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Moderate Hypothermia (moderate + hypothermia)
Selected AbstractsMechanism of the protective effect of hypothermia on ammonia toxicity in astrocytesJOURNAL OF NEUROCHEMISTRY, Issue 2002C. Zwingmann Ammonia is a key factor in the pathogenesis of hepatic encephalopathy (HE). Acute ammonia treatment causes energy failure of astrocytes, which are able to compensate partly by increased anaerobic metabolism as a means of making up for the energetic shortfall. As hypothermia offers protection from severe encephalopathy and lactate accumulation in liver failure, we investigated the mechanism by which hypothermia protects against ammonia toxicity by multinuclear NMR spectroscopy. 12 h exposure to 5 mm NH4CL decreased the phosphocreatine (PCr)/creatine (Cr) and ATP/ADP ratios to 65 and 76% of control, increased synthesis and release of glutamine to 200,250% and led to a significant stimulation of glycolytic activity reflected by increased uptake and consumption of glucose and accumulation of de novo synthesized intra- and extracellular lactate to 161 and 230% of control. The protective effect of mild hypothermia was evident from inhibiton of lactate accumulation and restoration of ammonia-induced depletion of PCr/Cr. Moderate hypothermia led to an increase of PCr/Cr ratio and inhibited lactate synthesis to 14% of normothermic control, but did not prevent the ATP decrease. While hypothermia inhibited glycolytic flux, intracellular glutamine remained elevated. The results suggest that hypothermia-induced protection against ammonia toxicity results from reduction of cellular energy demand leading to inhibition of anaerobic glucose metabolism and a compensatory stimulation of mitochondrial energy production. Acknowledgements:, Funded by CIHR Canada. [source] Induced hypothermia following out-of-hospital cardiac arrest; initial experience in a community hospitalCLINICAL CARDIOLOGY, Issue 12 2006Brook D. Scott M.D. Abstract Background Successful resuscitation from sudden cardiac death is frequently accompanied by severe and often fatal neurologic injury. Induced hypothermia (IH) may attenuate the neurologic damage observed in patients after cardiac arrest. Hypothesis This study examined a population of nonselected patients presenting to a community hospital following successful resuscitation of sudden cardiac death. We sought to determine whether a program of induced hypothermia would improve the clinical outcome of these critically ill patients. Methods We initiated a protocol of IH at the Oklahoma Heart Hospital in August of 2003. Study patients were consecutive adults admitted following successful resuscitation of out-of-hospital cardiac arrest. Moderate hypothermia was induced by surface cooling and maintained for 24 to 36 h in the Intensive Care Unit with passive rewarming over 8 h. Results Forty-nine patients who were resuscitated and had the return of spontaneous circulation completed the hypothermia protocol. The cause of cardiac arrest was acute myocardial infarction in 24 patients and cardiac arrhythmias in 19 patients. Nineteen patients (39%) survived and were discharged. Sixteen of the patients discharged had no or minimal residual neurologic dysfunction and 3 patients had clinically significant residual neurologic injury. Conclusion A program of induced hypothermia based in a community hospital is feasible, practical, and requires limited additional financial and nursing resources. Survival and neurologic recovery compare favorably with clinical trial outcomes. Copyright © 2006 Wiley Periodicals, Inc. Wiley Periodicals, Inc. [source] Apoptosis and Cardiopulmonary BypassJOURNAL OF CARDIAC SURGERY, Issue 2 2007M.S., Miljenko Kova Apoptotic index (AI) obtained with in situ terminal deoxynucleotidyl transferase-labeled dUTP nick end labeling (TUNEL) method and Bak protein expression were compared. Patients and Methods: Twenty consecutive patients who underwent coronary artery bypass surgery, myocardial samples from the right atrium were taken in three stages: before cannulation (the first sample group), after declamping (the second sample group), and 20 minutes after reperfusion (the third sample group). The percentage of apoptotic cells was determined by TUNEL method. Expression of Bak protein was immunohistochemically analyzed. Intermittent ischemia and moderate hypothermia were used as methods of myocardial management during surgery. A statistical analysis was performed by using the Friedman ANOVA analysis of variances, the Kendall coefficient of concordance and the Wilcoxon matched pair test. Results: In the first sample group mean value of Bak expression was 2.61 ± 2.18, compared with AI 5.38 ± 3.58, after declamping (the