Influence of Hypoxic and Hyperoxic Preconditioning on Endothelial
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Role of C5ar1 and C5L2 Receptors in Ischemia-Reperfusion Injury
Journal of Clinical Medicine Article Role of C5aR1 and C5L2 Receptors in Ischemia-Reperfusion Injury Carlos Arias-Cabrales 1,* , Eva Rodriguez-Garcia 1, Javier Gimeno 2, David Benito 3, María José Pérez-Sáez 1, Dolores Redondo-Pachón 1, Anna Buxeda 1, Carla Burballa 1, Marta Crespo 1, Marta Riera 3,* and Julio Pascual 1,* 1 Department of Nephrology, Parc de Salut Mar, 08003 Barcelona, Spain; [email protected] (E.R.-G.); [email protected] (M.J.P.-S.); [email protected] (D.R.-P.); [email protected] (A.B.); [email protected] (C.B.); [email protected] (M.C.) 2 Department of Pathology, Parc de Salut Mar, 08003 Barcelona, Spain; [email protected] 3 Kidney Research Group, Hospital del Mar Medical Research Institute, IMIM, 08003 Barcelona, Spain; [email protected] * Correspondence: [email protected] (C.A.-C.); [email protected] (M.R.); [email protected] (J.P.) Abstract: The role of C5a receptors (C5aR1 and C5L2) in renal ischemia-reperfusion injury (IRI) is uncertain. We generated an in vitro model of hypoxia/reoxygenation with human proximal tubule epithelial cells to mimic some IRI events. C5aR1, membrane attack complex (MAC) and factor H (FH) deposits were evaluated with immunofluorescence. Quantitative polymerase chain reaction evaluated the expression of C5aR1, C5L2 genes as well as genes related to tubular injury, inflammation, and profibrotic pathways. Additionally, C5aR1 and C5L2 deposits were evaluated in kidney graft biopsies (KB) from transplant patients with delayed graft function (DGF, n = 12) and compared with Citation: Arias-Cabrales, C.; a control group (n = 8). We observed higher immunofluorescence expression of C5aR1, MAC and FH Rodriguez-Garcia, E.; Gimeno, J.; as higher expression of genes related to tubular injury, inflammatory and profibrotic pathways and Benito, D.; Pérez-Sáez, M.J.; of C5aR1 in the hypoxic cells; whereas, C5L2 gene expression was unaffected by the hypoxic stimulus. -
Respiratory and Gastrointestinal Involvement in Birth Asphyxia
Academic Journal of Pediatrics & Neonatology ISSN 2474-7521 Research Article Acad J Ped Neonatol Volume 6 Issue 4 - May 2018 Copyright © All rights are reserved by Dr Rohit Vohra DOI: 10.19080/AJPN.2018.06.555751 Respiratory and Gastrointestinal Involvement in Birth Asphyxia Rohit Vohra1*, Vivek Singh2, Minakshi Bansal3 and Divyank Pathak4 1Senior resident, Sir Ganga Ram Hospital, India 2Junior Resident, Pravara Institute of Medical Sciences, India 3Fellow pediatrichematology, Sir Ganga Ram Hospital, India 4Resident, Pravara Institute of Medical Sciences, India Submission: December 01, 2017; Published: May 14, 2018 *Corresponding author: Dr Rohit Vohra, Senior resident, Sir Ganga Ram Hospital, 22/2A Tilaknagar, New Delhi-110018, India, Tel: 9717995787; Email: Abstract Background: The healthy fetus or newborn is equipped with a range of adaptive, strategies to reduce overall oxygen consumption and protect vital organs such as the heart and brain during asphyxia. Acute injury occurs when the severity of asphyxia exceeds the capacity of the system to maintain cellular metabolism within vulnerable regions. Impairment in oxygen delivery damage all organ system including pulmonary and gastrointestinal tract. The pulmonary effects of asphyxia include increased pulmonary vascular resistance, pulmonary hemorrhage, pulmonary edema secondary to cardiac failure, and possibly failure of surfactant production with secondary hyaline membrane disease (acute respiratory distress syndrome).Gastrointestinal damage might include injury to the bowel wall, which can be mucosal or full thickness and even involve perforation Material and methods: This is a prospective observational hospital based study carried out on 152 asphyxiated neonates admitted in NICU of Rural Medical College of Pravara Institute of Medical Sciences, Loni, Ahmednagar, Maharashtra from September 2013 to August 2015. -
