scholarly journals Lung-Protective Ventilation Strategies for Relief from Ventilator-Associated Lung Injury in Patients Undergoing Craniotomy: A Bicenter Randomized, Parallel, and Controlled Trial

2017 ◽  
Vol 2017 ◽  
pp. 1-12 ◽  
Author(s):  
Chaoliang Tang ◽  
Juan Li ◽  
Shaoqing Lei ◽  
Bo Zhao ◽  
Zhetao Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Mechanical Ventilation ◽  
Lung Injury ◽  
Inflammatory Response ◽  
Protective Ventilation ◽  
Current Evidence ◽  
Lung Protective Ventilation ◽  
Hemodynamic Variables ◽  
And Oxidative Stress

Current evidence indicates that conventional mechanical ventilation often leads to lung inflammatory response and oxidative stress, while lung-protective ventilation (LPV) minimizes the risk of ventilator-associated lung injury (VALI). This study evaluated the effects of LPV on relief of pulmonary injury, inflammatory response, and oxidative stress among patients undergoing craniotomy. Sixty patients undergoing craniotomy received either conventional mechanical (12 mL/kg tidal volume [VT] and 0 cm H2O positive end-expiratory pressure [PEEP]; CV group) or protective lung (6 mL/kg VT and 10 cm H2O PEEP; PV group) ventilation. Hemodynamic variables, lung function indexes, and inflammatory and oxidative stress markers were assessed. The PV group exhibited greater dynamic lung compliance and lower respiratory index than the CV group during surgery (P<0.05). The PV group exhibited higher plasma interleukin- (IL-) 10 levels and lower plasma malondialdehyde and nitric oxide and bronchoalveolar lavage fluid, IL-6, IL-8, tumor necrosis factor-α, IL-10, malondialdehyde, nitric oxide, and superoxide dismutase levels (P<0.05) than the CV group. There were no significant differences in hemodynamic variables, blood loss, liquid input, urine output, or duration of mechanical ventilation between the two groups (P>0.05). Patients receiving LPV during craniotomy exhibited low perioperative inflammatory response, oxidative stress, and VALI.

Interactive effects of mechanical ventilation, inhaled nitric oxide and oxidative stress in acute lung injury

2014 ◽  
Vol 190 ◽  
pp. 118-123 ◽  
Author(s):  
Carlos Fernando Ronchi ◽  
Ana Lucia Anjos Ferreira ◽  
Fabio Joly Campos ◽  
Cilmery Suemi Kurokawa ◽  
Mario Ferreira Carpi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Mechanical Ventilation ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Inhaled Nitric Oxide ◽  
Interactive Effects ◽  
And Oxidative Stress

Noninvasive and Invasive Ventilatory Support II

2018 ◽  
Author(s):  
Pauline K. Park ◽  
Nicole L Werner ◽  
Carl Haas
Keyword(s):  
Mechanical Ventilation ◽  
Respiratory Failure ◽  
Lung Injury ◽  
Acute Respiratory Failure ◽  
Ventilatory Support ◽  
Underlying Disease ◽  
Protective Ventilation ◽  
Lung Protective Ventilation ◽  
Pulmonary Mechanics ◽  
Ventilator Induced Lung Injury

Invasive and noninvasive ventilation are important tools in the clinician’s armamentarium for managing acute respiratory failure. Although these modalities do not treat the underlying disease, they can provide the necessary oxygenation and ventilatory support until the causal pathology resolves. Care must be taken as even appropriate application can cause harm. Knowledge of pulmonary mechanics, appreciation of the basic machine settings, and an understanding of how common and advanced modes function allows the clinician to optimally tailor support to the patient while limiting iatrogenic injury. This second chapter reviews indications for mechanical ventilation, routine management, troubleshooting, and liberation from mechanical ventilation This review contains 6 figures, 7 tables and 60 references Keywords: Mechanical ventilation, lung protective ventilation, sedation, ventilator-induced lung injury, liberation from mechanical ventilation 

scholarly journals Angiotensin-converting enzyme 2 attenuates inflammatory response and oxidative stress in hyperoxic lung injury by regulating NF-κB and Nrf2 pathways

QJM ◽  
2019 ◽  
Vol 112 (12) ◽  
pp. 914-924 ◽  
Author(s):  
Y Fang ◽  
F Gao ◽  
Z Liu
Keyword(s):  
Oxidative Stress ◽  
Lung Injury ◽  
Inflammatory Response ◽  
Lung Tissue ◽  
Ang Ii ◽  
Converting Enzyme ◽  
Angiotensin Converting Enzyme 2 ◽  
Hyperoxic Lung Injury ◽  
Expression Activity ◽  
And Oxidative Stress

