scholarly journals Modern strategies of adaptation to the respiratory support as a way to reduce self-induced lung injury (SILI)

2020 ◽  
pp. 243-244
Author(s):  
M.M. Pylypenko ◽  
O.Yu. Khomenko
Keyword(s):  
Lung Injury ◽  
Dead Space ◽  
Body Position ◽  
Lung Damage ◽  
Respiratory Support ◽  
Shortness Of Breath ◽  
Respiratory Effort ◽  
Psychomotor Agitation ◽  
Obese People ◽  
Mechanical Lung Ventilation

Background. The success of respiratory support depends on the effectiveness of improving gas exchange, reducing lung damage, and adaptation of the respirator. Reduction of lung damage has previously been reported in the context of ventilator-associated injury: barotrauma in case of high plateau pressure and driving pressure, volume trauma in case of large tidal volume, atelectasis trauma due to the cyclic collapse of lungs on exhalation and opening on inspiration. Objective. To describe the features of lung damage during mechanical lung ventilation (MLV) and the possibility of its prevention. Materials and methods. Analysis of literature sources on this topic. Results and discussion. The main causes of “air hunger” breathing type and shortness of breath include hypoxia, acidosis, increased anatomical and functional dead space, psychomotor agitation and fear. Metabolic acidosis is compensated by hyperventilation and respiratory alkalosis, but it is treated by improving oxygenation. High-flow oxygenation helps to leach CO2 from the dead space. Psychomotor agitation and pain aggravate shortness of breath, so all components of these processes should be influenced by effective analgesia, providing the patient with a comfortable body position (especially obese people), ensuring the absence of hunger and thirst, creating conditions for night sleep and more. If all these measures are taken, but the patient’s agitation is maintained, sedation should be considered. Propofol and dexmedetomidine are increasingly used for short-term sedation. Approaches to sedation have been changing abroad in recent years. First, non-pharmacological methods are used and only then – pharmacological ones. First of all, it is recommended to achieve analgesia, and then – sedation. It is advisable to maintain moderate sedation (from 0 to -2 on the RASS scale) and avoid deep sedation (from -3 to -5 points on the RASS scale). Sedation should be stopped each morning for the wake-up test and the respirator quitting test. To improve the immediate consequences of treatment (duration of MLV and stay in the intensive care unit), it is advisable to minimize the use of benzodiazepines and prefer propofol or dexmedetomidine. The depth of sedation should be constantly monitored, however, even experienced physicians may not always be able to detect asynchrony and excessive sedation. Asynchrony is associated with the increased mortality and prolonged weaning. To assess the intensity of the patient’s respiratory effort, the index of rapid shallow breathing, the maximum vacuum in the airways and the pressure in 0.1 second after the start of the breathing attempt are used. If the latter exceeds 3.5 cm H2O, it indicates the excessive respiratory effort of the patient (Telias I. et al., 2020). Conclusions. 1. The term “self-induced lung injury” has become widely used in the practice of anesthesiologists. 2. The need for respiratory support is determined primarily by the patient’s breathing efforts. 3. The ability to timely identify and respond to asynchrony helps to avoid self-induced lung damage.

scholarly journals Increased effort during partial ventilatory support is not associated with lung damage in experimental acute lung injury

2019 ◽  
Vol 7 (1) ◽  
Author(s):  
Dietrich Henzler ◽  
Alf Schmidt ◽  
Zhaolin Xu ◽  
Nada Ismaiel ◽  
Haibo Zhang ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Pressure Support ◽  
Diffuse Alveolar Damage ◽  
Ventilatory Support ◽  
Lung Damage ◽  
Respiratory Effort ◽  
Sprague Dawley ◽  
Mechanical Pressure ◽  
Acid Aspiration