Reperfusion Injury in Stroke
Reperfusion Injury in Stroke Thanapon Songthammawat,MD Outlines • Overview • Symptoms of cerebral reperfusion syndrome • Causes of cerebral reperfusion injury • Reperfusion Injury After Thrombolytic Therapy • Reperfusion Injury After Endovascular Mechanical Thrombectomy • Assessment of Risk for Reperfusion Injury in Carotid Endarterectomy and Stenting • Prevention of Reperfusion Injury Reperfusion syndrome • Cerebral hyperperfusion, or reperfusion syndrome • Rare, but serious • Complication following revascularization • Rapid restoration of normal perfusion pressure • Reperfusion syndrome can occur as a complication of thrombolytic therapy for AIS, carotid endarterectomy (CEA), intracranial stenting, and even bland cerebral infarction. • However, not all patients with hyperperfusion are symptomatic • Patients with only moderate rises in CBF can have severe outcomes • Outcomes are dependent on timely recognition and prevention of precipitating factors • Most important is the treatment of hypertension • Reperfusion injury is involved directly in the potentiation of stroke damage • Components of the inflammatory response, including cytokine release and leukocyte adhesion, appear to play key roles in these effects. • Damage to the blood-brain barrier (BBB), an important factor in reperfusion injury • Postcontrast image 24 hours after a right middle cerebral artery stroke, demonstrating contrast extravasation through a faulty blood-brain barrier. Causes of Cerebral Reperfusion Injury • Several mechanisms • As time passes following arterial -
Acute Effects of Mechanical Ventilation with Hyperoxia on the Morphometry of the Rat Diaphragm
ISSN 1413-3555 Rev Bras Fisioter, São Carlos, v. 13, n. 6, p. 487-92, nov./dez. 2009 ARTIGO ORIGIN A L ©Revista Brasileira de Fisioterapia Efeitos agudos da ventilação mecânica com hiperoxia na morfometria do diafragma de ratos Acute effects of mechanical ventilation with hyperoxia on the morphometry of the rat diaphragm Célia R. Lopes1, André L. M. Sales2, Manuel De J. Simões3, Marco A. Angelis4, Nuno M. L. Oliveira5 Resumo Contextualização: A asssistência ventilória mecânica (AVM) prolongada associada a altas frações de oxigênio produz impacto negativo na função diafragmática. No entanto, não são claros os efeitos agudos da AVM associada a altas frações de oxigênio em pulmões aparentemente sadios. Objetivo: Analisar os efeitos agudos da ventilação mecânica com hiperóxia na morfometria do diafragma de ratos. Métodos: Estudo experimental prospectivo, com nove ratos Wistar, com peso de 400±20 g, randomizados em dois grupos: controle (n=4), anestesiados, traqueostomizados e mantidos em respiração espontânea em ar ambiente por 90 minutos e experimental (n=5), também anestesiados, curarizados, traqueostomizados e mantidos em ventilação mecânica controlada pelo mesmo tempo. Foram submetidos à toracotomia mediana para coleta da amostra das fibras costais do diafragma que foram seccionadas a cada 5 µm e coradas pela hematoxilina e eosina para o estudo morfométrico. Para a análise estatística, foi utilizado o teste t de Student não pareado, com nível de significância de p<0,05. Resultados: Não foram encontrados sinais indicativos de lesão muscular aguda, porém observou-se dilatação dos capilares sanguíneos no grupo experimental. Os dados morfométricos do diâmetro transverso máximo da fibra muscular costal foram em média de 61,78±17,79 µm e de 70,75±9,93 µm (p=0,045) nos grupos controle e experimental respectivamente. -
