Early physiological and biological features in three animal models of induced acute lung injury

López-Aguilar, Josefina; Quilez, María Elisa; Martí-Sistac, Octavi; García-Martín, Carolina; Fuster, Gemma; Puig, Ferranda; Flores, Carlos; Villar, Jesús; Artigas, Antonio; Blanch, Lluís

doi:10.1007/s00134-009-1695-x

Cited by 24 publications

(20 citation statements)

References 33 publications

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“…The OA model is one of the three most widely used animal models (broncho-alveolar lavage, OA injection and LPS injection) in research concerning acute respiratory diseases, such as acute lung injury and acute respiratory distress syndrome [26,27]. This model causes the increasing in the permeability in endothelial cells and impairs gas exchange [28][29][30].…”

Section: Discussionmentioning

confidence: 99%

Somatostatin Reduces the Acute Lung Injury of Mice via Increasing the Affinity of Glucocorticoid Receptor

Zhao

Zhang

Xiong

et al. 2016

Cell Physiol Biochem

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Background/Aims: Although it has been reported that somatostatin (SOM) upregulated the level of 90-kD heat shock protein (Hsp90), which participates in the inflammatory regulation by its client proteins, such as glucocorticoid receptor (GR), it remains unclear if it has a protective role against acute lung injury (ALI). Methods: ALI model was established by the injection of oleic acid (OA) into the tail vein of mice. Lung injury was assessed by histological analysis, lung water content and arterial blood gases. The levels of Hsp90 and GR, the binding capacity and the affinity of GR were examined. Results: It was showed that pretreatment with SOM significantly increased Hsp90 levels and alleviated lung injuries in OA-injected mice. Furthermore, SOM increased the GR expression and improved the affinity of the GR in animals with lung injury. However, little alteration was found in the maximum binding capacity of the GR in mice with or without SOM. Conclusion: The data indicate SOM exerts a protective effect by increasing Hsp90 abundant and further enhancing the affinity of the GR. The beneficial effects of SOM treatment provide a new strategy for modulation of GR efficiency and alleviation of acute lung injury.

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Section: Discussionmentioning

confidence: 99%

Somatostatin Reduces the Acute Lung Injury of Mice via Increasing the Affinity of Glucocorticoid Receptor

Zhao

Zhang

Xiong

et al. 2016

Cell Physiol Biochem

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“…25 In addition, acute brain injury may lead to the release of systemic inflammatory mediators that ultimately can induce lung injury. 26 Thus, it seems that CNS injury can have detrimental effects on remote organs. This study provided the first clinical evidence that markers of brain injury are associated with mechanical ventilation requirements in general critically ill patients.…”

Section: Respiratory Failure and Biomarkersmentioning

confidence: 99%

Lack of association of S100β and neuron-specific enolase with mortality in critically ill patients

Macedo

Tomasi

Giombelli

et al. 2013

Rev. Bras. Psiquiatr.

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Objective: To evaluate the relationship between brain damage biomarkers and mortality in the intensive care unit (ICU). Methods: The sample comprised 70 patients admitted to an ICU. Blood samples were collected from all patients on ICU admission, and levels of S100b and neuron-specific enolase (NSE) were determined by ELISA. Results: Acute Physiologic and Chronic Health Evaluation (APACHE II) score was associated with mortality, but NSE and S100b were not associated with this outcome. In contrast, S100b levels were significantly higher in delirious and non-delirious patients who required mechanical ventilation during ICU stay. Conclusion: Levels of brain biomarkers at the time of ICU admission did not predict mortality in critically ill patients.

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“…Moreover, models of experimental brain injury have also shown that neurokinins and neuropeptides also play a role in bronchoconstriction, mucosal edema, and leukocyte adhesion. Lastly, acute brain injury is associated with high levels of proinflammatory cytokines in the brain that may trigger the release of systemic inflammatory mediators and cause a severe systemic imbalance associated with an elevated risk of complications [26]. All together, clinical and experimental data support the idea that damage to the central nervous system can have detrimental effects on remote organs and systems; however, little is known about the mechanisms through which injury to distal organs may affect the brain [27].…”

Section: The Importance Of Brain-lung Crosstalkmentioning

confidence: 98%

Organ crosstalk during acute lung injury, acute respiratory distress syndrome, and mechanical ventilation

Quilez

López-Aguilar

Blanch

2012

Current Opinion in Critical Care

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Early physiological and biological features in three animal models of induced acute lung injury

Abstract: The early responses to direct or remote lung insult in our three models of ALI captured different physiological and biological features that could lead to respiratory and/or multiorgan failure.

Cited by 24 publications

References 33 publications

Somatostatin Reduces the Acute Lung Injury of Mice via Increasing the Affinity of Glucocorticoid Receptor

Somatostatin Reduces the Acute Lung Injury of Mice via Increasing the Affinity of Glucocorticoid Receptor

Lack of association of S100β and neuron-specific enolase with mortality in critically ill patients

Organ crosstalk during acute lung injury, acute respiratory distress syndrome, and mechanical ventilation

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