			Home About us Contact

Hypothermia Treatment (hypothermia + treatment)

Distribution by Scientific Domains

Medical Sciences	80%

Selected Abstracts

Antiapoptotic Cardioprotective Effect of Hypothermia Treatment Against Oxidative Stress Injuries

ACADEMIC EMERGENCY MEDICINE, Issue 9 2009
Chien-Hua Huang MD
Abstract Objectives:, The effect of hypothermia on cardiomyocyte injury induced by oxidative stress remains unclear. The authors investigated the effects of hypothermia on apoptosis and mitochondrial dysfunction in cardiomyocytes exposed to oxidative stress. Methods:, Cardiomyocytes (H9c2) derived from embryonic rat heart cell culture were exposed to either normothermic (37°C) or hypothermic (31°C) environments before undergoing oxidative stress via treatment with hydrogen peroxide (H2O2). The degree of apoptosis was determined by annexin V and terminal deoxynucleotidyl transferase (TUNEL) staining. The amount of reactive oxygen species (ROS) was compared after H2O2 exposure between normo- and hypothermic-pretreated groups. Mitochondrial dysfunction in both groups was measured by differential reductase activity and transmembrane potential (,,m). Results:, Hydrogen peroxide induced significant apoptosis in both normothermic and hypothermic cardiomyocytes. Hypothermia ameliorated apoptosis as demonstrated by decreased annexin V staining (33 ± 1% vs. 49 ± 4%; p < 0.05) and TUNEL staining (27 ± 17% vs. 80 ±25%; p < 0.01). The amount of intracellular ROS increased after H2O2 treatment and was higher in the hypothermic group than that in the normothermic group (237.9 ± 31.0% vs. 146.6 ± 20.6%; p < 0.05). In the hypothermic group, compared with the normothermic group, after H2O2 treatment mitochondrial reductase activity was greater (72.0 ± 17.9% vs. 27.0 ± 13.3%; p < 0.01) and the mitochondria ,,m was higher (101.0 ± 22.6% vs. 69.7 ± 12.9%; p < 0.05). Pretreatment of cardiomyocytes with the antioxidant ascorbic acid diminished the hypothermia-induced increase in intracellular ROS and prevented the beneficial effects of hypothermia on apoptosis and mitochondrial function. Conclusions:, Hypothermia at 31°C can protect cardiomyocytes against oxidative stress,induced injury by decreasing apoptosis and mitochondrial dysfunction through intracellular ROS-dependent pathways. [source]

Hypothermia treatment potentiates ERK1/2 activation after traumatic brain injury

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 4 2007
Coleen M. Atkins
Abstract Traumatic brain injury (TBI) results in significant hippocampal pathology and hippocampal-dependent memory loss, both of which are alleviated by hypothermia treatment. To elucidate the molecular mechanisms regulated by hypothermia after TBI, rats underwent moderate parasagittal fluid-percussion brain injury. Brain temperature was maintained at normothermic or hypothermic temperatures for 30 min prior and up to 4 h after TBI. The ipsilateral hippocampus was assayed with Western blotting. We found that hypothermia potentiated extracellular signal-regulated kinase 1/2 (ERK1/2) activation and its downstream effectors, p90 ribosomal S6 kinase (p90RSK) and the transcription factor cAMP response element-binding protein. Phosphorylation of another p90RSK substrate, Bad, also increased with hypothermia after TBI. ERK1/2 regulates mRNA translation through phosphorylation of mitogen-activated protein kinase-interacting kinase 1 (Mnk1) and the translation factor eukaryotic initiation factor 4E (eIF4E). Hypothermia also potentiated the phosphorylation of both Mnk1 and eIF4E. Augmentation of ERK1/2 activation and its downstream signalling components may be one molecular mechanism that hypothermia treatment elicits to improve functional outcome after TBI. [source]

Hypothetical pathophysiology of acute encephalopathy and encephalitis related to influenza virus infection and hypothermia therapy

