A crucial role of nitric oxide in acute lung injury secondary to the acute necrotizing pancreatitis

2010 ◽  
Vol 29 (4) ◽  
pp. 329-337 ◽  
Author(s):  
Shi Cheng ◽  
Wen-Mao Yan ◽  
Bin Yang ◽  
Jing-dong Shi ◽  
Mao-min Song ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Lung Injury ◽  
Lung Inflammation ◽  
Necrotizing Pancreatitis ◽  
Acute Necrotizing Pancreatitis ◽  
No Production ◽  
Acute Lung Inflammation ◽  
Tnf Α ◽  
Acute Necrotizing

To investigate the role of nitric oxide (NO) in acute lung inflammation and injury secondary to acute necrotizing pancreatitis (ANP), 5% sodium taurocholate was retrogradely injected into the biliopancreatic duct of rats to ANP model. These ANP rats were given L-Arginine (L-Arg, 100 mg/kg), L-NAME (10 mg/kg), or their combination by intraperitoneal injection 30 min prior to ANP induction. At 1, 3, 6, and 12 hours after ANP induction, lung NO production, and inducible NO synthase (iNOS) expression were measured. Lung histopathological changes, bronchoalveolar lavage (BAL) protein concentration, proinflammatory mediators tumor necrotic factor alpha (TNF-α), and lung tissue myeloperoxidase (MPO) activity were examined. Results showed that NO production and iNOS mRNA expression in alveolar macrophages (AMs) were significantly increased along with significant increases in lung histological abnormalities and BAL proteins in the ANP group, all of which were further enhanced by pretreatment with L-Arg and attenuated by pretreatment with L-NAME, respectively. These markers were slightly attenuated by pretreatment with combination of L-Arg + L-NAME, suggesting that NO is required for initiating the acute lung damage in ANP rats, and also that L-Arg-enhanced lung injury is mediated by its NO generation rather than its direct effect. MPO activity and TNF-α expression in lung were upregulated in the ANP rats and further enhanced by pretreatment with L-Arg and attenuated by pretreatment with L-NAME, respectively. These results suggest that overproduction of NO mediated by iNOS in the lung is required for the acute lung inflammation and damage secondary to ANP.

scholarly journals Lung Inflammation Associated With Clinical Acute Necrotizing Pancreatitis in Dogs

2016 ◽  
Vol 54 (1) ◽  
pp. 129-140 ◽  
Author(s):  
V. Vrolyk ◽  
B. K. Wobeser ◽  
A. N. Al-Dissi ◽  
A. Carr ◽  
B. Singh
Keyword(s):  
Lung Injury ◽  
Alveolar Macrophages ◽  
Lung Inflammation ◽  
Necrotizing Pancreatitis ◽  
Inflammatory Cells ◽  
Mononuclear Phagocyte ◽  
Acute Necrotizing Pancreatitis ◽  
Median Score ◽  
Acute Necrotizing ◽  
Clinical Cases

Although dogs with acute necrotizing pancreatitis (ANP) can develop respiratory complications, there are no data describing lung injury in clinical cases of ANP in dogs. Therefore, we conducted a study to characterize lung injury and determine if pulmonary intravascular macrophages (PIMs) are induced in dogs with ANP ( n = 21) compared with control dogs ( n = 6). Two pathologists independently graded histologic sections of pancreas from clinical cases to characterize the severity of ANP (total scores of 3–10) compared with controls showing histologically normal pancreas (total scores of 0). Based on histological grading, lungs from dogs with ANP showed inflammation (median score, 1.5; range, 0–3), but the scores did not differ statistically from the control lungs (median score, 0.5; range, 0–2). A grid intersects-counting method showed an increase in the numbers of MAC387-positive alveolar septal mononuclear phagocyte profiles in lungs of dogs with ANP (ratio median, 0.0243; range, 0.0093–0.0734, with 2 outliers at 0.1523 and 0.1978) compared with controls (ratio median, 0.0019; range, 0.0017–0.0031; P < .0001). Only dogs with ANP showed labeling for von Willebrand factor in alveolar septal capillary endothelial cells, septal inflammatory cells, and alveolar macrophages. Toll-like receptor 4 and interleukin 6 were variably expressed in alveolar macrophages and septal inflammatory cells in lungs from both ANP and control dogs. Inducible nitric oxide synthase was detected in alveolar macrophages of dogs with ANP only. These data show that dogs with ANP have lung inflammation, including the recruitment of PIMs and expression of inflammatory mediators.

Effects of Berberine on Acute Necrotizing Pancreatitis and Associated Lung Injury

Pancreas ◽  
2017 ◽  
Vol 46 (8) ◽  
pp. 1046-1055 ◽  
Author(s):  
Sun-Bok Choi ◽  
Gi-Sang Bae ◽  
Il-Joo Jo ◽  
Ho-Joon Song ◽  
Sung-Joo Park
Keyword(s):  
Lung Injury ◽  
Necrotizing Pancreatitis ◽  
Acute Necrotizing Pancreatitis ◽  
Acute Necrotizing

Author's reply to ‘The role of the bloody microbiology in acute necrotizing pancreatitis’

2021 ◽  
Vol 33 (5) ◽  
pp. 762-763
Author(s):  
Elmas Biberci Keskin ◽  
Gülay Okay ◽  
Duygu Muhiddin ◽  
Rasul Sharif ◽  
Bahadir Taşlidere ◽  
...  
Keyword(s):  
Necrotizing Pancreatitis ◽  
Acute Necrotizing Pancreatitis ◽  
Acute Necrotizing

scholarly journals Protective effects of erythropoietin against acute lung injury in a rat model of acute necrotizing pancreatitis