Abstract Background An on-going debate exists as to whether partial ventilatory support is lung protective in an acute phase of ARDS. So far, the effects of different respiratory efforts on the development of ventilator-associated lung injury (VALI) have been poorly understood. To test the hypothesis whether respiratory effort itself promotes VALI, acute lung injury (ALI) was induced in 48 Sprague Dawley rats by hydrochloric acid aspiration model. Hemodynamics, gas-exchange, and respiratory mechanics were measured after 4 h of ventilation in pressure control (PC), assist-control (AC), or pressure support with 100% (PS100), 60% (PS60), or 20% (PS20) of the driving pressure during PC. VALI was assessed by histological analysis and biological markers. Results ALI was characterized by a decrease in PaO2/FiO2 from 447 ± 75 to 235 ± 90 mmHg (p < 0.001) and dynamic respiratory compliance from 0.53 ± 0.2 to 0.28 ± 0.1 ml/cmH2O (p < 0.001). There were no differences in hemodynamics or respiratory function among groups at baseline or after 4 h of ventilation. The reduction of mechanical pressure support was associated with a compensatory increase in an inspiratory effort such that peak inspiratory transpulmonary pressures were equal in all groups. The diffuse alveolar damage score showed significant lung injury but was similar among groups. Pro- and anti-inflammatory proteins in the bronchial fluid were comparable among groups. Conclusions In experimental ALI in rodents, the respiratory effort was increased by reducing the pressure support during partial ventilatory support. In the presence of a constant peak inspiratory transpulmonary pressure, an increased respiratory effort was not associated with worsening ventilator-associated lung injury measured by histologic score and biologic markers.

scholarly journals Patient-Self Inflicted Lung Injury: A Practical Review

2021 ◽  
Vol 10 (12) ◽  
pp. 2738
Author(s):  
Guillaume Carteaux ◽  
Mélodie Parfait ◽  
Margot Combet ◽  
Anne-Fleur Haudebourg ◽  
Samuel Tuffet ◽  
...  
Keyword(s):  
Lung Injury ◽  
Transpulmonary Pressure ◽  
Inspiratory Effort ◽  
Lung Damage ◽  
Respiratory Drive ◽  
Inhomogeneous Distribution ◽  
Respiratory Effort ◽  
Ventilatory Strategy ◽  
Clinical Observations ◽  
Severe Lung

Patients with severe lung injury usually have a high respiratory drive, resulting in intense inspiratory effort that may even worsen lung damage by several mechanisms gathered under the name “patient-self inflicted lung injury” (P-SILI). Even though no clinical study has yet demonstrated that a ventilatory strategy to limit the risk of P-SILI can improve the outcome, the concept of P-SILI relies on sound physiological reasoning, an accumulation of clinical observations and some consistent experimental data. In this review, we detail the main pathophysiological mechanisms by which the patient’s respiratory effort could become deleterious: excessive transpulmonary pressure resulting in over-distension; inhomogeneous distribution of transpulmonary pressure variations across the lung leading to cyclic opening/closing of nondependent regions and pendelluft phenomenon; increase in the transvascular pressure favoring the aggravation of pulmonary edema. We also describe potentially harmful patient-ventilator interactions. Finally, we discuss in a practical way how to detect in the clinical setting situations at risk for P-SILI and to what extent this recognition can help personalize the treatment strategy.

Class B Scavenger Receptors BI and BII Protect Against LPS-induced Acute Lung Injury in Mice by Mediating LPS Clearance

2021 ◽  
Author(s):  
Irina N. Baranova ◽  
Alexander V. Bocharov ◽  
Tatyana G. Vishnyakova ◽  
Zhigang Chen ◽  
Anna A. Birukova ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Transgenic Mice ◽  
Neutrophil Infiltration ◽  
Lavage Fluid ◽  
Protective Role ◽  
Lung Damage ◽  
Wild Type ◽  
Class B ◽  
Anti Inflammatory