Subacute Normobaric Oxygen and Hyperbaric Oxygen Therapy in Drowning, Reversal of Brain Volume Loss: a Case Report
[Downloaded free from http://www.medgasres.com on Monday, July 3, 2017, IP: 12.22.86.35] CASE REPORT Subacute normobaric oxygen and hyperbaric oxygen therapy in drowning, reversal of brain volume loss: a case report Paul G. Harch1, *, Edward F. Fogarty2 1 Department of Medicine, Section of Emergency Medicine, University Medical Center, Louisiana State University School of Medicine, New Orleans, LA, USA 2 Department of Radiology, University of North Dakota School of Medicine, Bismarck, ND, USA *Correspondence to: Paul G. Harch, M.D., [email protected] or [email protected]. orcid: 0000-0001-7329-0078 (Paul G. Harch) Abstract A 2-year-old girl experienced cardiac arrest after cold water drowning. Magnetic resonance imaging (MRI) showed deep gray mat- ter injury on day 4 and cerebral atrophy with gray and white matter loss on day 32. Patient had no speech, gait, or responsiveness to commands on day 48 at hospital discharge. She received normobaric 100% oxygen treatment (2 L/minute for 45 minutes by nasal cannula, twice/day) since day 56 and then hyperbaric oxygen treatment (HBOT) at 1.3 atmosphere absolute (131.7 kPa) air/45 minutes, 5 days/week for 40 sessions since day 79; visually apparent and/or physical examination-documented neurological improvement oc- curred upon initiating each therapy. After HBOT, the patient had normal speech and cognition, assisted gait, residual fine motor and temperament deficits. MRI at 5 months after injury and 27 days after HBOT showed near-normalization of ventricles and reversal of atrophy. Subacute normobaric oxygen and HBOT were able to restore drowning-induced cortical gray matter and white matter loss, as documented by sequential MRI, and simultaneous neurological function, as documented by video and physical examinations. -
Mechanisms of Ischemia-Reperfusion Injury (IRI)
MechanismsMechanisms ofof IschemiaIschemia--ReperfusionReperfusion InjuryInjury (IRI)(IRI) To make a complex story simple Pasquale Pagliaro Dpt of Clinical and Biological Sciences University of Torino, Italy The Bad Ischemia: the occlusion of a coronary artery http://amazingworldofbiol.wix.com/ The Good REPERFUSION: the reopening of a coronary artery The Ugly Reperfusion Injury: at the re-opening of a coronary artery Diagram depicts critical events in cardiac ischemia reperfusion injury (Suleiman et al 2001) ImportantImportant FactorsFactors toto DetermineDetermine IschemiaIschemia andand ReperfusionReperfusion InjuryInjury IS Duration of ischemia t Collateral circulation formation Dependency on Condition of Reperfusion and Oxygen Supply The speed/modality of reperfusion The components of reperfusion solution Why Reperfusion Injury? ExperimentalExperimental studystudy showedshowed thethe importanceimportance ofof Calcium overload pH recovery ( pH paradox ) The Central Role of Mitochondria, mitochondrial Permeability Transition Pore (mPTP) and «Reactive Oxygen Species» (ROS) Why Coronary Ischemia ? •• 1010 FactorsFactors ThatThat IncreaseIncrease thethe RiskRisk ofof HeartHeart DiseaseDisease andand HeartHeart AttackAttack :: • 1) Tobacco Smoke • 2) High Blood Cholesterol • 3) High Blood Pressure • 4) Physical Inactivity • 5) Obesity and Overweight • 6) Diabetes Mellitus • 7) Stress • 8) Alcohol • 9) Diet and Nutrition • 10) Age Ischemic Heart Disease (IHD) The leading cause of death in human population • It is the most common type -
Short-Time Intermittent Preexposure of Living Human Donors To
