Publications by authors named "Hoegl S"

The MACCS (Medical Assistant for Chronic Care Service) platform enables secure sharing of key medical information between patients after kidney transplantation and physicians. Patients provide information such as vital signs, well-being, and medication intake via smartphone apps. The information is transferred directly into a database and electronic health record at the kidney transplant center, which is used for routine patient care and research.

View Article and Find Full Text PDF

Severe acute respiratory distress syndrome (ARDS) presents typically with an initializing event, followed by the need for mechanical ventilation. Most animal models of ALI are limited by the fact that they focus on a singular cause of acute lung injury (ALI) and therefore fail to mimic the complex, multifactorial pathobiology of ARDS. To better capture this scenario, we provide a comprehensive characterization of models of ALI combining two injuries: intra tracheal (i.

View Article and Find Full Text PDF

A critical step in the pathogenesis of acute lung injury (ALI) is excessive recruitment of polymorphonuclear neutrophils (PMNs) into the lungs, causing significant collateral tissue damage. Defining the molecular and cellular steps that control neutrophil infiltration and activation during ALI is therefore of important therapeutic relevance. Based on previous findings implicating the transcription factor Tbet in mucosal Th1-inflammation, we hypothesized a detrimental role for Tbet during ALI.

View Article and Find Full Text PDF

Purpose Of Review: This review gives an update on current treatment options and novel concepts on the prevention and treatment of the acute respiratory distress syndrome (ARDS) in cardiovascular surgery patients.

Recent Findings: The only proven beneficial therapeutic options in ARDS are those that help to prevent further ventilator-induced lung injury, such as prone position, use of lung-protective ventilation strategies, and extracorporeal membrane oxygenation. In the future also new approaches like mesenchymal cell therapy, activation of hypoxia-elicited transcription factors or targeting of purinergic signaling may be successful outside the experimental setting.

View Article and Find Full Text PDF

Acute lung injury (ALI) is an acute inflammatory lung disease that causes morbidity and mortality in critically ill patients. However, there are many instances where ALI resolves spontaneously through endogenous pathways that help to control excessive lung inflammation. Previous studies have implicated the extracellular signaling molecule adenosine and signaling events through the A2B adenosine receptor in lung protection.

View Article and Find Full Text PDF

Acute lung injury (ALI) is an inflammatory lung disease that manifests itself in patients as acute respiratory distress syndrome and thereby contributes significantly to the morbidity and mortality of patients experiencing critical illness. Even though it may seem counterintuitive, as the lungs are typically well-oxygenated organs, hypoxia signaling pathways have recently been implicated in the resolution of ALI. For example, functional studies suggest that transcriptional responses under the control of the hypoxia-inducible factor (HIF) are critical in optimizing alveolar epithelial carbohydrate metabolism, and thereby dampen lung inflammation during ALI.

View Article and Find Full Text PDF

Objectives: To evaluate the feasibility and incremental diagnostic value of xenon-enhanced dual-energy CT in mechanically ventilated intensive care patients with worsening respiratory function.

Methods: The study was performed in 13 mechanically ventilated patients with severe pulmonary conditions (acute respiratory distress syndrome (ARDS), n=5; status post lung transplantation, n=5; other, n=3) and declining respiratory function. CT scans were performed using a dual-source CT scanner at an expiratory xenon concentration of 30%.

View Article and Find Full Text PDF
Article Synopsis
  • Lipopolysaccharide (LPS) is commonly used in inflammation studies, but this research introduces a new short-term sepsis model in rats via cecal ligation and incision (CLI) to compare its effects with LPS.
  • Both LPS and CLI caused significant drops in blood pressure and metabolic issues, but there were no notable differences between the two in terms of blood pressure and gas parameters.
  • LPS triggered higher levels of inflammatory markers (IL-1β, IL-6, TNF-α) than CLI, suggesting that the CLI model is effective for understanding hemodynamic changes in sepsis while indicating potential immunosuppression due to lower TNF-α levels.
View Article and Find Full Text PDF

Long-term administration of PUFA is known to modulate immune functions and apoptotic pathways depending on the respective amount of n-6 and n-3 fatty acids (FA). Data on short-term effects on apoptotic pathways are rare. Apoptosis of splenic lymphocytes is the hallmark of detrimental sepsis.

View Article and Find Full Text PDF

Objective: To evaluate the feasibility of dual-energy CT (DECT) ventilation imaging in combination with DE perfusion mapping for a comprehensive assessment of ventilation, perfusion, morphology and structure of the pulmonary parenchyma.

Methods: Two dual-energy CT acquisitions for xenon-enhanced ventilation and iodine-enhanced perfusion mapping were performed in patients under artificial respiration. Parenchymal xenon and iodine distribution were mapped and correlated with structural or vascular abnormalities.

View Article and Find Full Text PDF

High-pressure ventilation induces barotrauma and pulmonary inflammation, thus leading to ventilator-induced lung injury (VILI). IL-22 has both immunoregulatory and tissue-protective properties. Functional IL-22 receptor expression is restricted to nonleukocytic cells, such as alveolar epithelial cells.

