Sevoflurane, but not propofol, reduces the lung inflammatory response and improves oxygenation in an acute respiratory distress syndrome model (original) (raw)
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Sevoflurane Abolishes Oxygenation Impairment in a Long-Term Rat Model of Acute Lung Injury
Anesthesia and analgesia, 2017
Patients experiencing acute lung injury (ALI) often need mechanical ventilation for which sedation may be required. In such patients, usually the first choice an intravenously administered drug. However, growing evidence suggests that volatile anesthetics such as sevoflurane are a valuable alternative. In this study, we evaluate pulmonary and systemic effects of long-term (24-hour) sedation with sevoflurane compared with propofol in an in vivo animal model of ALI. Adult male Wistar rats were subjected to ALI by intratracheal lipopolysaccharide (LPS) application, mechanically ventilated and sedated for varying intervals up to 24 hours with either sevoflurane or propofol. Vital parameters were monitored, and arterial blood gases were analyzed. Inflammation was assessed by the analysis of bronchoalveolar lavage fluid (BALF), cytokines (monocyte chemoattractant protein-1 [MCP-1], cytokine-induced neutrophil chemoattractant protein-1 [CINC-1], interleukin [IL-6], IL-12/12a, transforming ...
European Journal of Anaesthesiology, 2013
Mechanical ventilation (MV), a life-saving intervention for critically ill patients with respiratory failure caused by acute lung injury (ALI), can cause an inflammatory response in both diseased and normal lungs. MV itself can also cause ventilator-induced lung injury (VILI), a form of ALI [1]. VILI results not only from barotraumas caused by alveolar disruption, capillary leakage, or lung edema, but also from biotraumas caused by the secretion of pro-inflammatory cytokines and mediators in pulmonary cells Experimental Research Article Background: Ventilator-induced lung injury (VILI) sustained during mechanical ventilator support is still a cause of a high rate of morbidity and mortality in intensive care units and in operating rooms. VILI is characterized by pulmonary inflammation that appears to be mediated by proinflammatory cytokines. This study investigates whether the volatile anesthetic sevoflurane has an anti-inflammatory effect that attenuates VILI. Methods: Twenty one male rabbits were anesthetized and were mechanically ventilated with 50% oxygen at a peak inspiratory pressure (PIP) of 10 cmH 2 O, I : E ratio of 1 : 4, and positive end expiratory pressure of 5 cmH 2 O. All animals were randomly assigned to one of three groups that were ventilated for 5 h with 10 cmH 2 O of PIP (Sham group, n = 7); 30 cmH 2 O of PIP (Control group, n = 7); or 30 cmH 2 O of PIP and 0.8 vol% sevoflurane (Sevoflurane group, n = 7). The wet/dry weight (W/D) ratio and histopathology of the lung; concentration of interleukin-8 (IL-8) in the bronchoalveolar lavage fluid; and activation of extracellular signal-regulated kinases (ERK) 1/2, p38 mitogen-activated protein kinase, and Akt were measured in the lung tissue after completing the protocol. Results: Histopathology indicated that the sevoflurane group showed fewer inflammatory cells and architectural changes than the control group did. The W/D ratio [(5.36 ± 0.13) versus (6.61 ± 0.20)], expression of IL-8 [(144.08 ± 14.61) versus (228.56 ± 15.13) pg/ml] and phosphorylation of ERK1/2 and Akt decreased significantly in the sevoflurane group relative to the control group. Conclusions: Sevoflurane attenuates VILI in rabbits mainly by inhibiting expression of IL-8, and Sevoflurane-induced inhibition of phosphorylated ERK1/2 and Akt might be a possible pathway for protection.
