distress Syndrome ◽  
Neutrophil Migration ◽  
Lavage Fluid ◽  
Neutrophil Influx ◽  
Lung Lymph

The adult respiratory distress syndrome and bacterial pneumonia are both characterized by an influx of neutrophils into the lung. The neutrophil has been implicated as having a “pathological” role in adult respiratory distress syndrome, in contrast to its role in bacterial pneumonia. We hypothesized that processes resulting in neutrophil recruitment to the lung are distinct, depending on whether the inflammatory stimulus arises in the intravascular or the alveolar compartment of the lung. Anesthetized sheep with lung lymph fistulas were utilized to access the three compartments of the lung relevant to studies of transpulmonary neutrophil migration. Serum, lung lymph, and bronchoalveolar lavage fluid were studied for neutrophil influx and chemotactic activity before and after administration of endotoxin by either an intravascular or inhaled alveolar route. Both groups developed significant neutrophil influx into the lymph and bronchoalveolar lavage fluid by 3 h postendotoxin. Those animals receiving intravascular endotoxin developed chemotactic gradients opposing neutrophil migration into the lung in contrast to animals receiving alveolar endotoxin, suggesting that neutrophil influx into the lung occurs by random migration.

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