Hindawi Publishing Corporation Journal of Transplantation Volume 2011, Article ID 204843, 8 pages doi:10.1155/2011/204843 Clinical Study Short-Time Intermittent Preexposure of Living Human Donors to Hyperoxia Improves Renal Function in Early Posttransplant Period: A Double-Blind Randomized Clinical Trial Kamran Montazeri,1 Mohammadali Vakily,1 Azim Honarmand,1 Parviz Kashefi,1 Mohammadreza Safavi,1 Shahram Taheri,2 and Bahram Rasoulian3 1 Anesthesiology and Critical Care Research Center, Isfahan University of Medical Sciences, P.O. Box 8174675731, Isfahan 81744, Iran 2 Isfahan Kidney Diseases Research Center (IKRC) and Internal Medicine Department, Alzahra Hospital, Isfahan University of Medical Sciences, P.O. Box 8174675731, Isfahan 81744, Iran 3 Research Center and Department of Physiology, Lorestan University of Medical Sciences, P.O. Box 6814617767, Khorramabad, Iran Correspondence should be addressed to Azim Honarmand, [email protected] Received 6 November 2010; Revised 5 January 2011; Accepted 26 January 2011 Academic Editor: Wojciech A. Rowinski´ Copyright © 2011 Kamran Montazeri et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The purpose of this human study was to investigate the effect of oxygen pretreatment in living kidney donors on early renal function of transplanted kidney. Sixty living kidney donor individuals were assigned to receive either 8–10 L/min oxygen (Group I) by a non-rebreather mask with reservoir bag intermittently for one hour at four times (20, 16, 12, and 1 hours before transplantation) or air (Group II). -
Oxygen Content in Semi-Closed Rebreathing Apparatuses for Underwater Use. Measurements and Modeling
Doctoral Thesis in Technology and Health Stockholm, Sweden 2015 Oxygen content in semi-closed rebreathing apparatuses for underwater use. Measurements and modeling OSKAR FRÅNBERG KTH ROYAL INSTITUTE OF TECHNOLOGY ENGINEERING SCIENCES Oxygen content in semi-closed rebreathing apparatuses for underwater use. Measurements and modeling OSKAR FRÅNBERG Doctoral thesis No. 6 2015 KTH Royal Institute of Technology Engineering Sciences Department of Environmental Physiology SE-171 65, Solna, Sweden ii TRITA-STH Report 2015:6 ISSN 1653-3836 ISRN/KTH/STH/2015:6-SE ISBN 978-91-7595-616-9 Akademisk avhandling som med tillstånd av KTH i Stockholm framlägges till offentlig granskning för avläggande av teknisk doktorsexamen fredagen den 25/9 2015 kl. 09:00 i sal D2 KTH, Lindstedtsvägen 5, Stockholm. iii Messen ist wissen, aber messen ohne Wissen ist kein Wissen Werner von Siemens Å meta e å veta Som man säger på den Kungliga Tekniska Högskolan i Hufvudstaden Att mäta är att väta Som man säger i dykeriforskning Till min familj Olivia, Artur och Filip iv v Abstract The present series of unmanned hyperbaric tests were conducted in order to investigate the oxygen fraction variability in semi-closed underwater rebreathing apparatuses. The tested rebreathers were RB80 (Halcyon dive systems, High springs, FL, USA), IS-Mix (Interspiro AB, Stockholm, Sweden), CRABE (Aqua Lung, Carros Cedex, France), and Viper+ (Cobham plc, Davenport, IA, USA). The tests were conducted using a catalytically based propene combusting metabolic simulator. The metabolic simulator connected to a breathing simulator, both placed inside a hyperbaric pressure chamber, was first tested to demonstrate its usefulness to simulate human respiration in a hyperbaric situation. -
Hyperoxia Induces Glutamine-Fuelled Anaplerosis in Retinal Mã¼ller Cells