Summary Objective To investigate the role of angiotensin-converting enzyme 2 (ACE2) in hyperoxic lung injury. Methods Adult mice were exposed to 95% O2 for 72 h to induce hyperoxic lung injury, and simultaneously treated with ACE2 agonist diminazene aceturate (DIZE) or inhibitor MLN-4760. ACE2 expression/activity in lung tissue and angiotensin (Ang)-(1–7)/Ang II in bronchoalveolar lavage fluid (BALF), and the severity of hyperoxic lung injury were evaluated. The levels of inflammatory factors in BALF and lung tissue and the expression levels of phospho-p65, p65 and IkBα were measured. Oxidative parameter and antioxidant enzyme levels in lung tissue were measured to assess oxidative stress. Finally, the expression levels of nuclear factor-erythroid-2-related factor (Nrf2), NAD(P)H quinine oxidoreductase 1 (NQO1) and heme oxygenase-1 (HO-1) were measured using Western blotting. Results Hyperoxia treatment significantly decreased lung ACE2 expression/activity and increased the Ang II/Ang-(1–7) ratio, while co-treatment with hyperoxia and DIZE significantly increased lung ACE2 expression/activity and decreased the Ang II/Ang-(1–7) ratio. By contrast, co-treatment with hyperoxia and MLN-4760 significantly decreased lung ACE2 expression/activity and increased the Ang II/Ang-(1–7) ratio. Hyperoxia treatment induced significant lung injury, inflammatory response and oxidative stress, which were attenuated by DIZE but aggravated by MLN-4760. The NF-κB pathways were activated by hyperoxia and MLN-4760 but inhibited by DIZE. The Nrf2 pathway and its downstream proteins NQO1 and HO-1 were activated by DIZE but inhibited by MLN-4760. Conclusion Activation of ACE2 can reduce the severity of hyperoxic lung injury by inhibiting inflammatory response and oxidative stress. ACE2 can inhibit the NF-κB pathway and activate the Nrf2/HO-1/NQO1 pathway, which may be involved in the underlying mechanism.

scholarly journals Evidence for Negative Effects of Elevated Intra-Abdominal Pressure on Pulmonary Mechanics and Oxidative Stress

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
I. Davarcı ◽  
M. Karcıoğlu ◽  
K. Tuzcu ◽  
K. İnanoğlu ◽  
T. D. Yetim ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protective Ventilation ◽  
Lung Mechanics ◽  
Lung Protective Ventilation ◽  
Ventilation Strategy ◽  
Negative Effects ◽  
30Th Minute ◽  
Protective Ventilation Strategy ◽  
And Oxidative Stress ◽  
Lung Protective Ventilation Strategy

Objective. To compare the effects of pneumoperitoneum on lung mechanics, end-tidal CO2(ETCO2), arterial blood gases (ABG), and oxidative stress markers in blood and bronchoalveolar lavage fluid (BALF) during laparoscopic cholecystectomy (LC) by using lung-protective ventilation strategy.Materials and Methods. Forty-six patients undergoing LC and abdominal wall hernia (AWH) surgery were assigned into 2 groups. Measurements and blood samples were obtained before, during pneumoperitoneum, and at the end of surgery. BALF samples were obtained after anesthesia induction and at the end of surgery.Results. Peak inspiratory pressure, ETCO2, and pCO2values at the 30th minute were significantly increased, while there was a significant decrease in dynamic lung compliance, pH, and pO2values in LC group. In BALF samples, total oxidant status (TOS), arylesterase, paraoxonase, and malondialdehyde levels were significantly increased; the glutathione peroxidase levels were significantly decreased in LC group. The serum levels of TOS and paraoxonase were significantly higher at the end of surgery in LC group. In addition, arylesterase level in the 30th minute was increased compared to baseline. Serum paraoxonase level at the end of surgery was significantly increased when compared to AWH group.Conclusions. Our study showed negative effects of pneumoperitoneum in both lung and systemic levels despite lung-protective ventilation strategy.

scholarly journals Synergistic Effect of Hyperoxia and Biotrauma On Ventilator-Induced Lung Injury

