Fluid Resuscitation With Isotonic or Hypertonic Saline Solution Avoids Intraneural Calcium Influx After Traumatic Brain Injury Associated With Hemorrhagic Shock
Contribuinte(s) |
UNIVERSIDADE DE SÃO PAULO |
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Data(s) |
19/10/2012
19/10/2012
2010
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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. FAPESP (Fundacao de Amparo a Pesquisa do Estado de Sao Paulo)[04/15964-6] |
Identificador |
JOURNAL OF TRAUMA-INJURY INFECTION AND CRITICAL CARE, v.68, n.4, p.859-864, 2010 0022-5282 http://producao.usp.br/handle/BDPI/21520 10.1097/TA.0b013e3181af69d3 |
Idioma(s) |
eng |
Publicador |
LIPPINCOTT WILLIAMS & WILKINS |
Relação |
Journal of Trauma-injury Infection and Critical Care |
Direitos |
restrictedAccess Copyright LIPPINCOTT WILLIAMS & WILKINS |
Palavras-Chave | #Calcium metabolism #Hemorrhage #Hypertonic saline #Traumatic brain injury #Shock #INTRACRANIAL-PRESSURE #MULTICENTER TRIAL #LACTATED RINGERS #SODIUM-CHLORIDE #HEAD-INJURY #HYPOTENSION #7.5-PERCENT #EPIDEMIOLOGY #MANNITOL #DEATHS #Critical Care Medicine #Surgery |
Tipo |
article original article publishedVersion |