ARTICLE https://doi.org/10.1038/s41467-020-15066-6 OPEN Hyperoxia induces glutamine-fuelled anaplerosis in retinal Müller cells Charandeep Singh 1, Vincent Tran1, Leah McCollum1, Youstina Bolok1, Kristin Allan1,2, Alex Yuan1, ✉ George Hoppe1, Henri Brunengraber3 & Jonathan E. Sears 1,4 Although supplemental oxygen is required to promote survival of severely premature infants, hyperoxia is simultaneously harmful to premature developing tissues such as in the retina. 1234567890():,; Here we report the effect of hyperoxia on central carbon metabolism in primary mouse Müller glial cells and a human Müller glia cell line (M10-M1 cells). We found decreased flux from glycolysis entering the tricarboxylic acid cycle in Müller cells accompanied by increased glutamine consumption in response to hyperoxia. In hyperoxia, anaplerotic catabolism of glutamine by Müller cells increased ammonium release two-fold. Hyperoxia induces glutamine-fueled anaplerosis that reverses basal Müller cell metabolism from production to consumption of glutamine. 1 Ophthalmic Research, Cole Eye Institute, Cleveland Clinic, Cleveland, OH 44195, USA. 2 Molecular Medicine, Case Western Reserve School of Medicine Cleveland, Cleveland, OH 44106, USA. 3 Department of Nutrition, Case Western Reserve School of Medicine Cleveland, Cleveland, OH 44106, USA. ✉ 4 Cardiovascular and Metabolic Sciences, Cleveland Clinic, Cleveland, OH 44195, USA. email: [email protected] NATURE COMMUNICATIONS | (2020) 11:1277 | https://doi.org/10.1038/s41467-020-15066-6 | www.nature.com/naturecommunications 1 ARTICLE NATURE COMMUNICATIONS | https://doi.org/10.1038/s41467-020-15066-6 remature infants require oxygen supplementation to sur- We first ensured that the isotopic steady state was established for Pvive, but excess oxygen causes retinovascular growth sup- at least 20 h before treating part of the cells with hyperoxia. -
Life-Threatening Rhabdomyolysis Complicating Surgical Reperfusion of Peripheral Arterial Occlusive Disease — a Case Report and Literature Review
Case Report Chih-Hsuan Yen et al. Acta Cardiol Sin 2004;20:120-124 Life-threatening Rhabdomyolysis Complicating Surgical Reperfusion of Peripheral Arterial Occlusive Disease — A Case Report and Literature Review Chih-Hsuan Yen,1 Ping-Ying Lee,1,2 Charles Jia-Yin Hou,1 Yu-San Chou,1 Cheng-Ho Tsai1 Rhabdomyolysis is a rare complication following successful reperfusion of occluded peripheral arteries. Acute renal failure frequently develops in these patients, and it carries a high mortality rate. We report a 78-year-old female with near-total occlusion of bilateral femoral arteries. After successful femoral-popliteal artery bypass, she developed rhabdomyolysis with acute renal failure. Despite intensive support and treatment, she died of multiple-organ failure. Key Words: Rhabdomyolysis · Acute renal · Failure peripheral · Arterial occlusive disease INTRODUCTION nal failure after successful peripheral vascular surgery. Rhabdomyolysis, compartment syndrome, and crush syndrome represent a spectrum of the same disease,1,2 CASE REPORT which may be induced by numerous factors, including alcoholism, crush injury to a limb, overuse of skeletal A 78-year-old female suffered from right leg swell- muscle, heat, viral infections, metabolic disorder, ing, pallor, and pain and was not able to move her leg for myopathies, drugs, toxins, and hyperkalemia.1,3 2 weeks prior to admission. The patient had a history of Rhabdomyolysis is a rare complication after successful hypertension treated with amlodipine for 2 years and bypass surgery for peripheral vascular disease. Acute type 2 diabetes mellitus for 3 years. She did not smoke. myoglobinuric renal failure may further complicate the Toes of both legs were cyanotic and cold, and dorsalis situation, with catastrophic results. -
Improvement of Ischemic Cholangiopathy in Three Patients with Hereditary Hemorrhagic Telangiectasia Following Treatment with Bevacizumab