2007 ◽  
Vol 13 (46) ◽  
pp. 6172 ◽  
Author(s):  
Oge Tascilar ◽  
Güldeniz Karadeniz Cakmak ◽  
Ishak Ozel Tekin ◽  
Ali Ugur Emre ◽  
Bulent Hamdi Ucan ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Rat Model ◽  
Necrotizing Pancreatitis ◽  
Acute Necrotizing Pancreatitis ◽  
Protective Effects ◽  
Acute Necrotizing

scholarly journals Pretreatment with atorvastatin ameliorates cobra venom factor-induced acute lung inflammation in mice

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Jing Guo ◽  
Min Li ◽  
Yi Yang ◽  
Lin Zhang ◽  
Li-wei Zhang ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Inflammatory Response ◽  
Protein Content ◽  
Complement System ◽  
Complement Activation ◽  
Lung Inflammation ◽  
Acute Lung Inflammation ◽  
Tnf Α ◽  
The Complement System

Abstract Background The complement system plays a critical role as the pathogenic factor in the models of acute lung injury due to various causes. Cobra venom factor (CVF) is a commonly used complement research tool. The CVF can cause acute inflammation in the lung by producing complement activation components. Atorvastatin (ATR) is a 3-hydroxy-3-methylglutaryl coenzyme A inhibitor approved for control of plasma cholesterol levels. This inhibitor can reduce the acute pulmonary inflammatory response. However, the ability of ATR in treating acute lung inflammation caused by complement activation is still unknown. Therefore, we investigated the effect of ATR on lung inflammation in mice induced by activation of the complement alternative pathway in this study. Methods ATR (10 mg/kg/day via oral gavage) was administered for 7 days before tail vein injection of CVF (25 μg/kg). On the seventh day, all mice were sacrificed 1 h after injection. The lung lobe, bronchoalveolar lavage fluid (BALF), and blood samples were collected. The myeloperoxidase (MPO) activity of the lung homogenate, the leukocyte cell count, and the protein content of BALF were measured. The levels of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), P-selectin, and Intercellular cell adhesion molecule-1 (ICAM-1) in BALF and serum were determined by enzyme-linked immunosorbent assay. The pathological change of the lung tissue was observed by hematoxylin and eosin staining. The deposition of C5b-9 in the lung tissue was detected by immunohistochemistry. The phosphorylation of NF-κB p65 in the lung tissues was examined by immunohistochemistry and western blotting. Results The lung inflammation levels were determined by measuring the leukocyte cell numbers and protein content of BALF, the lung MPO activity, and expression and staining of the inflammatory mediators (IL-6 and TNF-α), and adhesion molecules (P-selectin and ICAM-1) for lung lesion. A significant reduction in the lung inflammation levels was observed after 7 days in ATR pre-treated mice with a CVF-induced lung disease. Deposition of C5b-9 was significantly alleviated by ATR pretreatment. Early intervention with ATR significantly reduced the development of acute lung inflammation on the basis of phosphorylation of NF-κB p65 in the lung. Conclusion These findings suggest the identification of ATR treatment for the lung inflammation induced by activating the complement system on the basis of its anti-inflammatory response. Together with the model replicating the complement activating characteristics of acute lung injury, the results may be translatable to the overactivated complement relevant diseases.

TNF-α causes reversible in vivo systemic vascular barrier dysfunction via NO-dependent and -independent mechanisms

1997 ◽  
Vol 273 (6) ◽  
pp. H2565-H2574 ◽  
Author(s):  
Neil K. Worrall ◽  
Kathy Chang ◽  
Wanda S. Lejeune ◽  
Thomas P. Misko ◽  
Patrick M. Sullivan ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Lung Injury ◽  
Water Content ◽  
Selective Inhibition ◽  
No Production ◽  
Barrier Dysfunction ◽  
Barrier Integrity ◽  
Tnf Α ◽  
Severe Lung

Tumor necrosis factor (TNF-α) and nitric oxide (NO) are important vasoactive mediators of septic shock. This study used a well-characterized quantitative permeation method to examine the effect of TNF-α and NO on systemic vascular barrier function in vivo, without confounding endotoxemia, hypotension, or organ damage. Our results showed 1) TNF-α reversibly increased albumin permeation in the systemic vasculature (e.g., lung, liver, brain, etc.); 2) TNF-α did not affect hemodynamics or blood flow or cause significant tissue injury; 3) pulmonary vascular barrier dysfunction was associated with increased lung water content and impaired oxygenation; 4) TNF-α caused inducible nitric oxide synthase (iNOS) mRNA expression in the lung and increased in vivo NO production; 5) selective inhibition of iNOS with aminoguanidine prevented TNF-α-induced lung and liver vascular barrier dysfunction; 6) aminoguanidine prevented increased tissue water content in TNF-α-treated lungs and improved oxygenation; and 7) nonselective inhibition of NOS with N G-monomethly-l-arginine increased vascular permeation in control lungs and caused severe lung injury in TNF-α-treated animals. We conclude that 1) TNF-α reversibly impairs vascular barrier integrity through NO-dependent and -independent mechanisms; 2) nonselective NOS inhibition increased vascular barrier dysfunction and caused severe lung injury, whereas selective inhibition of iNOS prevented impaired endothelial barrier integrity and pulmonary dysfunction; and 3) selective inhibition of iNOS may be beneficial in treating increased vascular permeability that complicates endotoxemia and cytokine immunotherapy.

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