Recent studies suggest an anti-inflammatory protective role for class B scavenger receptor BI (SR-BI) in endotoxin-induced inflammation and sepsis. Other data, including ours, provide evidence for an alternative role of SR-BI, facilitating bacterial and endotoxin uptake, and contributing to inflammation and bacterial infection. Enhanced endotoxin susceptibility of SR-BI deficient mice due to their anti-inflammatory glucocorticoid deficiency complicates understanding SR-BI’s role in endotoxemia/sepsis, calling for use of alternative models. In this study, using hSR-BI and hSR-BII transgenic mice, we found that SR-BI and to a lesser extent its splicing variant SR-BII, protects against LPS-induced lung damage. At 20 hours after intratracheal LPS instillation the extent of pulmonary inflammation and vascular leakage was significantly lower in hSR-BI and hSR-BII transgenic mice compared to wild type mice. Higher bronchoalveolar lavage fluid (BALF) inflammatory cell count and protein content as well as lung tissue neutrophil infiltration found in wild type mice was associated with markedly (2-3 times) increased pro-inflammatory cytokine production as compared to transgenic mice following LPS administration. Markedly lower endotoxin levels detected in BALF of transgenic vs. wild type mice along with the significantly increased BODIPY-LPS uptake observed in lungs of hSR-BI and hSR-BII mice 20 hours after the IT LPS injection suggest that hSR-BI and hSR-BII-mediated enhanced LPS clearance in the airways could represent the mechanism of their protective role against LPS-induced acute lung injury.

scholarly journals Garcinia Multiflora Inhibits FPR1-Mediated Neutrophil Activation and Protects Against Acute Lung Injury

2018 ◽  
Vol 51 (6) ◽  
pp. 2776-2793 ◽  
Author(s):  
Yung-Fong Tsai ◽  
Shun-Chin Yang ◽  
Wen-Yi Chang ◽  
Jih-Jung Chen ◽  
Chun-Yu Chen ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Superoxide Anion ◽  
Calcium Influx ◽  
Neutrophil Activation ◽  
Lung Damage ◽  
Hek293 Cells ◽  
Human Neutrophils ◽  
Therapeutic Effects

Background/Aims: Formyl peptide receptors (FPRs) recognize different endogenous and exogenous molecular stimuli and mediate neutrophil activation. Dysregulation of excessive neutrophil activation and the resulting immune responses can induce acute lung injury (ALI) in the host. Accordingly, one promising approach to the treatment of neutrophil-dominated inflammatory diseases involves therapeutic FPR1 inhibition. Methods: We extracted a potent FPR1 antagonist from Garcinia multiflora Champ. (GMC). The inhibitory effects of GMC on superoxide anion release and elastase degranulation from activated human neutrophils were determined with spectrophotometric analysis. Reactive oxygen species (ROS) production and the FPR1 binding ability of neutrophils were assayed by flow cytometry. Signaling transduction mediated by GMC in response to chemoattractants was assessed with a calcium influx assay and western blotting. A lipopolysaccharide (LPS)-induced ALI mouse model was used to determine the therapeutic effects of GMC in vivo. Results: GMC significantly reduced superoxide anion release, the reactive oxidants derived therefrom, and elastase degranulation mediated through selective, competitive FPR1 blocking in N-formyl-L-methionyl-L-leucyl-L-phenylalanine (fMLF)-stimulated human neutrophils. In cell-free systems, GMC was unable to scavenge superoxide anions or suppress elastase activity. GMC produced a right shift in fMLF-activated concentration-response curves and was confirmed to be a competitive FPR1 antagonist. GMC binds to FPR1 not only in neutrophils, but also FPR1 in neutrophil-like THP-1 and hFPR1-transfected HEK293 cells. Furthermore, the mobilization of calcium and phosphorylation of mitogen-activated protein kinases and Akt, which are involved in FPR1-mediated downstream signaling, was competitively blocked by GMC. In an in vivo study, GMC significantly reduced pulmonary edema, neutrophil infiltration, and alveolar damage in LPS-induced ALI mice. Conclusion: Our findings demonstrate that GMC is a natural competitive FPR1 inhibitor, which makes it a possible anti-inflammatory treatment option for patients critically inflicted with FPR1-mediated neutrophilic lung damage.

Dexpanthenol therapy reduces lung damage in a hyperoxic lung injury in neonatal rats

2015 ◽  
pp. 1-7 ◽  
Author(s):  
Ramazan Ozdemir ◽  
Gulsum Demirtas ◽  
Hakan Parlakpinar ◽  
Alaadin Polat ◽  
Kevser Tanbag ◽  
...  
Keyword(s):  
Lung Injury ◽  
Lung Damage ◽  
Neonatal Rats ◽  
Hyperoxic Lung Injury

scholarly journals M1 macrophage activation in severe Plasmodium falciparum malaria patients with pulmonary oedema

