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RESEARCH PRODUCT
Lung injury does not aggravate mechanical ventilation-induced early cerebral inflammation or apoptosis in an animal model.
Rainer ThomasSerge C. ThalErik K. HartmannKonstantin FolkertAndreas Garcia-bardonAlexander ZiebartKatrin FrauenknechtJens Kamufsubject
MaleARDSCritical Care and Emergency MedicinePulmonologySwinePhysiologymedicine.medical_treatmentVentilator-Induced Lung InjuryInterleukin-1betalcsh:MedicineApoptosisPathology and Laboratory MedicineHippocampusPositive-Pressure RespirationRandom Allocation0302 clinical medicineAnimal CellsImmune PhysiologyMedicine and Health Scienceslcsh:ScienceImmune ResponseAcute Respiratory Distress SyndromeTidal volumeCerebral CortexNeuronsCognitive ImpairmentRespiratory Distress SyndromeInnate Immune SystemMultidisciplinarymedicine.diagnostic_testCognitive NeurologyBrainGeneral MedicineLung InjuryNeurologyAnesthesiaBreathingCytokinesTumor necrosis factor alphamedicine.symptomAnatomyCellular TypesGeneral Agricultural and Biological SciencesResearch ArticleHistologyCognitive NeuroscienceImmunology10208 Institute of NeuropathologyInflammation610 Medicine & healthGenetics and Molecular BiologyGlial Cells1100 General Agricultural and Biological SciencesLung injury03 medical and health sciencesSigns and SymptomsRespiratory Failure1300 General Biochemistry Genetics and Molecular BiologyDiagnostic MedicinemedicineAnimalsMicroglial CellsMechanical ventilationInflammation1000 Multidisciplinarybusiness.industryInterleukin-6Tumor Necrosis Factor-alphalcsh:RBiology and Life Sciences030208 emergency & critical care medicineCell BiologyMolecular Developmentmedicine.diseaseRespiration ArtificialBronchoalveolar lavage030228 respiratory systemImmune SystemCellular NeuroscienceGeneral Biochemistry570 Life sciences; biologyCognitive Sciencelcsh:QbusinessDevelopmental BiologyNeurosciencedescription
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.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 2018-08-09 | PloS one |