Long-lasting neuroprotective effect of postischemic hypothermia and treatment with an anti-inflammatory/antipyretic drug - Evidence for chronic encephalopathic processes following ischemia

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dc.contributor.authorCoimbra, Cicero [UNIFESP]
dc.contributor.authorDrake, M.
dc.contributor.authorBorisMoller, F.
dc.contributor.authorWieloch, T.
dc.contributor.institutionLUND UNIV
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.date.accessioned2018-06-18T12:12:07Z
dc.date.available2018-06-18T12:12:07Z
dc.date.issued1996-09-01
dc.description.abstractBackground and Purpose It has been recognized that post ischemic pharmacological interventions may delay the evolution of neuronal damage rather than provide long-lasting neuroprotection. Also, fever complicates recovery after stroke in humans. Here we report the effects of late postischemic treatment with hypothermia and an antipyretic/anti-inflammatory drug, dipyrone, on cell damage at 1 week and 2 months of survival.Methods Rats were subjected to 10 minutes of forebrain ischemia. Hypothermia (33 degrees C) was induced at 2 hours of recovery and maintained for 7 hours. Dipyrone (100 mg . kg(-1)IP) was given every 3 hours from 14 to 72 hours of recovery. Temperature was measured every 6 hours for 60 days. Neuronal damage was assessed at 7 days and 2 months of recovery.Results From 17 to 72 hours of recovery, a period of hyperthermia was observed, which dipyrone abolished but postischemic hypothermia treatment did not. Dipyrone treatment diminished neuronal damage by 43% at 7 days, and at 2 months of survival, a minor (168) protection was seen. Postischemic hypothermia treatment alone delayed neuronal damage. In contrast, combined treatment of hypothermia followed by dipyrone markedly diminished neuronal damage by more than 50% at both 7 days and 2 months of recovery.Conclusions Neuronal degeneration may be ongoing for months after a transient ischemic insult, and prolonged protective measures need to be instituted for long-lasting neuroprotective effects. Hyperthermia during recovery worsens ischemic damage, and processes associated with inflammation may contribute to the development of neuronal damage. An early and extended period of postischemic hypothermia provides a powerful and long-lasting protection if followed by treatment with anti-inflammatory/antipyretic drugs.en
dc.description.affiliationLUND UNIV,EXPT BRAIN RES LAB,S-22101 LUND,SWEDEN
dc.description.sourceWeb of Science
dc.format.extent1578-1585
dc.identifierhttp://dx.doi.org/10.1161/01.STR.27.9.1578
dc.identifier.citationStroke. Dallas: Amer Heart Assoc, v. 27, n. 9, p. 1578-1585, 1996.
dc.identifier.doi10.1161/01.STR.27.9.1578
dc.identifier.issn0039-2499
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/45633
dc.identifier.wosWOS:A1996VF03200023
dc.language.isoeng
dc.publisherAmer Heart Assoc
dc.relation.ispartofStroke
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjecttemperatureen
dc.subjectneuronal damageen
dc.subjectratsen
dc.subjecthypothermiaen
dc.subjectanti-inflammatory agentsen
dc.titleLong-lasting neuroprotective effect of postischemic hypothermia and treatment with an anti-inflammatory/antipyretic drug - Evidence for chronic encephalopathic processes following ischemiaen
dc.typeinfo:eu-repo/semantics/article
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