2019 ◽  
Author(s):  
Aekkarin Klinkhamhom ◽  
Supattra Glaharn ◽  
Charit Sris ◽  
Sumate Ampawong ◽  
Srivicha Krudsood ◽  
...  
Keyword(s):  
Lung Injury ◽  
Falciparum Malaria ◽  
Malaria Infection ◽  
Plasmodium Falciparum Malaria ◽  
Lung Damage ◽  
M2 Macrophage ◽  
Tissue Samples ◽  
Macrophage Polarisation ◽  
Lung Macrophages ◽  
M1 Macrophage

Abstract BackgroundPulmonary oedema (PE) is a serious complication of severe P. falciparum malaria which can lead to acute lung injury in severe cases. Lung macrophages are activated during malaria infection due to a complex host-immune response. The molecular basis for macrophage polarisation is still unclear but understanding the predominant subtypes could lead to new therapeutic strategies where the diseases present with lung involvement. The present study was designed to study the polarisation of lung macrophages, as M1 or M2 macrophages, in the lungs of severe P. falciparum malaria patients with and without evidence of PE.Methods Lung tissue samples, taken from patients who died from severe P. falciparum malaria, were categorised into severe malaria with PE and without PE (non-PE). Expression of surface markers (CD68- all macrophages, CD40- M1 macrophage and CD163- M2 macrophage) on activated lung macrophages was used to quantify M1/M2 macrophage subtypes.Results Lung injury was demonstrated in malaria patients with PE. The expression of CD40 (M1 macrophage) was prominent in the group of severe P. falciparum malaria patients with PE ( p < 0.05), whereas there was no difference observed for CD163 (M2 macrophage) between PE and non-PE groups.Conclusions The study demonstrates M1 polarisation in lung tissues from severe P. falciparum malaria infections with PE. Understanding the nature of macrophage characterisation in malaria infection may provide new insights into therapeutic approaches that could be deployed to reduce lung damage in severe P. falciparum malaria.

Protective effects of hydrogen against irradiation

2021 ◽  
Vol 27 ◽  
Author(s):  
Yasuhiro Terasaki ◽  
Mika Terasaki ◽  
Akira Shimizu
Keyword(s):  
Oxidative Stress ◽  
Lung Injury ◽  
Cultured Cells ◽  
Animal Experiments ◽  
Lung Epithelial Cells ◽  
Lung Damage ◽  
Protective Effects ◽  
Chronic Radiation ◽  
Radiation Induced ◽  
Reactive Oxidants

: Radiation-induced lung injury is characterized by an acute pneumonia phase followed by a fibrotic phase. At the time of irradiation, a rapid, short-lived burst of reactive oxygen species (ROS) such as hydroxyl radicals (•OH) occurs, but chronic radiation-induced lung injury may occur due to excess ROS such as H2O2 , O2•− , ONOO− , and •OH. Molecular hydrogen (H2 ) is an efficient antioxidant that quickly diffuses cell membranes, reduces ROS such as •OH and ONOO− , and suppresses damage caused by oxidative stress in various organs. In 2011, through the evaluation of electron-spin resonance and fluorescent indicator signals, we had reported that H2 can eliminate •OH and can protect against oxidative stress-related apoptotic damage induced by irradiation of cultured lung epithelial cells. We had explored for the first time the radioprotective effects of H2 treatment on acute and chronic radiation-induced lung damage in mice by inhaled H2 gas (for acute) and imbibed H2 -enriched water (for chronic). Thus, we had proposed that H2 be considered a potential radioprotective agent. Recent publications have shown that H2 directly neutralizes highly reactive oxidants and indirectly reduces oxidative stress by regulating the expression of various genes. By regulating gene expression, H2 functions as an anti-inflammatory and anti-apoptotic molecule and promotes energy metabolism. The increased evidence obtained from cultured cells or animal experiments reveal a putative place for H2 treatment and its radioprotective effect clinically. This review focuses on major scientific advances of in the treatment of H2 as a new class of radioprotective agents.