second sample group) the mean value of Bak expression was 4.31 ± 2.68 while AI was 7.63 ± 4.38 and after 20 minutes of reperfusion in the third sample group mean value of Bak expression was 8.89 ± 4.45, while AI was 15.6 ± 8.45. When compared by using Wilcoxon matched pair test two methods significantly correlated, p > 0.0001. Conclusion: The positive correlation between AI obtained by TUNEL method and expression of Bak protein may suggest that apoptosis is activated mainly through mitochondrial activation pathway in ischemic reperfusion injury. The results suggest that ischemic reperfusion injury increases the AI in the right atrial tissue. If so, immunohistochemical expression of Bak protein could be used as a marker of myocardial ischemia induced injury. [source] Neuroprotective effect of hypothermia at defined intraischemic time courses in cortical culturesJOURNAL OF NEUROSCIENCE RESEARCH, Issue 6 2001Sriranganathan Varathan Abstract Many experimental and clinical studies have shown that hypothermia confers cerebroprotective benefits against ischemic insults. Because of the many conflicting reports on hypothermic neuroprotection, we undertook this cellular study to identify the optimal temperature or a range of temperatures for maximal neuroprotection at different times (6,24 hr) during ischemic insults. Cultured Wistar rat cortical neurons were exposed to oxygen deprivation at defined times and temperatures (37°C normothermia, 32°C mild hypothermia, 27°C moderate hypothermia, 22°C deep hypothermia, and 17°C profound hypothermia). The survival rate of neurons was evaluated by assessing viable neurons on photomicrographs. The normothermic group demonstrated a significantly lower survival rate of cultured neurons (6 hr, 80.3% ± 2.7%; 12 hr, 56.1% ± 2.1%; 18 hr, 34.2% ± 1%; 24 hr, 18.1% ± 2.2%) compared to hypothermic groups (P < 0.001). The survival rate for the profound hypothermic group was significantly reduced (P < 0.01) compared to other hypothermic groups (at 17°C: 12 hr, 85.9% ± 2.5%, 18 hr, 74.7% ± 3.7%, 24 hr, 58.7% ± 2.7%). Almost equal survival rates were observed among mild, moderate, and deep hypothermic groups following <18 hr exposure to hypoxia, but the deep hypothermic group showed a significantly higher survival rate (84.1% ± 1.6%; P < 0.001) when subjected to hypoxia for 24 hr. In conclusion, hypothermia offers marked neuroprotection against hypoxia, but attenuation of neuronal cell death was less with profound hypothermia compared to mild, moderate, and deep hypothermia. Deep hypothermia affords maximal protection of neurons compared to mild and moderate hypothermia during long-lasting hypoxia (>18 hr). J. Neurosci. Res. 65:583,590, 2001. © 2001 Wiley-Liss, Inc. [source] Management of critically ill children with traumatic brain injuryPEDIATRIC ANESTHESIA, Issue 6 2008GILLES A. ORLIAGUET MD PhD Summary The management of critically ill children with traumatic brain injury (TBI) requires a precise assessment of the brain lesions but also of potentially associated extra-cranial injuries. Children with severe TBI should be treated in a pediatric trauma center, if possible. Initial assessment relies mainly upon clinical examination, trans-cranial Doppler ultrasonography and body CT scan. Neurosurgical operations are rarely necessary in these patients, except in the case of a compressive subdural or epidural hematoma. On the other hand, one of the major goals of resuscitation in these children is aimed at protecting against secondary brain insults (SBI). SBI are mainly because of systemic hypotension, hypoxia, hypercarbia, anemia and hyperglycemia. Cerebral perfusion pressure (CPP = mean arterial blood pressure , intracranial pressure: ICP) should be monitored and optimized as soon as possible, taking into account age-related differences in optimal CPP goals. Different general maneuvers must be applied in these patients early during their treatment (control of fever, avoidance of jugular venous outflow obstruction, maintenance of adequate arterial oxygenation, normocarbia, sedation,analgesia and normovolemia). In the case of increased ICP and/or decreased CPP, first-tier ICP-specific treatments may be implemented, including cerebrospinal fluid drainage, if possible, osmotic therapy and moderate hyperventilation. In the case of refractory intracranial hypertension, second-tier therapy (profound hyperventilation with PaCO2 < 35 mmHg, high-dose barbiturates, moderate hypothermia, decompressive craniectomy) may be introduced, after a new cerebral CT scan. [source] The prognostic value of early aEEG in asphyxiated infants undergoing systemic hypothermia treatmentACTA PAEDIATRICA, Issue 4 2010B 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] | |||||||||||||