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Mild hypothermia alone or in combination with anesthetic post-conditioning reduces expression of inflammatory cytokines in the cerebral cortex of pigs after cardiopulmonary resuscitation
Patrick Meybohm, Matthias Gruenewald, Kai D Zacharowski, Martin Albrecht, Ralph Lucius, Nikola F?sel, Johannes Hensler, Karina Zitta, Berthold Bein
Critical Care , 2010, DOI: 10.1186/cc8879
Abstract: Thirty pigs (28 to 34 kg) were subjected to cardiac arrest following temporary coronary artery occlusion. After seven minutes of ventricular fibrillation and two minutes of basic life support, advanced cardiac life support was started according to the current American Heart Association guidelines. Return of spontaneous circulation was achieved in 21 animals who were randomized to either normothermia at 38°C, hypothermia at 33°C or hypothermia at 33°C combined with sevoflurane (each group: n = 7) for 24 hours. The effects of hypothermia and the combination of hypothermia with sevoflurane on cerebral inflammatory response after cardiopulmonary resuscitation were studied using tissue samples from the cerebral cortex of pigs euthanized after 24 hours and employing quantitative RT-PCR and ELISA techniques.Global cerebral ischemia following resuscitation resulted in significant upregulation of cerebral tissue inflammatory cytokine mRNA expression (mean ± SD; interleukin (IL)-1β 8.7 ± 4.0, IL-6 4.3 ± 2.6, IL-10 2.5 ± 1.6, tumor necrosis factor (TNF)α 2.8 ± 1.8, intercellular adhesion molecule-1 (ICAM-1) 4.0 ± 1.9-fold compared with sham control) and IL-1β protein concentration (1.9 ± 0.6-fold compared with sham control). Hypothermia was associated with a significant (P < 0.05 versus normothermia) reduction in cerebral inflammatory cytokine mRNA expression (IL-1β 1.7 ± 1.0, IL-6 2.2 ± 1.1, IL-10 0.8 ± 0.4, TNFα 1.1 ± 0.6, ICAM-1 1.9 ± 0.7-fold compared with sham control). These results were also confirmed for IL-1β on protein level. Experimental settings employing hypothermia in combination with sevoflurane showed that the volatile anesthetic did not confer additional anti-inflammatory effects compared with hypothermia alone.Mild therapeutic hypothermia resulted in decreased expression of typical cerebral inflammatory mediators after cardiopulmonary resuscitation. This may confer, at least in part, neuroprotection following global cerebral ischemia and resuscitation.Althoug
Molecular Mechanisms Underlying Hypothermia-Induced Neuroprotection  [PDF]
Yasushi Shintani,Yasuko Terao,Hiroyuki Ohta
Stroke Research and Treatment , 2011, DOI: 10.4061/2011/809874
Abstract: Stroke is a dynamic event in the brain involving heterogeneous cells. There is now compelling clinical evidence that prolonged, moderate cerebral hypothermia initiated within a few hours after severe ischemia can reduce subsequent neuronal death and improve behavioral recovery. The neuroprotective role of hypothermia is also well established in experimental animals. However, the mechanism of hypothermic neuroprotection remains unclear, although, presumably involves the ability of hypothermia to suppress a broad range of injurious factors. In this paper, we addressed this issue by utilizing comprehensive gene and protein expression analyses of ischemic rat brains. To predict precise target molecules, we took advantage of the therapeutic time window and duration of hypothermia necessary to exert neuroprotective effects. We proposed that hypothermia contributes to protect neuroinflammation, and identified candidate molecules such as MIP-3α and Hsp70 that warrant further investigation as targets for therapeutic drugs acting as “hypothermia-like neuroprotectants.” 1. Introduction Stroke is the second leading cause of death in the world [1], and is a primary cause of long-term disability in adults [2, 3]. One potential approach for treating acute stroke involves neuroprotective agents. Although more than 100 clinical trials of potential agents have been conducted, none of these agents proved to be clinically efficacious except for a free radical scavenger edaravone [4–6]. However, recent progress in understanding the disease have unveiled the cellular and molecular events underlying ischemic cell death, such as loss of metabolic stores, excessive intracellular calcium accumulation, oxidative stress, and neuroinflammatory response. For instance, expression of stress, apoptosis, and inflammation-related genes is known to be upregulated upon reperfusion and reoxygenation [7, 8]. Therapeutic hypothermia is a promising neuroprotective intervention shown to improve outcome from brain ischemia in humans. The neuroprotective role of hypothermia has been well established in experimental animals [9–11] and in patients with cardiac arrest [12, 13]. Although the key mechanism has not been clarified, hypothermic neuroprotection may provide insight into stroke pathology and suggest novel therapeutic drug targets. To date, reactive oxygen species production [14], NF-κB activation [15], neutrophil infiltration [16] and cytochrome c release [17] have been observed to be inhibited in hypothermia-treated ischemic brains. However, it is difficult to discern an intrinsic hallmark
Hypothermia and pediatric cardiac arrest  [cached]
Schlunt Michelle,Wang Lynn
Journal of Emergencies, Trauma and Shock , 2010,
Abstract: The survival outcome following pediatric cardiac arrest still remains poor. Survival to hospital discharge ranges anywhere from 0 to 38% when considering both out-of-hospital and in-hospital arrests, with up to 50% of the survivors having neurologic injury. The use of mild induced hypothermia has not been definitively proven to improve outcomes following pediatric cardiac arrest. This may be due to the lack of consensus regarding target temperature, best method of cooling, optimal duration of cooling and identifying the patient population who will receive the greatest benefit. We review the current applications of induced hypothermia in pediatric patients following cardiac arrest after searching the current literature through Pubmed and Ovid journal databases. We put forth compiled recommendations/guidelines for initiating hypothermia therapy, its maintenance, associated monitoring and suggested adjunctive therapies to produce favorable neurologic and survival outcomes.
