Effects of Hypothermic Metabolic Suppression on Hippocampal Glutamate Concentrations After Transient Global Cerebral Ischemia

Illievich, U. M.; Zornow, Mark H.; Choi, Kyu Taek; Scheller, Mark S.; Strnat, Martin A. P.

doi:10.1213/00000539-199405000-00012

Cited by 88 publications

(28 citation statements)

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“…37,41,[43][44][45] Hypothermia is thought to play a neuroprotective role after ROSC by decreasing metabolic demand, 46,47 decreasing the release of excitatory neurotransmitters, 16 and decreasing inflammation. 48 Animal studies since the 1980s [49][50][51][52][53][54][55][56][57] have suggested that mild induced hypothermia may be beneficial as a neuroprotectant after cardiac arrest. In addition, human literature describes a beneficial effect of mild induced hypothermia in resuscitated post cardiac arrest patients.…”

Section: Discussionmentioning

confidence: 99%

Systematic review of randomized controlled trials of therapeutic hypothermia as a neuroprotectant in post cardiac arrest patients

Cheung

Green

Magee

2006

CJEM

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Objective: Several randomized controlled trials have suggested that mild induced hypothermia may improve neurologic outcome in comatose cardiac arrest survivors. This systematic review of randomized controlled trials was designed to determine if mild induced hypothermia improves neurologic outcome, decreases mortality, or is associated with an increased incidence of adverse events. Science (1989 to November 2005. For each included study, references were reviewed and the primary author contacted to identify any additional studies. Study selection: Studies that met inclusion criteria were randomized controlled trials of adult patients (>18 years of age) with primary cardiac arrest who remained comatose after return of spontaneous circulation. Patients had to be randomized to mild induced hypothermia (32°C-34°C) or normothermia within 24 hours of presentation. Only studies reporting pre-determined outcomes including discharge neurologic outcome, mortality or significant treatment-related adverse events were included. There were no language or publication restrictions. Data synthesis: Four studies involving 436 patients, with 232 cooled to a core temperature of 32°C-34°C met inclusion criteria. Pooled data demonstrated that mild hypothermia decreased inhospital mortality (relative ratio [RR] 0.75; 95% confidence interval [CI], 0.62-0.92) and reduced the incidence of poor neurologic outcome (RR 0.74; 95% CI, 0.62-0.84). Numbers needed to treat were 7 patients to save 1 life, and 5 patients to improve neurologic outcome. There was no evidence of treatment-limiting side effects. Conclusions: Therapeutically induced mild hypothermia decreases in-hospital mortality and improves neurologic outcome in comatose cardiac arrest survivors. The possibility of treatment-limiting side effects cannot be excluded. RÉSUMÉObjectif : Plusieurs essais comparatifs randomisés ont suggéré qu'une légère hypothermie provoquée peut améliorer le résultat clinique chez les victimes d'arrêt cardiaque dans le coma. La

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Section: Discussionmentioning

confidence: 99%

Systematic review of randomized controlled trials of therapeutic hypothermia as a neuroprotectant in post cardiac arrest patients

Cheung

Green

Magee

2006

CJEM

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“…Neuroprotection would appear to function by enhancing maintenance of intracellular ATP levels during short HI episodes [19,[27][28] . Mild hypothermia also suppresses the release of free oxygen radicals, cytokines and excitatory neurotransmitters [29][30][31] .…”