European Journal of Anaesthesiology
BACKGROUND: Septic encephalopathy is believed to be a result of neuro-inflammation possibly triggered by endotoxins, such as lipopolysaccharides (LPS). Modulation of the immune system is a property of volatile anaesthetics. OBJECTIVE: We aimed to investigate the systemic and cerebral inflammatory response in a LPS-induced sepsis model in rats. We compared two different sedation strategies, intravenous propofol and the volatile anaesthetic sevoflurane, with the hypothesis that the latter may attenuate neuro-inflammatory processes. DESIGN: Laboratory rat study. SETTING: Basic research laboratories at the University Hospital Zurich and University Zurich Irchel between August 2014 and June 2016. PATIENTS: A total of 32 adult male Wistar rats. INTERVENTIONS: After tracheotomy and mechanical ventilation, the anaesthetised rats were monitored before sepsis was induced by using intravenous LPS or phosphate-buffered saline as control. Rats were sedated with propofol (10 mg kg h) or sevoflurane (2 vol%) continuously for 12 h. MAIN OUTCOME MEASURES: Systemic inflammatory markers such as cytokine-induced neutrophil chemo-attractant protein 1, monocyte chemo-tactic protein-1 and IL-6 were determined. The same cytokines were measured in brain tissue. Cellular response in the brain was assessed by defining neutrophil accumulation with myeloperoxidase and also activation of microglia with ionised calcium-binding adaptor molecule-1 and astrocytes with glial fibrillary acidic protein. Finally, brain injury was determined. RESULTS: Animals were haemodynamically stable in both sedation groups treated with LPS. Blood cytokine peak values were lower in the sevoflurane-LPS compared with propofol-LPS animals. In brain tissue of LPS animals, chemoattractant protein-1 was the only significantly increased cytokine (P = 0.003), however with no significance between propofol and sevoflurane. After LPS challenge, cerebral accumulation of neutrophils was observed. Microglia activation was pronounced in the hippocampus of animals treated with LPS (P = 0.006). LPS induced prominent astrogliosis (P < 0.001). There was no significant difference in microglia or astrocyte activation or apoptosis in the brain between sevoflurane and propofol. CONCLUSION: We have shown that systemic attenuation of inflammation by the volatile anaesthetic sevoflurane did not translate into attenuated neuro-inflammation in this LPS-induced inflammation model. TRIAL REGISTRATION: Animal approval No. 134/2014, Veterinäramt Zürich.
Effects of sevoflurane and propofol on pulmonary inflammatory responses during lung resection
Journal of Anesthesia, 2012
Purpose Pulmonary inflammatory reactions are affected by one-lung ventilation (OLV) and anesthetic agents. However, the effects of anesthetic agents on pulmonary inflammatory reactions may vary. Our previous investigations suggested that inflammatory reactions were more pronounced in the dependent lung during lung resection under general anesthesia with propofol and remifentanil. Therefore, in the present study we attempted to determine the difference in pulmonary inflammatory reaction using either sevoflurane or propofol in both dependent and nondependent lungs during OLV. Methods Forty adult patients undergoing elective lung resection were randomized to receive either propofol (n = 20) or sevoflurane (n = 20) as the main anesthetic agent. Intraoperative analgesia was provided by remifentanil in both groups. Epithelial lining fluid (ELF) was obtained from each lung using a bronchoscopic microsampling method. ELF and plasma levels of inflammatory cytokines were measured using multiplexed bead-based immunoassays before and after OLV.