Hipotermia intravascular prolongada en un paciente con hipertensión endocraneana refractaria Prolonged hypothermia in refractory intracranial hypertension. Report of one case
Maximiliano Rovegno,José Luis Valenzuela,Patricio Mellado,Max Andresen
Revista médica de Chile , 2012,
Abstract: The use of hypothermia after cardiac arrest caused by ventricular fibrillation is a standard clinical practice, however its use for neuroprotection has been extended to other conditions. We report a 23-year-old male with intracranial hypertension secondary to a parenchymal hematoma associated to acute hydrocephalus. An arterial malformation was found and embolized. Due to persistent intracranial hypertension, moderate hypothermia with a target temperature of 33°C was started. After 12 hours of hypothermia, intracranial pressure was controlled. After 13 days of hypothermia a definitive control of intracranial pressure was achieved. The patient was discharged 40 days after admission, remains with a mild hemiparesia and is reassuming his university studies.
Out-of-hospital therapeutic hypothermia in cardiac arrest victims
Wilhelm Behringer, Jasmin Arrich, Michael Holzer, Fritz Sterz
Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine , 2009, DOI: 10.1186/1757-7241-17-52
Abstract: Sudden cardiac arrest remains a major unresolved public health problem. In Europe and the USA, approximately 425.000 people suffer of sudden cardiac death with very poor survival, usually less than 10% [1,2]. After cardiac arrest and brain ischemia, reperfusion initiates multiple independent chemical cascades and fatal pathways, resulting in neuronal death due to necrosis and apoptosis [3]. Because of the multi-factorial pathogenesis of post-arrest neuronal death, a multifaceted treatment strategy is required to achieve survival without brain damage. Hypothermia, a re-discovered promising treatment strategy, exerts its beneficial effects on brain ischemia by various mechanisms, and perfectly fulfils the requirements of a multifaceted treatment strategy [4].In therapeutic hypothermia, different degrees of cooling can be differentiated, though definition of these temperature levels may differ slightly between authors: mild (34 to 32°C), moderate (31 to 28°C), deep (27 to 11°C), profound (10 to 6°C), and ultra-profound (5 to 0°C) hypothermia. Protective hypothermia, induced before cardiac arrest, has to be differentiated from preservative hypothermia, induced during cardiac arrest treatment, and from resuscitative hypothermia, induced after successful resuscitation. Protective hypothermia is used in cardiac surgery and neurosurgery, but is clinically unrealistic in sudden cardiac death. This review will focus on a) preservative mild hypothermia during cardiac arrest treatment and b) resuscitative mild hypothermia after successful resuscitation in respect to its clinical application in the out-of-hospital setting.Preservative hypothermia can further be differentiated into the induction of hypothermia during ischemia (before initiation of resuscitation - or before reperfusion) and the induction of hypothermia during resuscitation.Research in myocytes showed that injury to cells not only occurs during ischemia itself, but mainly with reperfusion by initiating several casc
Intra-arrest hypothermia during cardiac arrest: a systematic review
Sabino Scolletta, Fabio Taccone, Per Nordberg, Katia Donadello, Jean-Louis Vincent, Maaret Castren
Critical Care , 2012, DOI: 10.1186/cc11235
