Respiratory mechanics and lung tissue remodeling in a hepatopulmonary syndrome rat model

2011 ◽  
Vol 179 (2-3) ◽  
pp. 326-333 ◽  
Author(s):  
César Augusto Melo-Silva ◽  
Eduardo Gaio ◽  
José E. Trevizoli ◽  
Caio S. Souza ◽  
Alessandra S. Gonçalves ◽  
...  
Keyword(s):  
Lung Tissue ◽  
Rat Model ◽  
Respiratory Mechanics ◽  
Tissue Remodeling ◽  
Hepatopulmonary Syndrome

Impaired pulmonary artery contractile responses in a rat model of microgravity: role of nitric oxide

2002 ◽  
Vol 92 (1) ◽  
pp. 33-40 ◽  
Author(s):  
Daniel Nyhan ◽  
Soonyul Kim ◽  
Stacey Dunbar ◽  
Dechun Li ◽  
Artin Shoukas ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Pulmonary Artery ◽  
Lung Tissue ◽  
Rat Model ◽  
Orthostatic Intolerance ◽  
Volume Distribution ◽  
Contractile Responses ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Vascular contractile hyporesponsiveness is an important mechanism underlying orthostatic intolerance after microgravity. Baroreceptor reflexes can modulate both pulmonary resistance and capacitance function and thus cardiac output. We hypothesized, therefore, that pulmonary vasoreactivity is impaired in the hindlimb-unweighted (HLU) rat model of microgravity. Pulmonary artery (PA) contractile responses to phenylephrine (PE) and U-46619 (U4) were significantly decreased in the PAs from HLU vs. control (C) animals. N G-nitro-l-arginine methyl ester (10−5 M) enhanced the contractile responses in the PA rings from both C and HLU animals and completely abolished the differential responses to PE and U4 in HLU vs. C animals. Vasorelaxant responses to ACh were significantly enhanced in PA rings from HLU rats compared with C. Moreover, vasorelaxant responses to sodium nitroprusside were also significantly enhanced. Endothelial nitric oxide synthase (eNOS) and soluble guanlyl cyclase expression were significantly enhanced in PA and lung tissue from HLU rats. In marked contrast, the expression of inducible nitric oxide synthase was unchanged in lung tissue. These data support the hypothesis that vascular contractile responsiveness is attenuated in PAs from HLU rats and that this hyporesponsiveness is due at least in part to increased nitric oxide synthase activity resulting from enhanced eNOS expression. These findings may have important implications for blood volume distribution and attenuated stroke volume responses to orthostatic stress after microgravity exposure.

scholarly journals Role of p53 in lung tissue remodeling

2015 ◽  
Vol 5 (1) ◽  
pp. 40 ◽  
Author(s):  
Shiro Mizuno ◽  
Harm Jan Bogaard ◽  
Takeshi Ishizaki ◽  
Hirohisa Toga
Keyword(s):  
Lung Tissue ◽  
Tissue Remodeling

scholarly journals Lung and Intestine: A Specific Link in an Ulcerative Colitis Rat Model

2013 ◽  
Vol 2013 ◽  
pp. 1-13 ◽  
Author(s):  
Yuan Liu ◽  
Xin-Yue Wang ◽  
Xue Yang ◽  
Shan Jing ◽  
Li Zhu ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Lung Tissue ◽  
Rat Model ◽  
Close Association ◽  
Trinitrobenzene Sulfonic Acid ◽  
Microvascular Endothelium ◽  
Functional Changes ◽  
Liver And Kidney ◽  
Embryonic Origin ◽  
Endothelial Growth Factor

