Large animal models are frequently used to investigate new medical approaches. In most cases, animals are kept under general anesthesia and mandatory mechanical ventilation during the experiments. However, in some situations assisted spontaneous breathing is essential, e.
View Article and Find Full Text PDFElectrical impedance tomography is a valuable tool for monitoring global and regional lung mechanics. To evaluate the recorded data, an accurate estimate of the lung area is crucial.We present two novel methods for estimating the lung area using functional tidal images or active contouring methods.
View Article and Find Full Text PDFHydrogen sulfide (HS) protects against stretch-induced lung injury. However, the impact of HS on individual cells or their crosstalk upon stretch remains unclear. Therefore, we addressed this issue in vitro using relevant lung cells.
View Article and Find Full Text PDFPersonalized antibiotherapy ensures that the antibiotic concentration remains in the optimal therapeutic window to maximize efficacy, minimize side effects, and avoid the emergence of drug resistance due to insufficient dosing. However, such individualized schemes need frequent sampling to tailor the blood antibiotic concentrations. To optimally integrate therapeutic drug monitoring (TDM) into the clinical workflow, antibiotic levels can either be measured in blood using point-of-care testing (POCT), or can rely on noninvasive sampling.
View Article and Find Full Text PDFNew Findings: What is the central question of the study? Does respiratory support ensure blood gas homeostasis and the relevance of experimental outcomes? What is the main finding and its importance? Spontaneous breathing during surgical intervention under anaesthesia results in impaired gas exchange and loss of diaphragm muscle strength in rats. Subsequent short-term mechanical ventilation restored blood gas homeostasis and diaphragm muscle strength. Blood gas homeostasis interferes substantially with experimental conditions and may alter study results.
View Article and Find Full Text PDFWe previously found that argon exerts its neuroprotective effect in part by inhibition of the toll-like receptors (TLR) 2 and 4. The downstream transcription factors signal transducer and activator of transcription 3 (STAT3) and nuclear factor kappa B (NF-κB) are also affected by argon and may play a role in neuroprotection. It also has been demonstrated that argon treatment could mitigate brain damage, reduce excessive microglial activation, and subsequently attenuate brain inflammation.
View Article and Find Full Text PDFMechanical ventilation is associated with the risk of ventilator induced lung injury. For reducing lung injury in mechanically ventilated patients, the application of small tidal volumes and positive end-expiratory pressures has become clinical standard. Recently, an approach based on linear airway pressure decline and decelerated expiratory flow during expiration implied lung protective capacities.
View Article and Find Full Text PDFFor investigating the effects of mechanical ventilation on the respiratory system, experiments in small mammal models are used. However, conventional ventilators for small animals are usually limited to a specific ventilation mode, and in particular to passive expiration. Here, we present a computer-controlled research ventilator for small animals which provides conventional mechanical ventilation as well as new type ventilation profiles.
View Article and Find Full Text PDFObjectives: Lung-protective ventilation for acute respiratory distress syndrome aims for providing sufficient oxygenation and carbon dioxide clearance, while limiting the harmful effects of mechanical ventilation. "Flow-controlled ventilation", providing a constant expiratory flow, has been suggested as a new lung-protective ventilation strategy. The aim of this study was to test whether flow-controlled ventilation attenuates lung injury in an animal model of acute respiratory distress syndrome.
View Article and Find Full Text PDFProtective mechanical ventilation is aimed at preventing ventilator-induced lung injury while ensuring sufficient gas exchange. A new approach focuses on the temporal profile of the mechanical ventilation. We hypothesized that the temporal mechanical strain profile modulates inflammatory signalling.
View Article and Find Full Text PDFTransmigration and activation of neutrophils in the lung reflect key steps in the progression of acute lung injury (ALI). It is known that hydrogen sulfide (HS) can limit neutrophil activation, but the respective mechanisms remain elusive. Here, we aimed to examine the underlying pathways in pulmonary inflammation.
View Article and Find Full Text PDFBackground: In contrast to conventional mandatory ventilation, a new ventilation mode, expiratory ventilation assistance (EVA), linearises the expiratory tracheal pressure decline.
Objective: We hypothesised that due to a recruiting effect, linearised expiration oxygenates better than volume controlled ventilation (VCV). We compared the EVA with VCV mode with regard to gas exchange, ventilation volumes and pressures and lung aeration in a model of peri-operative mandatory ventilation in healthy pigs.
Mechanical ventilation is a life-saving clinical treatment but it can induce or aggravate lung injury. New therapeutic strategies, aimed at reducing the negative effects of mechanical ventilation such as excessive production of reactive oxygen species, release of pro-inflammatory cytokines, and transmigration as well as activation of neutrophil cells, are needed to improve the clinical outcome of ventilated patients. Though the inhaled anesthetic sevoflurane is known to exert organ-protective effects, little is known about the potential of sevoflurane therapy in ventilator-induced lung injury.
View Article and Find Full Text PDFAlthough essential in critical care medicine, mechanical ventilation often results in ventilator-induced lung injury. Low concentrations of hydrogen sulfide have been proven to have anti-inflammatory and anti-oxidative effects in the lung. The aim of this study was to analyze the kinetic effects of pre- and posttreatment with hydrogen sulfide in order to prevent lung injury as well as inflammatory and oxidative stress upon mechanical ventilation.
View Article and Find Full Text PDFObjectives: Hydrogen sulfide reduces ventilator-induced lung injury in mice. Here, we have examined the underlying mechanisms of hydrogen sulfide-mediated lung protection and determined the involvement of cyclooxygenase 2, 15-deoxy Δ-prostaglandin J2, and peroxisome proliferator-activated receptor gamma in this response.
Design: Randomized, experimental study.
Background: Mechanical ventilation is an important perioperative tool in anesthesia and a lifesaving treatment for respiratory failure, but it can lead to ventilator-associated lung injury. Inhaled anesthetics have demonstrated protective properties in various models of organ damage. We compared the lung-protective potential of inhaled sevoflurane, isoflurane, and desflurane in a mouse model of ventilator-induced lung injury (VILI).
View Article and Find Full Text PDFRecently, we have shown that inhalation of hydrogen sulfide (H2S) protects against ventilator-induced lung injury (VILI). In the present study, we aimed to determine the underlying molecular mechanisms of H2S-dependent lung protection by analyzing gene expression profiles in mice. C57BL/6 mice were subjected to spontaneous breathing or mechanical ventilation in the absence or presence of H2S (80 parts per million).
View Article and Find Full Text PDFIschemic and traumatic brain injury is associated with increased risk for death and disability. The inhibition of penumbral tissue damage has been recognized as a target for therapeutic intervention, because cellular injury evolves progressively upon ATP-depletion and loss of ion homeostasis. In patients, thiopental is used to treat refractory intracranial hypertension by reducing intracranial pressure and cerebral metabolic demands; however, therapeutic benefits of thiopental-treatment are controversially discussed.
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