Abstract: We performed a systematic search of PubMed, EMBASE, CINAHL, the Cochrane Library and Ovid/Medline databases using "arrest" OR "cardiac arrest" OR "heart arrest" AND "hypothermia" OR "therapeutic hypothermia" OR "cooling" as keywords. Only studies using intra-arrest therapeutic hypothermia (IATH) were selected for this review. Three authors independently assessed the validity of included studies and extracted data regarding characteristics of the studied cohort (animal or human) and the main outcomes related to the use of IATH: Mortality, neurological status and cardiac function (particularly, rate of ROSC).A total of 23 animal studies (level of evidence (LOE) 5) and five human studies, including one randomized controlled trial (LOE 1), one retrospective and one prospective controlled study (LOE 3), and two prospective studies without a control group (LOE 4), were identified. IATH improved survival and neurological outcomes when compared to normothermia and/or hypothermia after ROSC. IATH was also associated with improved ROSC rates and with improved cardiac function, including better left ventricular function, and reduced myocardial infarct size, when compared to normothermia.IATH improves survival and neurological outcome when compared to normothermia and/or conventional hypothermia in experimental models of CA. Clinical data on the efficacy of IATH remain limited.Use of mild therapeutic hypothermia, or "targeted temperature management" as recently suggested [1], has been recommended in cardiac arrest (CA) patients since the publication of two randomized clinical trials in 2002, the results of which demonstrated a significant improvement in neurologically intact survival for comatose CA patients presenting with ventricular fibrillation (VF) or ventricular tachycardia (VT) [2,3]. Current guidelines suggest that mild therapeutic hypothermia should also be considered in patients presenting with other rhythms although this has been less well studied [4].Although therap
Therapeutic hypothermia and neurological outcome after cardiac arrest  [PDF]
Petrovi? Milovan,Pani? Gordana,Joveli? Aleksandra,?anji Tibor
Vojnosanitetski Pregled , 2011, DOI: 10.2298/vsp1106495p
Abstract: Introduction/Aim. The most important clinically relevant cause of global cerebral ischemia is cardiac arrest. Clinical studies showed a marked neuroprotective effect of mild hypothermia in resuscitation. The aim of this study was to evaluate the impact of mild hypothermia on neurological outcome and survival of the patients in coma, after cardiac arrest and return of spontaneous circulation. Methods. The prospective study was conducted on consecutive comatose patients admitted to our clinic after cardiac arrest and return of spontaneous circulation, between February 2005 and May 2009. The patients were divided into two groups: the patients treated with mild hypothermia and the patients treated conservatively. The intravascular in combination with external method of cooling or only external cooling was used during the first 24 hours, after which spontaneous rewarming started. The endpoints were survival rate and neurological outcome. The neurological outcome was observed with Cerebral Performance Category Scale (CPC). Follow-up was 30 days. Results. The study was conducted on 82 patients: 45 patients (age 57.93 ± 14.08 years, 77.8% male) were treated with hypothermia, and 37 patients (age 62.00 ± 9.60 years, 67.6% male) were treated conservatively. In the group treated with therapeutic hypothermia protocol, 21 (46.7%) patients had full neurological restitution (CPC 1), 3 (6.7%) patients had good neurologic outcome (CPC 2), 1 (2.2%) patient remained in coma and 20 (44.4%) patients finally died (CPC 5). In the normothermic group 7 (18.9%) patients had full neurological restitution (CPC 1), and 30 (81.1%) patients remained in coma and finally died (CPC 5). Between the two therapeutic groups there was statistically significant difference in frequencies of different neurologic outcome (p = 0.006), specially between the patients with CPC 1 and CPC 5 outcome (p = 0.003). In the group treated with mild hypothermia 23 (51.1%) patients survived, and in the normothermic group 30 (81.1%) patients died, while in the group of survived patients 23 (76.7%) were treated with mild hypothermia (p = 0.003). Conclusion. Mild therapeutic hypothermia applied after cardiac arrest improved neurological outcome and reduced mortality in the studied group of comatose survivors.
