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2. Nebulized Lipopolysaccharide Causes Delayed Cortical Neuroinflammation in a Murine Model of Acute Lung Injury.

Author

Ritter, Katharina, Rissel, René, Renz, Miriam, Ziebart, Alexander, Schäfer, Michael K. E., and Kamuf, Jens

Subjects
LUNG injuries, CEREBRAL cortex, LABORATORY mice, RESPIRATORY infections, LIPOPOLYSACCHARIDES, SEPSIS
Abstract

Lung injury caused by respiratory infection is a major cause of hospitalization and mortality and a leading origin of sepsis. Sepsis-associated encephalopathy and delirium are frequent complications in patients with severe lung injury, yet the pathogenetic mechanisms remain unclear. Here, 70 female C57BL/6 mice were subjected to a single full-body-exposure with nebulized lipopolysaccharide (LPS). Neuromotor impairment was assessed repeatedly and brain, blood, and lung samples were analyzed at survival points of 24 h, 48 h, 72 h, and 96 h after exposure. qRT-PCR revealed increased mRNA-expression of TNFα and IL-1β 24 h and 48 h after LPS-exposure in the lung, concomitantly with increased amounts of proteins in bronchoalveolar lavage and interstitial lung edema. In the cerebral cortex, at 72 h and/or 96 h after LPS exposure, the inflammation- and activity-associated markers TLR4, GFAP, Gadd45b, c-Fos, and Arc were increased. Therefore, single exposure to nebulized LPS not only triggers an early inflammatory reaction in the lung but also induces a delayed neuroinflammatory response. The identified mechanisms provide new insights into the pathogenesis of sepsis-associated encephalopathy and might serve as targets for future therapeutic approaches. [ABSTRACT FROM AUTHOR]

Published
2024
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3. Analysis of the Effects of Epidural Anesthesia on the Nociception Level Index (NOL ®) during Abdominal Surgery.

Author

Ziebart, Alexander, Rothgerber, David-Jonas, Woldt, Sophia, Mackert, Katharina, Heiden, Julia, Schuster, Michael, Kamuf, Jens, Griemert, Eva-Verena, and Ruemmler, Robert

Subjects
EPIDURAL anesthesia, LOCAL anesthesia, EPIDURAL catheters, UROLOGICAL surgery, LOCAL anesthetics, PHOTOPLETHYSMOGRAPHY
Abstract

Background: The NOL® system (PMD-200™ Nociception Level Monitor; Medasense Ltd., Ramat Gan, Israel) is used for the real-time detection of physiological nociception in anesthetized patients by assessing the parameters indicative of sympathetic activity, such as photoplethysmography, skin conductance, peripheral temperature, and accelerometry, which are quantified into the NOL®-Index. This index is more sensitive than traditional clinical parameters in estimating pain and stress responses. While its effectiveness in general anesthesia is well documented, its efficacy in epidural anesthesia needs further investigation. Methods: This retrospective study analyzed NOL®-Index dynamics compared to conventional parameters after epidural administration of bupivacaine. Following ethics committee approval, 119 NOL® measurements were retrospectively analyzed after thoracic epidural catheter administration in 40 patients undergoing abdominal and urological surgery. The NOL-Index® was assessed at 0, 1, 3, and 5 min post application and compared to heart rate, blood pressure, and bispectral index dynamics. Results: This study showed a significant decrease in the NOL®-Index post-local-anesthetic administration with better sensitivity than classical clinical parameters (0 min = 38 ± 11; 1 min = 22 ± 13*; 3 min = 17 ± 11*; 5 min = 12 ± 10*). Higher doses of local anesthetics led to a significant, dose-dependent decrease in NOL®-Index (low dose, 5 min = 15 ± 10*; high dose, 5 min = 8 ± 8*). Conclusions: This study is the first to demonstrate the effectiveness of the NOL®-Index in measuring nociceptive effects following epidural administration, highlighting its potential superiority over conventional parameters and its sensitivity to dose variations. [ABSTRACT FROM AUTHOR]

Published
2024
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11. Experimental lung injury induces cerebral cytokine mRNA production in pigs