PRILOZI ◽  
2017 ◽  
Vol 38 (1) ◽  
pp. 91-96 ◽  
Author(s):  
Mirjana Shosholcheva ◽  
Nikola Јankulovski ◽  
Andrijan Kartalov ◽  
Biljana Kuzmanovska ◽  
Daniela Miladinova
Keyword(s):  
Mechanical Ventilation ◽  
Lung Injury ◽  
Inflammatory Response ◽  
Synergistic Effect ◽  
Diffuse Alveolar Damage ◽  
Oxygen Toxicity ◽  
Plateau Pressure ◽  
Lung Protective Ventilation ◽  
Lung Protection ◽  
Ventilator Induced Lung Injury

Abstract Patients undergoing mechanical ventilation in intensive care units (ICUs) may develop ventilator-induced lung injury (VILI). Beside the high tidal volume (Vt) and plateau pressure (Pplat), hyperoxia is supposed to precipitate lung injury. Oxygen toxicity is presumed to occur at levels of fraction of inspired oxygen (FiO2) exceeding 0.40. The exposure time to hyperoxia is certainly very important and patients who spend extended time on mechanical ventilation (MV) are probably more exposed to severe hyperoxic acute lung injury (HALI). Together, hyperoxia and biotrauma (release of cytokines) have a synergistic effect and can induce VILI. In the clinical practice, the reduction of FiO2 to safe levels through the appropriate use of the positive end expiratory pressure (PEEP) and the alignment of mean airway pressure is an appropriate goal. The strategy for lung protective ventilation must include setting up FiO2 to a safe level that is accomplished by using PaO2/FiO2 ratio with a lower limit of FiO2 to achieve acceptable levels of PaO2, which will be safe for the patient without local (lungs) or systemic inflammatory response. The protocol from the ARDS-net study is used for ventilator setup and adjustment. Cytokines (IL-1, IL-6, TNFα and MIP-2) that are involved in the inflammatory response are determined in order to help the therapeutic approach in counteracting HALI. Computed tomography findings reflect the pathological phases of the diffuse alveolar damage. At least preferably the lowest level of FiO2 should be used in order to provide full lung protection against the damage induced by MV.

scholarly journals Oxypaeoniflorin Prevents Acute Lung Injury Induced by Lipopolysaccharide through the PTEN/AKT Pathway in a Sirt1-Dependent Manner

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Fan Guohua ◽  
Zhu Tieyuan ◽  
Wang Rui ◽  
Xiong Juan
Keyword(s):  
Oxidative Stress ◽  
Acute Lung Injury ◽  
Epithelial Cells ◽  
Lung Injury ◽  
Inflammatory Response ◽  
Alveolar Epithelial Cells ◽  
Dependent Manner ◽  
Alveolar Epithelial ◽  
And Oxidative Stress

Acute lung injury (ALI) is featured by pulmonary edema, alveolar barrier injury, inflammatory response, and oxidative stress. The activation of Sirt1 could relieve lipopolysaccharide- (LPS-) induced murine ALI by maintaining pulmonary epithelial barrier function. Oxypaeoniflorin (Oxy) serves as a major component of Paeonia lactiflora Pall., exerting cardioprotection by activating Sirt1. However, the role of Oxy in ALI induced by LPS remains unclear. The aim of the present study is to illustrate the modulatory effects and molecular mechanisms by which Oxy operates in ALI induced by LPS. The intraperitoneal injection of LPS was performed to establish the murine ALI model while LPS-treated alveolar epithelial cells were used to mimic the in vitro ALI model. Levels of lung injury, oxidative stress, and inflammatory response were detected to observe the potential effects of Oxy on ALI. Oxy treatment mitigated lung edema, inflammatory response, and oxidative stress in mouse response to LPS, apart from improving 7-day survival. Meanwhile, Oxy also increased the expression and activity of Sirt1. Intriguingly, Sirt1 deficiency or inhibition counteracted the protective effects of Oxy treatment in LPS-treated mice or LPS-treated alveolar epithelial cells by regulating the PTEN/AKT signaling pathway. These results demonstrated that Oxy could combat ALI in vivo and in vitro through inhibiting inflammatory response and oxidative stress in a Sirt1-dependent manner. Oxy owns the potential to be a promising candidate against ALI.

