Procedimiento de autotrasplante pulmonar en el cerdo como modelo experimental para el estudio del síndrome de isquemia-reperfusión

Adiego, Carlos Simón; González-Casaurrán, Guillermo; Perea, Leire Azcárate; Viña, Jesus Isea de la; Ameigeiras, Elena Vara; Martín, Cruz; Martı́nez, Ignacio; Casanova, Javier; López, Ángeles; Piñeiro, Beatriz Martín; González-Aragoneses, Federico

doi:10.1016/j.arbres.2011.02.008

Cited by 5 publications

(3 citation statements)

References 35 publications

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“…The left lung I/R injury model of minipigs was established as reported before. 47 Briefly, minipigs were anesthetized and left thoracotomies were performed in the fifth intercostal space. The left pulmonary hilum was dissected, and then the left pulmonary artery, left pulmonary vein and left bronchus from the left pulmonary hilum were clamped individually.…”

Section: Methodsmentioning

confidence: 99%

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Autophagy induced by DAMPs facilitates the inflammation response in lungs undergoing ischemia-reperfusion injury through promoting TRAF6 ubiquitination

Liu

Cao

et al. 2017

Cell Death Differ

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Lung ischemia-reperfusion (I/R) injury remains one of the most common complications after various cardiopulmonary surgeries. The inflammation response triggered by the released damage-associated molecular patterns (DAMPs) aggravates lung tissue damage. However, little is known about the role of autophagy in the pathogenesis of lung I/R injury. Here, we report that a variety of inflammation-related and autophagy-associated genes are rapidly upregulated, which facilitate the inflammation response in a minipig lung I/R injury model. Left lung I/R injury triggered inflammatory cytokine production and activated the autophagy flux as evidenced in crude lung tissues and alveolar macrophages. This was associated with the release of DAMPs, such as high mobility group protein B1 (HMGB1) and heat shock protein 60 (HSP60). Indeed, treatment with recombinant HMGB1 or HSP60 induced autophagy in alveolar macrophages, whereas autophagy inhibition by knockdown of ATG7 or BECN1 markedly reduced DAMPtriggered production of inflammatory cytokines including IL-1β, TNF and IL12 in alveolar macrophages. This appeared to be because of decreased activation of MAPK and NF-κB signaling. Furthermore, knockdown of ATG7 or BECN1 inhibited Lys63 (K63)-linked ubiquitination of TNF receptor-associated factor 6 (TRAF6) in DAMP-treated alveolar macrophages. Consistently, treatment with 3-MA inhibited K63-linked ubiquitination of TRAF6 in I/R-injured lung tissues in vivo. Collectively, these results indicate that autophagy triggered by DAMPs during lung I/R injury amplifies the inflammatory response through enhancing K63-linked ubiquitination of TRAF6 and activation of the downstream MAPK and NF-κB signaling.

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Section: Methodsmentioning

confidence: 99%

“…47, 49 Briefly, the BALF was collected by lavaging the left or right lung three times with phosphate-buffered saline (PBS) through a tracheal cannula, which was pooled and centrifuged at 300 × g for 10 min. The acellular supernatant was divided into aliquots and stored at −80 °C until further assay.…”

Section: Methodsmentioning

confidence: 99%

Autophagy induced by DAMPs facilitates the inflammation response in lungs undergoing ischemia-reperfusion injury through promoting TRAF6 ubiquitination

Liu

Cao

et al. 2017

Cell Death Differ

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“…In a model of one-lung IRI in mice, Altemeier et al [ 25 ] used immunohistochemistry analyses and showed an upregulation of MCP-1 and vascular dysfunction in both lungs as a direct result of unilateral IRI. Our group has previously observed that pulmonary IRI presents with an increase in MCP-1, TNF- α , and IL-1 and that ischemic preconditioning significantly reduces the expression of all these mediators [ 26 ]. Li et al [ 27 ] postulated that lidocaine causes a dose-dependent inhibition of MCP-1 secretion in human monocyte cultures, as well as the suppression of MCP-1 messenger RNA expression induced by lipopolysaccharide.…”

Section: Discussionmentioning

confidence: 99%

Effect of Intravenous Lidocaine on Inflammatory and Apoptotic Response of Ischemia‐Reperfusion Injury in Pigs Undergoing Lung Resection Surgery

Romera

Cebollero

Romero-Gómez

et al. 2021

BioMed Research International

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Background. Ischemia-reperfusion injury is one of the most critical phenomena in lung transplantation and causes primary graft failure. Its pathophysiology remains incompletely understood, although the inflammatory response and apoptosis play key roles. Lidocaine has anti-inflammatory properties. The aim of this research is to evaluate the effect of intravenous lidocaine on the inflammatory and apoptotic responses in lung ischemia-reperfusion injury. Methods. We studied the histological and immunohistochemical changes in an experimental model of lung transplantation in pigs. Twelve pigs underwent left pneumonectomy, cranial lobectomy, caudal lobe reimplantation, and 60 minutes of graft reperfusion. Six of the pigs made up the control group, while six other pigs received 1.5 mg/kg of intravenous lidocaine after induction and a 1.5 mg/kg/h intravenous lidocaine infusion during surgery. In addition, six more pigs underwent simulated surgery. Lung biopsies were collected from the left caudal lobe 60 minutes after reperfusion. We conducted a double study on these biopsies and assessed the degree of inflammation, predominant cell type (monocyte-macrophage, lymphocytes, or polymorphous), the degree of congestion, and tissue edema by hematoxylin and eosin stain. We also conducted an immunohistochemical analysis with antibodies against CD68 antigens, monocyte chemoattractant protein-1 (MCP-1), Bcl-2, and caspase-9. Results. The lungs subjected to ischemia-reperfusion injury exhibited a higher degree of inflammatory infiltration. The predominant cell type was monocyte-macrophage cells. Both findings were mitigated by intravenous lidocaine administration. Immunohistochemical detection of anti-CD68 and anti-MCP-1 showed higher infiltration in the lungs subjected to ischemia-reperfusion injury, while intravenous lidocaine decreased the expression. Ischemia-reperfusion induced apoptotic changes and decreased Bcl-2 expression. The group treated with lidocaine showed an increased number of Bcl-2-positive cells. No differences were observed in caspase-9 expression. Conclusions. In our animal model, intravenous lidocaine was associated with an attenuation of the histological markers of lung damage in the early stages of reperfusion.

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Sevoflurane anesthetic preconditioning protects the lung endothelial glycocalyx from ischemia reperfusion injury in an experimental lung autotransplant model

et al. 2016

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Procedimiento de autotrasplante pulmonar en el cerdo como modelo experimental para el estudio del síndrome de isquemia-reperfusión

Cited by 5 publications

References 35 publications

Autophagy induced by DAMPs facilitates the inflammation response in lungs undergoing ischemia-reperfusion injury through promoting TRAF6 ubiquitination

Autophagy induced by DAMPs facilitates the inflammation response in lungs undergoing ischemia-reperfusion injury through promoting TRAF6 ubiquitination

Effect of Intravenous Lidocaine on Inflammatory and Apoptotic Response of Ischemia‐Reperfusion Injury in Pigs Undergoing Lung Resection Surgery

Sevoflurane anesthetic preconditioning protects the lung endothelial glycocalyx from ischemia reperfusion injury in an experimental lung autotransplant model

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