Case Report Improvement of ischemic cholangiopathy in three patients with hereditary hemorrhagic telangiectasia following treatment with bevacizumab Paraskevi A. Vlachou1, Errol Colak1, Alexander Koculym1, Anish Kirpalani1, Tae Kyoung Kim2, ⇑ ⇑ Gideon M. Hirschfield3,4, , , Marie E. Faughnan5,6, , 1Department of Diagnostic Imaging, St. Michael’s Hospital, 30 Bond Street, Toronto, ON, Canada M5B 1W8; 2Department of Diagnostic Imaging, Toronto General Hospital, 200 Elizabeth St., Toronto, ON, Canada M5G 2C4; 3Department of Medicine, Division of Gastroenterology, University of Toronto, Toronto, Canada; 4Centre for Liver Research, Institute of Biomedical Research, NIHR Biomedical Research Unit, University of Birmingham, Birmingham B15 2TT, UK; 5Department of Medicine, Division of Respirology, Toronto HHT Centre, St. Michael’s Hospital, Toronto, Canada; 6Keenan Research Centre of the Li Ka Shing Knowledge Institute of St. Michael’s Hospital, 30 Bond Street, Toronto, ON, Canada M5B 1W8 Abstract sias and visceral arteriovenous malformations [1]. Although radiological signs of liver involvement occur in more than 70% The ischemic biliary phenotype of hereditary hemorrhagic telan- of patients, less than 10% of these patients develop symptoms giectasia (HHT) is rare but distinct, with progressive biliary tree [2]. Symptomatic liver HHT from intrahepatic shunting can lead ischemia usually resulting in an irreversible secondary sclerosing to patients presenting with high-output cardiac failure (HOCF), cholangiopathy. When clinically severe, liver transplant is often portal hypertension or ischemic biliary disease [3,4]. A recent indicated. We report three patients with marked HHT Italian prospective cohort study found that over prolonged fol- associated biliary disease, in whom prolonged anti-vascular low-up, substantial morbidity and mortality were associated endothelial growth factor therapy (bevacizumab) notably with liver vascular malformations in HHT patients [5]. -
Clinical Pathophysiology of Hypoxic Ischemic Brain Injury After Cardiac Arrest: a “Two-Hit” Model Mypinder S
Sekhon et al. Critical Care (2017) 21:90 DOI 10.1186/s13054-017-1670-9 REVIEW Open Access Clinical pathophysiology of hypoxic ischemic brain injury after cardiac arrest: a “two-hit” model Mypinder S. Sekhon1,2*, Philip N. Ainslie2 and Donald E. Griesdale1,3,4 Abstract Hypoxic ischemic brain injury (HIBI) after cardiac arrest (CA) is a leading cause of mortality and long-term neurologic disability in survivors. The pathophysiology of HIBI encompasses a heterogeneous cascade that culminates in secondary brain injury and neuronal cell death. This begins with primary injury to the brain caused by the immediate cessation of cerebral blood flow following CA. Thereafter, the secondary injury of HIBI takes place in the hours and days following the initial CA and reperfusion. Among factors that may be implicated in this secondary injury include reperfusion injury, microcirculatory dysfunction, impaired cerebral autoregulation, hypoxemia, hyperoxia, hyperthermia, fluctuations in arterial carbon dioxide, and concomitant anemia. Clarifying the underlying pathophysiology of HIBI is imperative and has been the focus of considerable research to identify therapeutic targets. Most notably, targeted temperature management has been studied rigorously in preventing secondary injury after HIBI and is associated with improved outcome compared with hyperthermia. Recent advances point to important roles of anemia, carbon dioxide perturbations, hypoxemia, hyperoxia, and cerebral edema as contributing to secondary injury after HIBI and adverse outcomes. Furthermore, breakthroughs in the individualization of perfusion targets for patients with HIBI using cerebral autoregulation monitoring represent an attractive area of future work with therapeutic implications. We provide an in-depth review of the pathophysiology of HIBI to critically evaluate current approaches for the early treatment of HIBI secondary to CA.