The Practice of Therapeutic Hypothermia after Cardiac Arrest in France: A National Survey  [PDF]
Jean-Christophe Orban, Florian Cattet, Jean-Yves Lefrant, Marc Leone, Samir Jaber, Jean-Michel Constantin, Bernard Allaouchiche, Carole Ichai, for the AzuRéa group
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0045284
Abstract: Aims Cardiac arrest is a major health concern worldwide accounting for 375,000 cases per year in Europe with a survival rate of <10%. Therapeutic hypothermia has been shown to improve patients’ neurological outcome and is recommended by scientific societies. Despite these guidelines, different surveys report a heterogeneous application of this treatment. The aim of the present study was to evaluate the clinical practice of therapeutic hypothermia in cardiac arrest patients. Methods This self-declarative web based survey was proposed to all registered French adult intensive care units (ICUs) (n = 357). Paediatrics and neurosurgery ICUs were excluded. The different questions addressed the structure, the practical modalities of therapeutic hypothermia and the use of prognostic factors in patients admitted after cardiac arrest. Results One hundred and thirty-two out of 357 ICUs (37%) answered the questionnaire. Adherence to recommendations regarding the targeted temperature and hypothermia duration were 98% and 94% respectively. Both guidelines were followed in 92% ICUs. During therapeutic hypothermia, sedative drugs were given in 99% ICUs, mostly midazolam (77%) and sufentanil (59%). Neuromuscular blocking agents (NMBA) were used in 97% ICUs, mainly cisatracurium (77%). Numerous prognostic factors were used after cardiac arrest such as clinical factors (95%), biomarkers (53%), electroencephalography (78%) and evoked potentials (35%). Conclusions In France, adherence to recommendations for therapeutic hypothermia after cardiac arrest is higher than those previously reported in other countries. Numerous prognostic factors are widely used even if their reliability remains controversial.
Hypothermia and cardiac arrest: the promise of intra-arrest cooling
Roger A Band, Benjamin S Abella
Critical Care , 2008, DOI: 10.1186/cc6845
Abstract: In the previous issue of Critical Care, Bruel and colleagues report findings from a small, prospective, observational study in which they investigate the feasibility, efficacy and safety of intra-arrest therapeutic hypothermia (TH) for victims of out-of-hospital cardiac arrest (OHCA) [1]. From an initial pool of 412 cardiac arrest victims, the study enrolled 33 patients with a variety of presenting rhythms. This represents the first study of its kind to investigate the feasibility of intra-arrest cooling in the clinical setting, an approach that has shown significant promise in animal models of cardiac arrest and brain injury [2-4].Sudden cardiac arrest, defined as the abrupt loss of mechanical cardiac activity and concomitant global loss of blood flow, is a leading cause of death in the United States and Europe. Approximately 200,000 people suffer OHCA in the United States each year, and over 90% will succumb during resuscitation efforts or during subsequent hospitalization [5,6]. Survival to hospital discharge depends on a number of factors, including prompt delivery of cardiopulmonary resuscitation and defibrillation when indicated, the initial cardiac rhythm of arrest, and the quality of post-resuscitation care including provision of TH.Despite the significant effort that has been invested in this field, few therapeutic or pharmacologic interventions have yielded meaningful increases in overall survival from OHCA over the past 20 years [6,7]. The relatively new and evolving treatment modality of TH, however, has been associated with markedly decreased mortality and neurologic injury among patients who initially survive OHCA [8,9].TH reduces both the cerebral metabolic rate and oxygen demand, and it is thought to attenuate reperfusion injury, global inflammation and endothelial dysfunction – all consequences of cerebral and other organ ischemia [10,11]. Through such mechanisms, TH is thought to improve clinical parameters and outcomes. Two landmark multicenter ra
Recent treatment of postischaemic anoxic brain damage after cardiac arrest by using therapeutic hypothermia
An?eli? Sla?ana
Srpski Arhiv za Celokupno Lekarstvo , 2008, DOI: 10.2298/sarh0810549a
Abstract: Organ injury caused by ischemia and anoxia during prolonged cardiac arrest is compounded by reperfusion injury that occurs when spontaneous circulation is restored. Mild hypothermia (32-35oC) is neuroprotective through several mechanisms, including suppression of apoptosis, reduced production of excitotoxins and free radicals, and anti-inflammatory actions. Experimental studies show that hypothermia is more effective the earlier it is started after return of spontaneous circulation (ROSC). Two randomized clinical trials show improved survival and neurological outcome in adults who remained comatose after initial resuscitation from prehospital VF cardiac arrest, and who were cooled after ROSC. Different strategies can be used to induce hypothermia. Optimal timing of therapeutic hypothermia for cardiac ischemia is unknown. In patients who failed to respond to standard cardiopulmonary resuscitation, intra-arrest cooling using ice-cold intravenous (i.v.) fluid improved the chance of survival. Recently, fasudil, a Rho kinase inhibitor, was reported to prevent cerebral ischaemia in vivo by increasing cerebral blood flow and inhibiting inflammatory responses. In future, two different kinds of protective therapies, BCL-2 overexpression and hypothermia, will both inhibit aspects of apoptotic cell death cascades, and that combination treatment can prolong the temporal 'therapeutic window' for gene therapy.
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