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Dive into the research topics where Sandra Hoegl is active.

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Featured researches published by Sandra Hoegl.


American Journal of Respiratory Cell and Molecular Biology | 2011

Protective Properties of Inhaled IL-22 in a Model of Ventilator-Induced Lung Injury

Sandra Hoegl; Patrick Scheiermann; Itamar Goren; Christian Hofstetter; Josef Pfeilschifter; Bernhard Zwissler; Heiko Mühl

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. When applied via inhalation, IL-22 reaches the pulmonary system directly and in high concentrations, and may protect alveolar epithelial cells against cellular stress and biotrauma associated with VILI. In A549 lung epithelial cells, IL-22 was able to induce rapid signal transducer and activator of transcription (STAT)-3 phosphorylation/activation, and hereon mediated stable suppressor of cytokine signaling (SOCS) 3 expression detectable even 24 hours after onset of stimulation. In a rat model of VILI, the prophylactic inhalation of IL-22 before induction of VILI (peak airway pressure = 45 cm H(2)O) protected the lung against pulmonary disintegration and edema. IL-22 reduced VILI-associated biotrauma (i.e., pulmonary concentrations of macrophage inflammatory protein-2, IL-6, and matrix metalloproteinase 9) and mediated pulmonary STAT3/SOCS3 activation. In addition, despite a short observation period of 4 hours, inhaled IL-22 resulted in an improved survival of the rats. These data support the hypothesis that IL-22, likely via activation of STAT3 and downstream genes (e.g., SOCS3), is able to protect against cell stretch and pulmonary baro-/biotrauma by enhancing epithelial cell resistibility.


European Radiology | 2010

Pulmonary ventilation and perfusion imaging with dual-energy CT

Sven F. Thieme; Sandra Hoegl; Konstantin Nikolaou; Juergen Fisahn; Michael Irlbeck; Daniel Maxien; Maximilian F. Reiser; Christoph Becker; Thorsten R. C. Johnson

ObjectiveTo 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.MethodsTwo 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.ResultsIn all datasets, image quality was sufficient for a comprehensive image reading of the pulmonary CTA images, lung window images and pulmonary functional parameter maps and led to expedient results in each patient.ConclusionWith dual-source CT systems, DECT of the lung with iodine or xenon administration is technically feasible and makes it possible to depict the regional iodine or xenon distribution representing the local perfusion and ventilation.


Intensive Care Medicine | 2009

Effects of intravenous and inhaled levosimendan in severe rodent sepsis

Patrick Scheiermann; Devan Ahluwalia; Sandra Hoegl; Andrea Dolfen; Marc Revermann; Bernhard Zwissler; Heiko Mühl; Kim A. Boost; Christian Hofstetter

PurposeWe aimed at comparing the effects of intravenous (i.v.) and inhaled (inh.) levosimendan (LEVO) on survival, inflammatory cytokines and the apoptotic mediator caspase-3 in a rat model of severe sepsis induced by cecal ligation and incision (CLI).MethodsTwenty-eight anesthetized/ventilated male Sprague–Dawley rats (body weight 528xa0±xa020xa0g) underwent laparotomy. Cecal mobilisation served as control (SHAM, nxa0=xa07). In all other groups, severe sepsis was induced by CLI. No further intervention occurred in the CLI-group (nxa0=xa07). 180xa0min after CLI, 24xa0μg/kg i.v. LEVO was administered in the CLIxa0+xa0LEVO-IV-group (nxa0=xa07), and 24xa0μg/kg inh. LEVO was administered via jet nebulizer in the CLIxa0+xa0LEVO-INH-group (nxa0=xa07).ResultsCLI induced arterial hypotension, with i.v. and inh. LEVO attenuating blood pressure decrease over 390xa0min [CLI 34(31/50), CLIxa0+xa0LEVO-IV 82(69/131)*, CLIxa0+xa0LEVO-INH 78(62/85)* mmHg; median(25/75% quartile), *Pxa0<xa00.05]. CLI induced metabolic acidosis. I.v. and inh. LEVO avoided arterial pH [CLI 7.18(7.16/7.2), CLIxa0+xa0LEVO-IV 7.27(7.24/7.31)*, CLIxa0+xa0LEVO-INH 7.26(7.24/7.28)*] and base excess deterioration [CLI −19(−21.8/−17.9), CLIxa0+xa0LEVO-IV −13(−14.8/−12)*, CLIxa0+xa0LEVO-INH −12.7(−14/−12.2)*xa0mmol/l]. Overall mortality in the CLI-group was 57% compared to 0%* in both LEVO-treated groups after 390xa0min. LEVO administration significantly attenuated the increase in proinflammatory interleukin (IL)-1β [CLI 896(739/911), CLIxa0+xa0LEVO-IV 302(230/385)*, CLIxa0+xa0LEVO-INH 346(271/548)xa0pg/ml] and IL-6 [CLI 35651(31413/35816), CLIxa0+xa0LEVO-IV 21156(18397/28026), CLIxa0+xa0LEVO-INH 13674(10105/24843)xa0pg/ml] in the plasma and reduced cleaved caspase-3 expression in the spleen.ConclusionsIn a rat model of severe sepsis induced by CLI, i.v. and inh. LEVO equally attenuated arterial hypotension, metabolic acidosis and prolonged survival. Moreover, i.v. and inh. LEVO inhibited proinflammatory mediator release and reduced splenic caspase-3 expression.


