Fluid Resuscitation With Isotonic or Hypertonic Saline Solution Avoids Intraneural Calcium Influx After Traumatic Brain Injury Associated With Hemorrhagic Shock

Fluid Resuscitation With Isotonic or Hypertonic Saline Solution Avoids Intraneural Calcium Influx After Traumatic Brain Injury Associated With Hemorrhagic Shock

Autor Balbino, Marcos Google Scholar
Capone Neto, Antonio Google Scholar
Prist, Ricardo Google Scholar
Ferreira, Alice Teixeira Autor UNIFESP Google Scholar
Poli-de-Figueiredo, Luiz F. Google Scholar
Instituição Universidade de São Paulo (USP)
Universidade Federal de São Paulo (UNIFESP)
Resumo Background: Calcium is one of the triggers involved in ischemic neuronal death. Because hypotension is a strong predictor of outcome in traumatic brain injury (TBI), we tested the hypothesis that early fluid resuscitation blunts calcium influx in hemorrhagic shock associated to TBI.Methods: Fifteen ketamine-halothane anesthetized mongrel dogs (18.7 kg +/- 1.4 kg) underwent unilateral cryogenic brain injury. Blood was shed in 5 minutes to a target mean arterial pressure of 40 mm Hg to 45 mm Hg and maintained at these levels for 20 minutes (shed blood volume = 26 mL/kg +/- 7 mL/kg). Animals were then randomized into three groups: CT (controls, no fluid resuscitation), HS (7.5% NaCl, 4 mL/kg, in 5 minutes), and LR (lactate Ringer's, 33 mL/kg, in 15 minutes). Twenty minutes later, a craniotomy was performed and cerebral biopsies were obtained next to the lesion (clinical penumbra) and from the corresponding contralateral side (lesion's mirror) to determine intracellular calcium by fluorescence signals of Fura-2-loaded cells.Results: Controls remained hypotensive and in a low-flow state, whereas fluid resuscitation improved hemodynamic profile. There was a significant increase in intracellular calcium in the injured hemisphere in CT (1035 nM +/- 782 nM), compared with both HS (457 nM +/- 149 nM, p = 0.028) and LR (392 nM +/- 178 nM, p = 0.017), with no differences between HS and LR (p = 0.38). Intracellular calcium at the contralateral, uninjured hemisphere was 438 nM +/- 192 nM in CT, 510 nM +/- 196 nM in HS, and 311 nM +/- 51 nM in LR, with no significant differences between them.Conclusion: Both small volume hypertonic saline and large volume lactated Ringer's blunts calcium influx in early stages of TBI associated to hemorrhagic shock. No fluid resuscitation strategy promotes calcium influx and further neural damage.
Palavra-chave Calcium metabolism
Hemorrhage
Hypertonic saline
Traumatic brain injury
Shock
Idioma Inglês
Financiador Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Número do financiamento FAPESP: 04/15964-6
Data de publicação 2010-04-01
Publicado em Journal of Trauma-injury Infection and Critical Care. Philadelphia: Lippincott Williams & Wilkins, v. 68, n. 4, p. 859-864, 2010.
ISSN 0022-5282 (Sherpa/Romeo, fator de impacto)
Publicador Lippincott Williams & Wilkins
Extensão 859-864
Fonte http://dx.doi.org/10.1097/TA.0b013e3181af69d3
Direito de acesso Acesso restrito
Tipo Artigo
Web of Science WOS:000276663100020
Endereço permanente http://repositorio.unifesp.br/handle/11600/32447

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