Exposure to mechanical ventilation promotes tolerance to ventilator-induced lung injury by Ccl3 downregulation

2015 ◽  
Vol 309 (8) ◽  
pp. L847-L856 ◽  
Author(s):  
Jorge Blázquez-Prieto ◽  
Inés López-Alonso ◽  
Laura Amado-Rodríguez ◽  
Estefanía Batalla-Solís ◽  
Adrián González-López ◽  
...  
Keyword(s):  
High Pressure ◽  
Lung Injury ◽  
Molecular Mechanisms ◽  
Peak Pressure ◽  
Lung Damage ◽  
Previous Exposure ◽  
Neutrophilic Infiltration ◽  
Ventilator Induced Lung Injury ◽  
Inflammatory Protein ◽  
Albumin Content

Inflammation plays a key role in the development of ventilator-induced lung injury (VILI). Preconditioning with a previous exposure can damp the subsequent inflammatory response. Our objectives were to demonstrate that tolerance to VILI can be induced by previous low-pressure ventilation, and to identify the molecular mechanisms responsible for this phenomenon. Intact 8- to 12-wk-old male CD1 mice were preconditioned with 90 min of noninjurious ventilation [peak pressure 17 cmH2O, positive end-expiratory pressure (PEEP) 2 cmH2O] and extubated. Seven days later, preconditioned mice and intact controls were submitted to injurious ventilation (peak pressure 20 cmH2O, PEEP 0 cmH2O) for 2 h to induce VILI. Preconditioned mice showed lower histological lung injury scores, bronchoalveolar lavage albumin content, and lung neutrophilic infiltration after injurious ventilation, with no differences in Il6 or Il10 expression. Microarray analyses revealed a downregulation of Calcb, Hspa1b, and Ccl3, three genes related to tolerance phenomena, in preconditioned animals. Among the previously identified genes, only Ccl3, which encodes the macrophage inflammatory protein 1 alpha (MIP-1α), showed significant differences between intact and preconditioned mice after high-pressure ventilation. In separate, nonconditioned animals, treatment with BX471, a specific blocker of CCR1 (the main receptor for MIP-1α), decreased lung damage and neutrophilic infiltration caused by high-pressure ventilation. We conclude that previous exposure to noninjurious ventilation induces a state of tolerance to VILI. Downregulation of the chemokine gene Ccl3 could be the mechanism responsible for this effect.

scholarly journals Recipient T lymphocytes modulate the severity of antibody-mediated transfusion-related acute lung injury

Blood ◽  
2010 ◽  
Vol 116 (16) ◽  
pp. 3073-3079 ◽  
Author(s):  
Yoke Lin Fung ◽  
Michael Kim ◽  
Arata Tabuchi ◽  
Rukhsana Aslam ◽  
Edwin R. Speck ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
T Lymphocytes ◽  
Lung Injury ◽  
Pulmonary Edema ◽  
Critical Role ◽  
Severe Combined Immunodeficiency ◽  
Lung Damage ◽  
Moderate Hypothermia ◽  
Combined Immunodeficiency ◽  
Histocompatibility Complex

Abstract Transfusion-related acute lung injury (TRALI) is a serious complication of transfusion and has been ranked as one of the leading causes of transfusion-related fatalities. Nonetheless, many details of the immunopathogenesis of TRALI, particularly with respect to recipient factors are unknown. We used a murine model of antibody-mediated TRALI in an attempt to understand the role that recipient lymphocytes might play in TRALI reactions. Intravenous injection of an IgG2a antimurine major histocompatibility complex class I antibody (34-1-2s) into BALB/c mice induced moderate hypothermia and pulmonary granulocyte accumulation but no pulmonary edema nor mortality. In contrast, 34-1-2s injections into mice with severe combined immunodeficiency caused severe hypothermia, severe pulmonary edema, and approximately 40% mortality indicating a critical role for T and B lymphocytes in suppressing TRALI reactions. Adoptive transfer of purified CD8+ T lymphocytes or CD4+ T cells but not CD19+ B cells into the severe combined immunodeficiency mice alleviated the antibody-induced hypothermia, lung damage, and mortality, suggesting that T lymphocytes were responsible for the protective effect. Taken together, these results suggest that recipient T lymphocytes play a significant role in suppressing antibody-mediated TRALI reactions. They identify a potentially new recipient mechanism that controls the severity of TRALI reactions.

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