Critical Care Medicine | 2008

Inhaled levosimendan reduces mortality and release of proinflammatory mediators in a rat model of experimental ventilator-induced lung injury.

Kim A. Boost; Sandra Hoegl; Andrea Dolfen; Holger Czerwonka; Patrick Scheiermann; Bernhard Zwissler; Christian Hofstetter

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. Design:Experimental animal model. Setting:University hospital. Subjects:Forty male Sprague-Dawley rats. Interventions:Rats were randomly treated as follows (n = 8, each group): 1) inhalation of the solvent only before induction of VILI, no further intervention; 2) inhalation of 240 &mgr;g of levosimendan before VILI induction; 3) inhalation of 24 &mgr;g of levosimendan before VILI induction; 4) intravenous administration of 24 &mgr;g/kg levosimendan before VILI induction; 5) control group with surgical preparation only. All groups were observed for 4 hrs. Measurements and Main Results:After 4 hrs following induction of VILI, levels of interleukin-1&bgr; and macrophage inflammatory protein-2 in plasma and bronchoalveolar lavage fluid were analyzed by enzyme-linked immunosorbent assay. Nitric oxide release from alveolar macrophages was measured by Griess assay. Content of matrix metalloproteinase-2 and matrix metalloproteinase-9 in bronchoalveolar lavage fluid was analyzed by gelatin zymography. Inhalation of 240 &mgr;g of levosimendan significantly improved survival after 4 hrs and mean arterial blood pressure compared with VILI only. Additionally, inhalation of 240 &mgr;g and infusion of 24 &mgr;g/kg levosimendan significantly reduced the release of interleukin-1&bgr;, the nitric oxide release from alveolar macrophages, macrophage inflammatory protein-2 in plasma, and the macrophage inflammatory protein-2 and matrix metalloproteinase-9 content in bronchoalveolar lavage fluid compared with VILI only. Conclusions:Our study demonstrates that prophylactic inhalation of 240 &mgr;g of levosimendan improves survival and reduces release of inflammatory mediators in our experimental model of VILI. This might affect the clinical prophylaxis and treatment of VILI.


Journal of Immunology | 2015

Alveolar Epithelial A2B Adenosine Receptors in Pulmonary Protection during Acute Lung Injury

Sandra Hoegl; Michael R. Blackburn; Harry Karmouty-Quintana; Bernhard Zwissler; Holger K. Eltzschig

