title: Whole-body periodic acceleration reduces brain damage in a focal ischemia model.
abstract: Stroke is the second most common cause of death and major cause of disability worldwide. Actual treatment involves surgery and/or thrombolytic drugs, but there is an urgent need for new approaches. Periodic acceleration, a rocking headward to footward movement of the whole body, is a non-invasive method to induce pulsatile shear stress on the vascular endothelium eliciting an enhanced production and secretion of endothelium-derived products such as nitric oxide, prostacyclin, prostaglandin E2, tissue plasminogen activator (tPA), and adrenomedullin. All these products have been shown to protect the brain from ischemic injuries. A rat model of focal brain ischemia was treated with application of periodic acceleration for 3 h immediately after the onset of ischemia. Controls remained static for the same period of time. Brain damage was assessed by magnetic resonance imaging (MRI) and biochemical markers. A significant reduction in brain damage was observed, 7 days post-ischemia, in rocked rats when compared with the static controls, through MRI. Furthermore, rocked animals had significantly lower levels of Beclin 1 and fractin than their static counterparts, and some isoforms of nitric oxide synthase were regulated by periodic acceleration. Our results show that periodic acceleration may provide a novel, affordable, non-invasive therapeutic option for the treatment of stroke.
authors.affiliation: Department of Cellular, Molecular, and Developmental Neurobiology, Consejo Superior de Investigaciones Científicas, Madrid, Spain.
authors.forename: R
authors.initials: R
authors.lastname: Martínez-Murillo
authors.forename: J
authors.initials: J
authors.lastname: Serrano
authors.forename: A P
authors.initials: AP
authors.lastname: Fernández
authors.forename: A
authors.initials: A
authors.lastname: Martínez
mesh_terms: D000054:Acceleration; D000818:Animals; D051017:Apoptosis Regulatory Proteins / Q000235:genetics / Q000378:metabolism; D000071186:Beclin-1; D001930:Brain Injuries / Q000209:etiology* / Q000378:metabolism / Q000473:pathology / Q000628:therapy*; D002545:Brain Ischemia / Q000139:chemically induced / Q000150:complications* / Q000209:etiology; D053148:Caspase 3 / Q000235:genetics / Q000378:metabolism; D004195:Disease Models, Animal; D019332:Endothelin-1; D005081:Exercise Therapy / Q000379:methods*; D005786:Gene Expression Regulation / Q000502:physiology; D008279:Magnetic Resonance Imaging / Q000379:methods; D008297:Male; D019001:Nitric Oxide Synthase / Q000235:genetics / Q000378:metabolism; D010507:Periodicity; D051381:Rats; D017208:Rats, Wistar; D013997:Time Factors
chemical_list: D051017:Apoptosis Regulatory Proteins; D000071186:Beclin-1; C512829:Becn1 protein, rat; D019332:Endothelin-1; D019001:Nitric Oxide Synthase; D053148:Caspase 3