Background. To investigate the link and mechanisms between intestine and lung in the ulcerative colitis (UC) rat model.Materials and Methods. We used the UC rat model by immunological sensitization combined with local 2, 4, 6-trinitrobenzene sulfonic acid (TNBS) in 50% ethanol enema, observed dynamically animal general state and body weight, examined the histological and functional changes in the colon, lung, liver, and kidney tissues, and detected microvascular endothelium response towards inflammation characterized with the expression of iNOS, TXB2, P-selectin, ICAM-1, and vascular endothelial growth factor A (VEGF-A) in the colon and lung tissue.Results. Pulmonary function results suggested ventilator disorder, and pathological findings showed interstitial pneumonia. There were no significant changes in the liver and kidney function and histopathology. The colon and lung tissue iNOS, TXB2, P-selectin, ICAM-1, and VEGF-A expression of the model rats was significantly higher than the normal rats at both time points.Conclusions. Our study is the first to demonstrate the close association between the large intestine and lung in the immune-TNBS-ethanol-induced UC rat model. Different organs and tissues with the same embryonic origin may share the same pathological specificities in a disease. The present study provided a new way of thinking for pathological changes in clinical complex diseases manifested with multiorgan damage.

Rat Model to Investigate the Treatment of Acute Nitrogen Dioxide Intoxication

1992 ◽  
Vol 11 (3) ◽  
pp. 179-187 ◽  
Author(s):  
J. Meulenbelt ◽  
J.A.M.A. Dormans ◽  
M. Marra ◽  
P.J.A. Rombout ◽  
B. Sangster
Keyword(s):  
Lung Injury ◽  
Nitrogen Dioxide ◽  
Lung Tissue ◽  
Rat Model ◽  
Therapeutic Interventions ◽  
Nitrite Concentration ◽  
Therapeutic Measures ◽  
Severe Lung

1 The pulmonary toxic events induced by acute nitrogen dioxide (NO)2 exposure were studied in the rat to develop an inhalation model to investigate therapeutic measures. 2 A good correlation was observed between the lung weights and severity of the atypical pneumonitis. The pulmonary effects observed, became more pronounced with increasing NO 2 concentrations (0, 25, 75, 125, 175 or 200 ppm, 1 ppm NO2=1.88 mg m-3 NO2) and exposure times (5, 10, 20 or 30 min). 3 An adequate NO 2 concentration is 175 ppm, because it can induce a severe lung injury without mortality. This makes it possible to investigate suitable therapeutic interventions for several days. 4 Following acute inhalatory NO2 intoxication, transformation of NO2 to nitrate is presumably more notable than transformation to nitrite. 5 The transformation of NO2 to nitrate in lung tissue causes a slight increase in the serum nitrite concentration, which does not induce measurable formation of methaemoglobin. 6 Presumably, methaemoglobin does not contribute to the toxicity of NO2 intoxication.

scholarly journals Desflurane Attenuates Ventilator-Induced Lung Injury in Rats with Acute Respiratory Distress Syndrome

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Xue Lin ◽  
Ying-nan Ju ◽  
Wei Gao ◽  
Dong-mei Li ◽  
Chang-chun Guo
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Lung Injury ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Tidal Volume ◽  
Lung Tissue ◽  
Rat Model ◽  
Distress Syndrome ◽  
Inflammatory Factors ◽  
Ventilator Induced Lung Injury

Ventilator-induced lung injury aggravates the existing lung injury. This study investigated the effect of desflurane on VILI in a rat model of acute respiratory distress syndrome. Forty-eight rats were randomized into a sham (S) group, control (C) group, lipopolysaccharide/ventilation (LV) group, lipopolysaccharide/ventilation/desflurane (LVD) group, or lipopolysaccharide/low ventilation with and without desflurane (LLV and LLVD) groups. Rats in the S group received anesthesia only. Rats in the LV and LVD groups received lipopolysaccharide and were ventilated with a high tidal volume. Rats in LLV and LLVD groups were treated as the LV and LVD groups and ventilated with a low tidal volume. PaO2/FiO2, lung wet-to-dry weight ratios, concentrations of inflammatory factors in serum and BALF, histopathologic analysis of lung tissue, and levels of nuclear factor- (NF-) κB protein in lung tissue were investigated. PaO2/FiO2 was significantly increased by desflurane. Total cell count, macrophages, and neutrophils in BALF and proinflammatory factors in BALF and serum were significantly decreased by desflurane, while IL-10 was increased. The histopathological changes and levels of NF-κB protein in lung tissue were decreased by desflurane. The results indicated that desflurane ameliorated VILI in a rat model of acute respiratory distress syndrome.

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