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. In this context, we hypothesized that tissue-specific expression of the A2B adenosine receptor is responsible for the previously described attenuation of ALI. To address this hypothesis, we exposed mice with tissue-specific deletion of Adora2b to ALI, utilizing a two-hit model where intratracheal LPS treatment is followed by injurious mechanical ventilation. Interestingly, a head-to-head comparison of mice with deletion of Adora2b in the myeloid lineage (Adora2bloxP/loxP LysM Cre+), endothelial cells (Adora2bloxP/loxP VE-cadherin Cre+), or alveolar epithelial cells (Adora2bloxP/loxP SPC Cre+) revealed a selective increase in disease susceptibility in Adora2bloxP/loxP SPC Cre+ mice. More detailed analysis of Adora2bloxP/loxP SPC Cre+ mice confirmed elevated lung inflammation and attenuated alveolar fluid clearance. To directly deliver an A2B adenosine receptor–specific agonist to alveolar epithelial cells, we subsequently performed studies with inhaled BAY 60-6583. Indeed, aerosolized BAY 60-6583 treatment was associated with attenuated pulmonary edema, improved histologic lung injury, and dampened lung inflammation. Collectively, these findings suggest that alveolar epithelial A2B adenosine receptor signaling contributes to lung protection, and they implicate inhaled A2B adenosine receptor agonists in ALI treatment.


Respiratory Medicine | 2009

Inhaled IL-10 reduces biotrauma and mortality in a model of ventilator-induced lung injury

Sandra Hoegl; Kim A. Boost; Holger Czerwonka; Andrea Dolfen; Patrick Scheiermann; Heiko Mühl; Bernhard Zwissler; Christian Hofstetter

BACKGROUNDnHigh-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.nnnMETHODSnThirty six male, anesthetized and mechanically ventilated Sprague-Dawley rats were randomly assigned to the following groups (n=9, each): SHAM: pressure controlled ventilation with p(max)=20cmH(2)O, PEEP=4; VILI: ventilator settings were changed for 20min to p(max)=45cmH(2)O, PEEP=0; IL-10(high): inhalation of 10microg/kg IL-10 prior to induction of VILI; and IL-10(low): inhalation of 1microg/kg IL-10 prior to induction of VILI. All groups were ventilated and observed for 4h.nnnRESULTSnHigh-pressure ventilation increased the concentrations of macrophage inflammatory protein (MIP)-2 and IL-1beta in bronchoalveolar lavage fluid (BALF) and plasma. This effect was reduced by the inhalation of IL-10 (10microg/kg). Additionally, IL-10 increased the animal survival time (78% vs. 22% 4-h mortality rate) and reduced NO-release from ex vivo cultured alveolar macrophages. Moreover, VILI-induced pulmonary heat shock protein-70 expression was reduced by IL-10 aerosol in a dose-dependent manner. Similarly, the activation of matrix metalloproteinase (MMP)-9 in BALF was reduced dose-dependently by IL-10. IL-10-treated animals showed a lower macroscopic lung injury score and less impairment of lung integrity and gas exchange.nnnCONCLUSIONSnProphylactic inhalation of IL-10 improved survival and reduced lung injury in experimental VILI. Results indicate that this effect may be mediated by the inhibition of stress-induced inflammation and pulmonary biotrauma.


Journal of Applied Physiology | 2015

Hypoxia signaling during acute lung injury

Christine U. Vohwinkel; Sandra Hoegl; Holger K. Eltzschig

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. In the present review we discuss functional roles of oxygenation, hypoxia and HIFs during ALI, mechanisms of how HIFs are stabilized during lung inflammation, and how HIFs can mediate lung protection during ALI.


European Journal of Radiology | 2013

Worsening respiratory function in mechanically ventilated intensive care patients: feasibility and value of xenon-enhanced dual energy CT.

Sandra Hoegl; Felix G. Meinel; Sven F. Thieme; Thorsten R. C. Johnson; Oliver Eickelberg; Bernhard Zwissler; Konstantin Nikolaou

OBJECTIVESnTo evaluate the feasibility and incremental diagnostic value of xenon-enhanced dual-energy CT in mechanically ventilated intensive care patients with worsening respiratory function.nnnMETHODSnThe 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%. Both ventilation images (Xe-DECT) and standard CT images were reconstructed from a single CT scan. Findings were recorded for Xe-DECT and standard CT images separately. Ventilation defects on xenon images were matched to morphological findings on standard CT images and incremental diagnostic information of xenon ventilation images was recorded if present.nnnRESULTSnMean xenon consumption was 2.95 l per patient. No adverse events occurred under xenon inhalation. In the visual CT analysis, the Xe-DECT ventilation defects matched with pathologic changes in lung parenchyma seen in the standard CT images in all patients. Xe-DECT provided additional diagnostic findings in 4/13 patients. These included preserved ventilation despite early pneumonia (n=1), more confident discrimination between a large bulla and pneumothorax (n=1), detection of an airway-to-pneumothorax fistula (n=1) and exclusion of a suspected airway-to-mediastinum fistula (n=1). In all 4 patients, the additional findings had a substantial impact on patients management.nnnCONCLUSIONSnXenon-enhanced DECT is safely feasible and can add relevant diagnostic information in mechanically ventilated intensive care patients with worsening respiratory function.


Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine | 2010

Cuff overinflation and endotracheal tube obstruction: case report and experimental study

Christian Hofstetter; Bertram Scheller; Sandra Hoegl; Martin G. Mack; Bernhard Zwissler; Christian Byhahn

BackgroundInitiated 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.MethodsFive different disposable ETTs (6.0, 7.0, and 8.0 mm inner diameter) were exposed to ambient outside temperature for 13 months. In addition, every second of these tubes was mechanically stressed by clamping its cuffed end between the covers of a metal emergency case for 10 min. Then, all tubes were heated up to normal body temperature, placed within the cock of a syringe, followed by stepwise inflation of their cuffs to pressures of 3 kPa and ≥12 kPa, respectively. The inner lumen of the ETT was checked with the naked eye for any obstruction caused by the external cuff pressure.ResultsNeither in tubes that were exposed to ambient temperature (range: -12°C to +44°C) nor in those that were also clamped, visible obstruction by inflated cuffs was detected at any of the two cuff pressure levels.ConclusionsWe could not demonstrate a critical obstruction of an ETT by its inflated cuff, neither when the cuff was over-inflated to a pressure of 12 kPa or higher, nor in ETTs that had been exposed to unfavorable storage conditions and significant mechanical stress.


International Immunopharmacology | 2011

Comparing hemodynamics, blood gas analyses and proinflammatory cytokines in endotoxemic and severely septic rats

Patrick Scheiermann; Sandra Hoegl; Christian Hofstetter; Josef Pfeilschifter; Bernhard Zwissler; Heiko Mühl; Kim A. Boost; Bertram Scheller

Lipopolysaccharide (LPS) is often used in short-term models of inflammation. Since endotoxemia and sepsis are different entities we have recently established a short-term sepsis model in rats induced by cecal ligation and incision (CLI). This retrospective study was conducted in order to identify similarities and differences between both experimental approaches. 32 anesthetized/ventilated male rats from the following four groups were analysed (each n=8): CTRL-group (0.9% NaCl i.v.); LPS-group (5mg/kg i.v.); SHAM-group (laparotomy); CLI-group (1.5 cm blade incision). Mean arterial blood pressure (MAP) and blood gas parameters (arterial base excess (BE) and pH) were continuously recorded. Total observation time was 300 min. Plasma samples were obtained afterwards. LPS and CLI induced significant arterial hypotension and metabolic acidosis compared to CTRL- or SHAM-group, respectively. Yet, between the LPS- and CLI-groups, there were no differences in MAP, BE and pH. LPS significantly induced IL-1β, IL-6 and TNF-α in the plasma. In contrast, CLI showed a clear tendency towards increased IL-1β and IL-6 plasma levels and did not affect TNF-α. Our results indicate that the CLI sepsis model is suitable for short-term investigations on hemodynamic alterations and blood gas analyses during sepsis. 300 min after the proinflammatory insult, plasma concentrations of IL-1β and IL-6 in the plasma remain considerably lower after CLI compared to endotoxemia. Low TNF-α concentrations 300 min after sepsis induction could be interpreted as considerable immunosuppression during CLI sepsis.

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Holger K. Eltzschig

University of Texas Health Science Center at Houston

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Heiko Mühl

Goethe University Frankfurt

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Andrea Dolfen

Goethe University Frankfurt

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Bertram Scheller

Goethe University Frankfurt

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Kim A. Boost

Ludwig Maximilian University of Munich

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Eóin N. McNamee

University of Colorado Denver

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Michael R. Blackburn

University of Texas Health Science Center at Houston

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