Mechanical versus humoral determinants of brain death-induced lung injury
| Autor: | Jacques Creteur, Birgit Weynand, Laurence Dewachter, Benoît Rondelet, Myriam Remmelink, Christian Melot, Asmae Belhaj, Céline Dewachter, Kathleen Mc Entee, Emeline Hupkens, Robert Naeije, Sandrine Rorive |
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| Přispěvatelé: | UCL - SSS/IREC/MONT - Pôle Mont Godinne, UCL - (MGD) Service de chirurgie cardio-vasculaire et thoracique |
| Jazyk: | angličtina |
| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
Pathology Physiology Neutrophils Sus scrofa lcsh:Medicine Lung -- pathology -- physiopathology Vascular permeability Blood Pressure Apoptosis Cushing reflex Pathology and Laboratory Medicine Vascular Medicine White Blood Cells 0302 clinical medicine Animal Cells Physiologie générale Reflexes Immune Physiology Medicine and Health Sciences Edema Brain Damage lcsh:Science Immune Response Lung Intracranial pressure Innate Immune System Multidisciplinary Oxygen -- metabolism Cell Death respiratory system Acute Lung Injury -- blood -- etiology -- physiopathology medicine.anatomical_structure Neurology Cell Processes Cytokines Female Cellular Types Brain Death -- blood -- pathology -- physiopathology Research Article medicine.medical_specialty Brain Death Immune Cells Partial Pressure Immunology Acute Lung Injury Lung injury Interleukins -- metabolism RNA Messenger -- genetics -- metabolism 03 medical and health sciences Signs and Symptoms Diagnostic Medicine Internal medicine medicine.artery medicine Animals RNA Messenger Peroxidase Inflammation Neutrophils -- pathology Blood Cells Cell Adhesion Molecules -- genetics -- metabolism Peroxidase -- metabolism business.industry Tumor Necrosis Factor-alpha Interleukins lcsh:R Hemodynamics Biology and Life Sciences Cell Biology Molecular Development respiratory tract diseases Immunity Humoral Oxygen Oxidative Stress 030104 developmental biology Blood pressure Endocrinology Gene Expression Regulation Immune System Pulmonary artery Multivariate Analysis Vascular resistance Respiratory Mechanics lcsh:Q Tumor Necrosis Factor-alpha -- metabolism business Cell Adhesion Molecules 030217 neurology & neurosurgery Neuroscience Developmental Biology |
| Zdroj: | PloS one, 12 (7 PLoS ONE PLoS One, Vol. 12, no. 7, p. e0181899 [1-22] (2017) PLoS ONE, Vol 12, Iss 7, p e0181899 (2017) |
| Popis: | Background: The mechanisms of brain death (BD)-induced lung injury remain incompletely understood, as uncertainties persist about time-course and relative importance of mechanical and humoral perturbations. Methods: Brain death was induced by slow intracranial blood infusion in anesthetized pigs after randomization to placebo (n = 11) or to methylprednisolone (n = 8) to inhibit the expression of pro-inflammatory mediators. Pulmonary artery pressure (PAP), wedged PAP (PAWP), pulmonary vascular resistance (PVR) and effective pulmonary capillary pressure (PCP) were measured 1 and 5 hours after Cushing reflex. Lung tissue was sampled to determine gene expressions of cytokines and oxidative stress molecules, and pathologically score lung injury. Results: Intracranial hypertension caused a transient increase in blood pressure followed, after brain death was diagnosed, by persistent increases in PAP, PCP and the venous component of PVR, while PAWP did not change. Arterial PO2/fraction of inspired O2 (PaO2/FiO2) decreased. Brain death was associated with an accumulation of neutrophils and an increased apoptotic rate in lung tissue together with increased pro-inflammatory interleukin (IL)-6/IL-10 ratio and increased heme oxygenase(HO)-1 and hypoxia inducible factor(HIF)-1 alpha expression. Blood expressions of IL-6 and IL-1β were also increased. Methylprednisolone pre-treatment was associated with a blunting of increased PCP and PVR venous component, which returned to baseline 5 hours after BD, and partially corrected lung tissue biological perturbations. PaO2/ FiO2 was inversely correlated to PCP and lung injury score. Conclusions: Brain death-induced lung injury may be best explained by an initial excessive increase in pulmonary capillary pressure with increased pulmonary venous resistance, and was associated with lung activation of inflammatory apoptotic processes which were partially prevented by methylprednisolone. SCOPUS: ar.j info:eu-repo/semantics/published |
| Databáze: | OpenAIRE |
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