PEDIATRICS INTERNATIONAL, Issue 2 2000
Shumpei Yokota
AbstractBackground: To establish a treatment strategy for acute encephalopathy and encephalitis associated with influenza virus infection, the pathophysiology of the disease was investigated through manifestations and laboratory findings of patients. Patients and Methods: A child with central nervous system (CNS) complications during the course of influenza virus infection was analyzed in view of immunologic abnormalities. In addition, four children with acute encephalopathy and encephalitis were enrolled in the hypothermia treatment for the purpose of stabilizing the cytokine storm in the CNS. Results: The CNS symptoms preceded the systemic progression to the failure of multiple organs (MOF) and disseminated intravascular coagulopathy (DIC). The mild hypothermia suppressed the brain edema on computed tomography (CT) scanning and protected the brain from the subsequent irreversible neural cell damage. Conclusion: The replicated viruses at the nasopharyngeal epithelium may disrupt the olfactory mucosa and gain access to the brain via the olfactory nerve system. The direct virus,glial cell interaction or viral stimulation of the glial cells induces the production and accumulation of the pro-inflammatory cytokines, especially tumor necrosis factor (TNF)-,, in the CNS. The cytokine storm results in neural cell damage as well as the apoptosis of astrocytes, due to the TNF-,,induced mitochondrial respiratory failure. The disruption of the blood,brain barrier progresses to the systemic cytokine storm, resulting in DIC and MOF. Mild hypothermia appears promising in stabilizing the immune activation and the brain edema to protect the brain from ongoing functional, apoptotic neural and glial damage and the systemic expansion of the cytokine storm. [source]

The prognostic value of early aEEG in asphyxiated infants undergoing systemic hypothermia treatment

ACTA PAEDIATRICA, Issue 4 2010
B Hallberg
Abstract Background:, Induced moderate hypothermia (HT) for 72 h has been shown to reduce the combined outcome of death or severe neurodevelopmental disabilities in asphyxiated full-term infants. A pathological amplitude integrated EEG background as early as 3,6 h after birth, has been shown to correlate to poor prognosis. Aim:, The aim of this study was to investigate the correlation between amplitude integrated EEG during HT treatment and short-term outcome in asphyxiated full-term infants with moderate/severe hypoxic-ischaemic encephalopathy. Methods:, Between December 2006 and December 2007, 24 infants were treated with moderate HT (33.5°C for 72 h) using a cooling mattress. Motor functions were assessed at 4 and 12 months of age. Results:, Of the total birth cohort of 28,837 infants, 26 infants fulfilled the criteria for HT treatment (0.9/1000) of whom 23 was treated with HT and all of these infants had available amplitude integrated EEG data. Normal 1-year outcome was found in 10/15 infants with severely abnormal burst-suppression pattern or worse at 6 h of age. Severe abnormalities were found to be significantly predictive for abnormal outcome after 36 h. Conclusion:, Among asphyxiated infants treated with HT, only those who had aEEG abnormalities persisting at and beyond 24 h after birth showed poor neurological outcome at 1 year. [source]

Passive induction of hypothermia during transport of asphyxiated infants: a risk of excessive cooling

ACTA PAEDIATRICA, Issue 6 2009
Boubou Hallberg
Abstract Background: Induced mild hypothermia is an emerging therapy that has been shown to reduce the combined outcome of death or severe neurodevelopmental disabilities in asphyxiated full-term infants if started within 6 h after birth. Aim: To study the feasibility and safety of inducing hypothermia in asphyxiated infants already at the referring hospital by stopping active warming. Methods: Temperatures during passive induction of hypothermia were prospectively collected from transported asphyxiated infants. Results: Between December 2006 and April 2008, 37 infants of the total birth cohort of 40 350 fulfilled the criteria for hypothermia treatment. Eighteen of 34 infants treated with induced hypothermia were outborn. The rectal temperatures of the infants were 33.0,36.4°C before transport and 31.0,36.5°C on arrival. Six of the infants had a sub-therapeutic (<33.0°C) rectal temperature on arrival. Conclusion: Passive induction of hypothermia by turning off active warming devices is possible, making an earlier start of hypothermia achievable. However, there is a substantial risk of unintended excessive cooling; therefore, continuous monitoring of the central temperature is mandatory when such a strategy is used. [source]