Noninvasive and Invasive Ventilatory Support II

2018 ◽  
Author(s):  
Pauline K. Park ◽  
Nicole L Werner ◽  
Carl Haas
Keyword(s):  
Mechanical Ventilation ◽  
Respiratory Failure ◽  
Lung Injury ◽  
Acute Respiratory Failure ◽  
Ventilatory Support ◽  
Underlying Disease ◽  
Protective Ventilation ◽  
Lung Protective Ventilation ◽  
Pulmonary Mechanics ◽  
Ventilator Induced Lung Injury

Invasive and noninvasive ventilation are important tools in the clinician’s armamentarium for managing acute respiratory failure. Although these modalities do not treat the underlying disease, they can provide the necessary oxygenation and ventilatory support until the causal pathology resolves. Care must be taken as even appropriate application can cause harm. Knowledge of pulmonary mechanics, appreciation of the basic machine settings, and an understanding of how common and advanced modes function allows the clinician to optimally tailor support to the patient while limiting iatrogenic injury. This second chapter reviews indications for mechanical ventilation, routine management, troubleshooting, and liberation from mechanical ventilation This review contains 6 figures, 7 tables and 60 references Keywords: Mechanical ventilation, lung protective ventilation, sedation, ventilator-induced lung injury, liberation from mechanical ventilation 

scholarly journals Diaphragm neurostimulation during mechanical ventilation reduces atelectasis and transpulmonary plateau pressure, preserving lung homogeneity and PaO2/FiO2

2021 ◽  
Author(s):  
Elizabeth C. Rohrs ◽  
Thiago G. Bassi ◽  
Karl C. Fernandez ◽  
Marlena Ornowska ◽  
Michelle Nicholas ◽  
...  
Keyword(s):  
Mechanical Ventilation ◽  
Lung Injury ◽  
Phrenic Nerve ◽  
Control Ventilation ◽  
Protective Ventilation ◽  
Lung Mechanics ◽  
Volume Control ◽  
Normal Lung ◽  
Lung Protective Ventilation ◽  
Volume Control Ventilation

Tidal volume delivered by mechanical ventilation to a sedated patient is distributed in a non-physiological pattern, causing atelectasis (underinflation) and overdistension (overinflation). Activation of the diaphragm during mechanical ventilation provides a way to reduce atelectasis and alveolar inhomogeneity, protecting the lungs from ventilator-induced lung injury while also protecting the diaphragm by preventing ventilator-induced diaphragm dysfunction. We studied the hypothesis that diaphragm contractions elicited by transvenous phrenic nerve stimulation, delivered in synchrony with volume-control ventilation, would reduce atelectasis and lung inhomogeneity in a healthy, normal-lung pig model. Twenty-five large pigs were ventilated for 50 hours with lung-protective volume-control ventilation combined with synchronous transvenous phrenic-nerve neurostimulation on every breath, or every second breath. This was compared to lung-protective ventilation alone. Lung mechanics and ventilation pressures were measured using esophageal pressure manometry and electrical impedance tomography. Alveolar homogeneity was measured using alveolar chord length of preserved lung tissue. Lung injury was measured using inflammatory cytokine concentration in bronchoalveolar lavage fluid and serum. We found that diaphragm neurostimulation on every breath preserved PaO2/FiO2 and significantly reduced the loss of end-expiratory lung volume after 50 hours of mechanical ventilation. Neurostimulation on every breath reduced plateau and driving pressures, improved both static and dynamic compliance and resulted in less alveolar inhomogeneity. These findings support that temporary transvenous diaphragm neurostimulation during volume-controlled, lung-protective ventilation may offer a potential method to provide both lung- and diaphragm-protective ventilation.

Disruption of Diffusion

2017 ◽  
Author(s):  
Shahzad Shaefi ◽  
Aaron Mittel
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Acute Lung Injury ◽  
Gas Exchange ◽  
Lung Injury ◽  
Inflammatory Response ◽  
Respiratory Distress Syndrome ◽  
Distress Syndrome ◽  
Protective Ventilation ◽  
Lung Protective Ventilation ◽  
Circulatory Overload

Acute respiratory distress syndrome (ARDS), transfusion-related acute lung injury (TRALI), and transfusion-associated circulatory overload (TACO) are common conditions in critically ill patients that lead to pulmonary edema and hypoxemia. The nonhydrostatic edema characteristic of ARDS and TRALI is caused by an intense inflammatory response leading to increased microvascular permeability and alveolar injury. TACO is an acute hydrostatic edema temporally associated with events that precipitate lung injury. Lung-protective ventilation is the mainstay of therapy for ARDS and TRALI; optimizing gas exchange is the goal for all three. Prompt recognition is an important skill for perioperative practitioners.

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