PMID- 34195274 OWN - NLM STAT- MEDLINE DCOM- 20211025 LR - 20220424 IS - 2314-6141 (Electronic) IS - 2314-6133 (Print) VI - 2021 DP - 2021 TI - Effect of Intravenous Lidocaine on Inflammatory and Apoptotic Response of Ischemia-Reperfusion Injury in Pigs Undergoing Lung Resection Surgery. PG - 6630232 LID - 10.1155/2021/6630232 [doi] LID - 6630232 AB - 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. CI - Copyright (c) 2021 Andrea Romera et al. FAU - Romera, Andrea AU - Romera A AUID- ORCID: 0000-0002-9062-2377 AD - Department of Anesthesiology, Gregorio Maranon University Hospital, Madrid, Spain. FAU - Cebollero, Maria AU - Cebollero M AUID- ORCID: 0000-0003-0696-3572 AD - Department of Anatomic Pathology, Gregorio Maranon University Hospital, Madrid, Spain. FAU - Romero-Gomez, Barbara AU - Romero-Gomez B AUID- ORCID: 0000-0002-2963-183X AD - Department of Immunology, Ophthalmology and Otorhinolaryngology, Faculty of Medicine, Complutense University of Madrid, Madrid, Spain. FAU - Carricondo, Francisco AU - Carricondo F AUID- ORCID: 0000-0003-1651-3356 AD - Department of Immunology, Ophthalmology and Otorhinolaryngology, Faculty of Medicine, Complutense University of Madrid, Madrid, Spain. FAU - Zapatero, Sara AU - Zapatero S AUID- ORCID: 0000-0003-0094-7571 AD - Department of Anesthesiology, Gregorio Maranon University Hospital, Madrid, Spain. FAU - Garcia-Aldao, Uxio AU - Garcia-Aldao U AUID- ORCID: 0000-0001-9743-4304 AD - Department of Anesthesiology, Gregorio Maranon University Hospital, Madrid, Spain. FAU - Martin-Albo, Lorena AU - Martin-Albo L AUID- ORCID: 0000-0002-6312-7346 AD - Department of Thoracic Surgery, Gregorio Maranon University Hospital, Madrid, Spain. FAU - Ortega, Javier AU - Ortega J AUID- ORCID: 0000-0001-6122-0072 AD - Department of Thoracic Surgery, Gregorio Maranon University Hospital, Madrid, Spain. FAU - Vara, Elena AU - Vara E AUID- ORCID: 0000-0002-5361-5215 AD - Department of Biochemistry and Molecular Biology III, Faculty of Medicine, Complutense University of Madrid, Madrid, Spain. FAU - Garutti, Ignacio AU - Garutti I AUID- ORCID: 0000-0001-8284-2903 AD - Department of Anesthesiology, Gregorio Maranon University Hospital, Madrid, Spain. FAU - Simon, Carlos AU - Simon C AUID- ORCID: 0000-0002-9337-6167 AD - Department of Thoracic Surgery, Gregorio Maranon University Hospital, Madrid, Spain. LA - eng PT - Journal Article DEP - 20210604 PL - United States TA - Biomed Res Int JT - BioMed research international JID - 101600173 RN - 0 (Anti-Inflammatory Agents) RN - 0 (Antigens, CD) RN - 0 (Antigens, Differentiation, Myelomonocytic) RN - 0 (CD68 antigen, human) RN - 0 (Chemokine CCL2) RN - 0 (Proto-Oncogene Proteins c-bcl-2) RN - 98PI200987 (Lidocaine) RN - EC 3.4.22.- (Caspase 9) SB - IM MH - Animals MH - Anti-Inflammatory Agents/administration & dosage MH - Antigens, CD/metabolism MH - Antigens, Differentiation, Myelomonocytic/metabolism MH - Apoptosis/*drug effects MH - Biopsy MH - Caspase 9/metabolism MH - Chemokine CCL2/metabolism MH - Hemodynamics MH - Inflammation/*drug therapy MH - *Injections, Intravenous MH - Lidocaine/*administration & dosage MH - Lung/drug effects/*surgery MH - Proto-Oncogene Proteins c-bcl-2/metabolism MH - Reperfusion Injury/*drug therapy MH - Swine PMC - PMC8203341 COIS- The authors declare that they have no conflicts of interest. EDAT- 2021/07/02 06:00 MHDA- 2021/10/26 06:00 PMCR- 2021/06/04 CRDT- 2021/07/01 07:04 PHST- 2020/11/22 00:00 [received] PHST- 2021/05/27 00:00 [accepted] PHST- 2021/07/01 07:04 [entrez] PHST- 2021/07/02 06:00 [pubmed] PHST- 2021/10/26 06:00 [medline] PHST- 2021/06/04 00:00 [pmc-release] AID - 10.1155/2021/6630232 [doi] PST - epublish SO - Biomed Res Int. 2021 Jun 4;2021:6630232. doi: 10.1155/2021/6630232. eCollection 2021.