Section: Discussionmentioning

confidence: 99%

Safety of Deep Hypothermia in Treating Neonatal Asphyxia

et al. 2007

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Background: Several studies have demonstrated the efficiency and safety of mild hypothermia (33°C) used for treating moderate encephalopathy. In animal models, deep hypothermia proved to be neuroprotective. Objectives: To determine the safety of whole-body deep hypothermia between 30 and 33°C in moderate-severe hypoxic-ischemic encephalopathy in newborn term infants. Methods: Mortality rates, incidence of brain damage detected by magnetic resonance imaging (MRI) and neurological outcomes of 39 term asphyxiated infants were retrospectively compared. A first group of patients (control group C) was treated with routine standard methods, a second group (MH) was treated with mild whole-body hypothermia (32–34°C) and a third group (DH) was treated with deep whole-body hypothermia (30–33°C), for 72 h. Mean arterial pH, basic excess (BE) and lactic acid in the blood were measured. Laboratory and clinical side effects of hypothermia were investigated. A conventional brain MRI was performed after the second week of life. Results: 39 term asphyxiated newborns were enrolled in the study: 11 in group C, 10 in group MH, and 18 in group DH. During the first 72 h, disseminated intravascular coagulation was recorded in 2 cases (18%) in group C, pulmonary hypertension in 2 patients (20%) in group MH, and pneumonia in 3 cases (16%) in group DH. Severe cerebral lesions and poor neurological outcome were observed in 4 cases (36%) in group C, 1 case (10%) in group MH, and 1 case (5%) in group DH. A statistically significant difference in brain damage and major clinical neurological abnormalities was observed between group C and groups MH and DH, whereas no differences were demonstrated between asphyxiated infants treated with mild or deep hypothermia. Conclusions: The results support the safety of deep hypothermia. Further studies are needed to confirm these results and the neuroprotective effect of this approach.

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“…Increasing evidence suggests that brain hypothermia improves neurologic outcome after successful resuscitation from cardiac arrest. 5,6 The mechanism by which this occurs is likely multifactorial and includes: reduced cerebral oxygen uptake (7% /ЊC), 25 attenuated cerebral energy failure, 26 reduced cerebral edema, 27 slowed adenosine triphosphate (ATP) depletion/depolarization, 28 delayed ischemic intercellular calcium elevation/intercellular acidosis, 29 reduced release of excitatory amino acids, including glutamate, glycine, and aspartate, 28,30,31 attenuated free radical-induced damage to lipids, 32,33 reduced activation of nitric oxide, 34 and decreased protein kinase C activity. 34 The optimal method by which hypothermic therapy is instituted continues to be debated.…”

Section: Discussionmentioning

confidence: 99%

Untitled

2001

Academic Emergency Medicine

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Abstract. Objectives: Increasing human and laboratory evidence suggests that post-resuscitative brain hypothermia reduces the pathologic consequences of brain ischemia. Using a swine model of prolonged cardiac arrest, this investigation sought to determine whether unilateral hypothermic carotid bypass was capable of inducing selective brain hypothermia and reducing neurohistologic damage. Methods: Ventricular fibrillation was induced in common swine (n = 12). After 20 minutes of cardiopulmonary arrest (without ventilatory support or cardiopulmonary resuscitation), systemic extracorporeal bypass was instituted to restore coronary and cerebral perfusion, followed by restoration of normal sinus rhythm. Animals randomized to the normal brain temperature (NBT) cohort received mechanical ventilation and intravenous fluids for 24 hours. The selective brain hypothermia (SBH) cohort received 12 hours of femoral/ carotid bypass at 32ЊC. The bypass temperature was then increased one degree per hour until reaching 37ЊC and continued at this temperature until completion of the protocol (24 hours). Histopathologic damage was evaluated in two areas of the hippocampus. Results: Normal sinus rhythm was restored in all animals after the systemic (femoral/femoral) bypass was initiated. Nasal temperature (surrogate measure of brain temperature) remained higher than 37.0ЊC throughout the 24-hour recovery period in the NBT animals. In the SBH cohort, right nasal temperature dropped to the mild hypothermic range (<34ЊC) two hours after institution of femoral/carotid bypass. This was maintained throughout the 12-hour cooling period without hemodynamic compromise. There was a significant improvement in the neurohistology scores in the CA1 region of the hippocampus of the SBH treated animals as compared with those of the NBT cohort. Conclusions: Post-resuscitative selective brain hypothermia reduced regional ischemic brain damage in swine with prolonged ventricular fibrillation.

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Effects of Hypothermic Metabolic Suppression on Hippocampal Glutamate Concentrations After Transient Global Cerebral Ischemia

Cited by 88 publications

References 0 publications

Systematic review of randomized controlled trials of therapeutic hypothermia as a neuroprotectant in post cardiac arrest patients

Systematic review of randomized controlled trials of therapeutic hypothermia as a neuroprotectant in post cardiac arrest patients

Safety of Deep Hypothermia in Treating Neonatal Asphyxia

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