Author

Kamuf, Jens, primary, Garcia Bardon, Andreas, additional, Ziebart, Alexander, additional, Frauenknecht, Katrin, additional, Folkert, Konstantin, additional, Schwab, Johannes, additional, Ruemmler, Robert, additional, Renz, Miriam, additional, Cana, Denis, additional, Thal, Serge C., additional, and Hartmann, Erik K., additional

Published
2020
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15. Lung injury does not aggravate mechanical ventilation-induced early cerebral inflammation or apoptosis in an animal model

Author

Eckle, Tobias, Eckle, T ( Tobias ), Kamuf, Jens; https://orcid.org/0000-0003-2170-8510, Garcia-Bardon, Andreas, Ziebart, Alexander, Thomas, Rainer, Folkert, Konstantin, Frauenknecht, Katrin; https://orcid.org/0000-0002-1372-3297, Thal, Serge C; https://orcid.org/0000-0002-1222-8729, Hartmann, Erik K, Eckle, Tobias, Eckle, T ( Tobias ), Kamuf, Jens; https://orcid.org/0000-0003-2170-8510, Garcia-Bardon, Andreas, Ziebart, Alexander, Thomas, Rainer, Folkert, Konstantin, Frauenknecht, Katrin; https://orcid.org/0000-0002-1372-3297, Thal, Serge C; https://orcid.org/0000-0002-1222-8729, and Hartmann, Erik K

Abstract

Introduction The acute respiratory distress syndrome is not only associated with a high mortality, but also goes along with cognitive impairment in survivors. The cause for this cognitive impairment is still not clear. One possible mechanism could be cerebral inflammation as result of a “lung-brain-crosstalk”. Even mechanical ventilation itself can induce cerebral inflammation. We hypothesized, that an acute lung injury aggravates the cerebral inflammation induced by mechanical ventilation itself and leads to neuronal damage. Methods After approval of the institutional and state animal care committee 20 pigs were randomized to one of three groups: lung injury by central venous injection of oleic acid (n = 8), lung injury by bronchoalveolar lavage in combination with one hour of injurious ventilation (n = 8) or control (n = 6). Brain tissue of four native animals from a different study served as native group. For six hours all animals were ventilated with a tidal volume of 7 ml kg-1 and a scheme for positive end-expiratory pressure and inspired oxygen fraction, which was adapted from the ARDS network tables. Afterwards the animals were killed and the brains were harvested for histological (number of neurons and microglia) and molecular biologic (TNFalpha, IL-1beta, and IL-6) examinations. Results There was no difference in the number of neurons or microglia cells between the groups. TNFalpha was significantly higher in all groups compared to native (p < 0.05), IL-6 was only increased in the lavage group compared to native (p < 0.05), IL-1beta showed no difference between the groups. Discussion With our data we can confirm earlier results, that mechanical ventilation itself seems to trigger cerebral inflammation. This is not aggravated by acute lung injury, at least not within the first 6 hours after onset. Nevertheless, it seems too early to dismiss the idea of lung-injury induced cerebral inflammation, as 6 hours might be just not enough time to see any profound eff

Published
2018

21. Pentaerythritol Tetranitrate Improves Angiotensin II–Induced Vascular Dysfunction via Induction of Heme Oxygenase-1

Author

Schuhmacher, Swenja, primary, Wenzel, Philip, additional, Schulz, Eberhard, additional, Oelze, Matthias, additional, Mang, Christian, additional, Kamuf, Jens, additional, Gori, Tommaso, additional, Jansen, Thomas, additional, Knorr, Maike, additional, Karbach, Susanne, additional, Hortmann, Marcus, additional, Mäthner, Falk, additional, Bhatnagar, Aruni, additional, Förstermann, Ulrich, additional, Li, Huige, additional, Münzel, Thomas, additional, and Daiber, Andreas, additional

Published
2010
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22. Abstract 5522: Improvement of Angiotensin-II-Induced Vascular Dysfunction and Oxidative Stress by the Organic Nitrate Pentaerithrityl Tetranitrate Depends on Heme Oxygenase-1-Induction

Author

Wenzel, Philip, primary, Schuhmacher, Swenja, additional, Schulz, Eberhard, additional, Oelze, Matthias, additional, Kamuf, Jens, additional, Gori, Tommaso, additional, Hortmann, Marcus, additional, Bhatnagar, Aruni, additional, Daiber, Andreas, additional, and Münzel, Thomas, additional