Sevoflurane Prevents Liver Inflammatory Response Induced by Lung Ischemia-Reperfusion
Transplantation, 2014
Background. Transplants cause ischemia-reperfusion (IR) injury that can affect distant organs. Liver is particularly sensitive to IR injury. The present randomized experimental study was designed to investigate a possible protective effect of sevoflurane against liver inflammatory response to lung IR in a lung upper lobe left autotransplant model. Methods. Two groups (sevoflurane and control) of eight swines each were submitted to upper lobe left lung autotransplant. Hypnotic maintenance was performed with sevoflurane 3% or propofol 8 to 10 mg/kg per hr until pneumonectomy was done; then propofol was used for all animals. Blood and liver samples were taken in four different moments: prepneumonectomy, prereperfusion, 10 min postreperfusion and 30 min postreperfusion to measure levels of interleukin (IL)-1A, IL-10, tumor necrosis factor (TNF)->, monocyte chemotactic protein (MCP)-1, nuclear factor (NF)-JB, C-reactive protein, ferritin and caspase 3. Non-parametric test was used to find statistical meaning. Results. Lung IR markedly increased the expression of TNF->, IL-1A, MCP-1, NF-JB and caspase activity in control livers compared with basal levels, whereas liver IL-10 expression decreased 10 and 30 min post-reperfusion. Sevoflurane significantly decreased TNF->, IL-1A, MCP-1, NF-JB liver expression and caspase 3 activity. Sevoflurane also reverted the lung IR-induced decrease in IL-10 expression. Conclusions. The present results indicate that lung IR caused hepatic injury. Sevoflurane attenuated liver injury in a model of upper lobe left lung autotransplant in pigs.
Background: Patients that are affected by severe induced respiratory failure (C-ARDS) formCOVID-19, frequently need deep sedation in order to perform adequate ventilator support. Volatile anesthetics (VAs) constitute a convenient alternative to intravenous molecules, allowing to fine-tune the desired level of sedation. Moreover, VAs might have anti-inflammatory and bronchodilatatory effects, which are particularly appropriate for COVID-19 patients. Methods: In this study, we show the results of a retrospective single-center non-profit observational cohort study. To achieve this, we enrolled patients hospitalized for C-ARDS in the COVID Intensive Care Unit of Hospital Santo Stefano (Prato, Italy) during the period March 2020 - June 2021. A total of 112 patients were enrolled in the study that were all submitted to invasive mechanical ventilation. Participants were divided in two groups: i) Group 1 received the VA sevoflurane and, ii) Group 2 were sedated with propofol and remifentani...
PloS one, 2015
Infection is a common cause of acute lung injury (ALI). This study was aimed to explore whether Toll-like receptors 4 (TLR4) of airway smooth muscle cells (ASMCs) play a role in lipopolysaccharide (LPS)-induced airway hyperresponsiveness and potential mechanisms. In vivo: A sensitizing dose of LPS (50 µg) was administered i.p. to female mice before anesthesia with either 3% sevoflurane or phenobarbital i.p. After stabilization, the mice were challenged with 5 µg of intratracheal LPS to mimic inflammatory attack. The effects of sevoflurane were assessed by measurement of airway responsiveness to methacholine, histological examination, and IL-1, IL-6, TNF-α levels in bronchoalveolar lavage fluid (BALF). Protein and gene expression of TLR4 and NF-κB were also assessed. In vitro: After pre-sensitization of ASMCs and ASM segments for 24h, levels of TLR4 and NF-κB proteins in cultured ASMCs were measured after continuous LPS exposure for 1, 3, 5, 12 and 24h in presence or absence of sevof...
2020
Background. The aim of this study is to compare the effects of sevoflurane and propofol on one lung ventilation (OLV) induced ischemia-reperfusion injury (IRI) by determining the blood gas, ischemia-modified albumin (IMA), and malonyldialdehyde (MDA). Material and Methods. Forty-four patients undergoing thoracic surgery with OLV were randomized in two groups (sevoflurane Group S, propofol Group P). Anesthesia was inducted with thiopental and was maintained with 1-2.5% of sevoflurane within the 40/60% of O 2 /N 2 O mixture in Group S. In Group P anesthesia was inducted with propofol and was maintained with infusion of propofol and remifentanil. Hemodynamic records and blood samples were obtained before anesthesia induction ( 1 ), 1 min before two lung ventilation ( 2 ), 30 min after two lung ventilation ( 3 ), and postoperative sixth hours ( 4 ). Results. Heart rate at 2 and 3 in Group P was significantly lower than that in Group S. While there were no significant differences in term...