View Article and Find Full Text PDF

Background: Initiated by a clinical case of critical endotracheal tube (ETT) obstruction, we aimed to determine factors that potentially contribute to the development of endotracheal tube obstruction by its inflated cuff. Prehospital climate and storage conditions were simulated.

Methods: Five different disposable ETTs (6.

View Article and Find Full Text PDF

The nuclear factor (NF)-kappaB/inhibitory (I)kappaBalpha pathway is one of the most important intracellular signal transduction pathways during inflammation which is induced by a variety of major early response cytokines. Recent studies suggest that volatile anesthetics interfere with inflammatory cytokine production through inhibition of intracellular signal transduction pathways. We, therefore, aimed to investigate the effects of the volatile anesthetics sevoflurane and isoflurane on NF-kappaB/IkappaBalpha-dependent intracellular signal transduction in human monocytic THP-1 cells induced by tumor necrosis factor-alpha (TNF-alpha) and production of interleukin-8 (IL-8) and downstream heme oxygenase-1 (HO-1).

View Article and Find Full Text PDF

Background: High-pressure ventilation induces barotrauma and pulmonary inflammation, thus leading to ventilator-induced lung injury (VILI). By limiting the pulmonal inflammation cascade the anti-inflammatory cytokine interleukin (IL)-10 may have protective effects. Via inhalation, IL-10 reaches the pulmonary system directly and in high concentrations.

View Article and Find Full Text PDF

Objectives: Mechanical ventilation during critical care can cause structural and functional disturbances in the lung with subsequent release of proinflammatory mediators, termed ventilator-induced lung injury (VILI). VILI progressively provokes decreased efficiency of gas exchange with subsequent hypoxic pulmonary vasoconstriction leading to cardiopulmonary alterations, such as pulmonary hypertension and right heart failure. We therefore aimed to evaluate whether inhalation therapy with levosimendan, a calcium-sensitizer with pulmonary vasodilating properties, could attenuate VILI and improve short-term survival in a rat experimental model.

View Article and Find Full Text PDF

Background: Sepsis is a leading cause of death among critically ill patients. Up to now, severe sepsis with acute onset in animals has been induced mainly through injection of single bacteria species or endotoxin and not through a surgical procedure, which might adequately mirror the situation in septic patients. We therefore aimed to establish a surgical model of severe sepsis in rodents fulfilling international sepsis criteria.

View Article and Find Full Text PDF

Though often lifesaving, mechanical ventilation itself bears the risk of lung damage [ventilator-induced lung injury (VILI)]. The underlying molecular mechanisms have not been fully elucidated, but stress-induced mediators seem to play an important role in biotrauma related to VILI. Our purpose was to evaluate an animal model of VILI that allows the observation of pathophysiologic changes along with parameters of biotrauma.

View Article and Find Full Text PDF

Volatile anesthetics such as isoflurane have been shown to offer anti-inflammatory effects during experimental endotoxemia whereas the alpha-adrenergic vasopressor norepinephrine exhibits proinflammatory properties on systemic cytokine release under the same conditions. However, during major surgery and in patients with systemic inflammatory response syndrome or sepsis both agents are frequently administered concurrently. We therefore aimed to investigate the influence of preexisting i.

View Article and Find Full Text PDF

Background: Recent studies suggest that volatile anaesthetics have anti-inflammatory and preconditioning properties and that beta-adrenoceptors are involved in the signalling pathways for these effects. Concurrently, the blockade of beta-adrenoceptors has been shown to augment the release of inflammatory mediators in response to pro-inflammatory stimuli. We therefore aimed to investigate whether the beta-adrenoceptor antagonist propranolol might modulate the anti-inflammatory effects of isoflurane on the systemic and pulmonary release of pro-inflammatory cytokines in endotoxemic rats.

View Article and Find Full Text PDF

Objective: We set out to investigate whether the nebulized and inhaled specific caspase-1 inhibitor Ac-YVAD-CHO has the potential to attenuate the pulmonary and systemic release of the caspase-1-dependent cytokines interleukin-1 beta (IL-1 beta) and interleukin-18 (IL-18) as well as their downstream enzymes iNOS and COX-2 in rat experimental endotoxaemia.

Design And Setting: Controlled, randomized animal study in a university research facility.

Subject: Male Sprague-Dawley rats (n=32) were randomly treated as follows: Inhaled Ac-YVAD-CHO was administered in eight rats at a inhaled total dosage of 5 mg and in eight rats at a inhaled total dose of 0.

View Article and Find Full Text PDF

Objective: We aimed to clarify if inhaled interleukin (IL)-10 attenuates pulmonary and systemic inflammation as indicated by reduced content of proinflammatory mediators in bronchoalveolar lavage fluid (BALF) and plasma in experimental endotoxemia in the rat.

Design: Laboratory experiment.

Setting: University research institute.

View Article and Find Full Text PDF

The authors have adjusted a jet nebulizer to a mechanical ventilator (Servo Ventilator, Siemens) to deliver an aerosol to rats. They aimed to clarify whether a modified jet nebulizer generating particles with a mass median aerodynamic diameter of 2 microm would be effective and safe in intubated ventilated rats. Fluorescent microspheres (diameter: 1.

View Article and Find Full Text PDF