Published
2009
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23. Lung injury does not aggravate mechanical ventilation-induced early cerebral inflammation or apoptosis in an animal model

Author

Rainer Thomas, Serge C. Thal, Erik K. Hartmann, Konstantin Folkert, Andreas Garcia-Bardon, Alexander Ziebart, Katrin Frauenknecht, Jens Kamuf, University of Zurich, Eckle, Tobias, and Kamuf, Jens

Subjects
Male, ARDS, Critical Care and Emergency Medicine, Pulmonology, Swine, Physiology, medicine.medical_treatment, Ventilator-Induced Lung Injury, Interleukin-1beta, lcsh:Medicine, Apoptosis, Pathology and Laboratory Medicine, Hippocampus, Positive-Pressure Respiration, Random Allocation, 0302 clinical medicine, Animal Cells, Immune Physiology, Medicine and Health Sciences, lcsh:Science, Immune Response, Acute Respiratory Distress Syndrome, Tidal volume, Cerebral Cortex, Neurons, Cognitive Impairment, Respiratory Distress Syndrome, Innate Immune System, Multidisciplinary, medicine.diagnostic_test, Cognitive Neurology, Brain, General Medicine, Lung Injury, Neurology, Anesthesia, Breathing, Cytokines, Tumor necrosis factor alpha, medicine.symptom, Anatomy, Cellular Types, General Agricultural and Biological Sciences, Research Article, Histology, Cognitive Neuroscience, Immunology, 10208 Institute of Neuropathology, Inflammation, 610 Medicine & health, Genetics and Molecular Biology, Glial Cells, 1100 General Agricultural and Biological Sciences, Lung injury, 03 medical and health sciences, Signs and Symptoms, Respiratory Failure, 1300 General Biochemistry, Genetics and Molecular Biology, Diagnostic Medicine, medicine, Animals, Microglial Cells, Mechanical ventilation, 1000 Multidisciplinary, business.industry, Interleukin-6, Tumor Necrosis Factor-alpha, lcsh:R, Biology and Life Sciences, 030208 emergency & critical care medicine, Cell Biology, Molecular Development, medicine.disease, Respiration, Artificial, Bronchoalveolar lavage, 030228 respiratory system, Immune System, Cellular Neuroscience, General Biochemistry, 570 Life sciences, biology, Cognitive Science, lcsh:Q, business, Developmental Biology, Neuroscience
Abstract

INTRODUCTION:The acute respiratory distress syndrome is not only associated with a high mortality, but also goes along with cognitive impairment in survivors. The cause for this cognitive impairment is still not clear. One possible mechanism could be cerebral inflammation as result of a "lung-brain-crosstalk". Even mechanical ventilation itself can induce cerebral inflammation. We hypothesized, that an acute lung injury aggravates the cerebral inflammation induced by mechanical ventilation itself and leads to neuronal damage. METHODS:After approval of the institutional and state animal care committee 20 pigs were randomized to one of three groups: lung injury by central venous injection of oleic acid (n = 8), lung injury by bronchoalveolar lavage in combination with one hour of injurious ventilation (n = 8) or control (n = 6). Brain tissue of four native animals from a different study served as native group. For six hours all animals were ventilated with a tidal volume of 7 ml kg-1 and a scheme for positive end-expiratory pressure and inspired oxygen fraction, which was adapted from the ARDS network tables. Afterwards the animals were killed and the brains were harvested for histological (number of neurons and microglia) and molecular biologic (TNFalpha, IL-1beta, and IL-6) examinations. RESULTS:There was no difference in the number of neurons or microglia cells between the groups. TNFalpha was significantly higher in all groups compared to native (p < 0.05), IL-6 was only increased in the lavage group compared to native (p < 0.05), IL-1beta showed no difference between the groups. DISCUSSION:With our data we can confirm earlier results, that mechanical ventilation itself seems to trigger cerebral inflammation. This is not aggravated by acute lung injury, at least not within the first 6 hours after onset. Nevertheless, it seems too early to dismiss the idea of lung-injury induced cerebral inflammation, as 6 hours might be just not enough time to see any profound effect.

Published
2018

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