therapeutic hypothermia has been shown to provide neuroprotection against ischemic injury after cardiac arrest in in vitro and in vivo models . in the previous issue of critical care , meybohm and colleagues   demonstrate that cardiac arrest triggers the release of cerebral inflammatory cytokines in pigs ' cerebral cortex . . the combination of hypothermia with sevoflurane post - conditioning does not confer additional anti - inflammatory effects compared with hypothermia alone . cardiac arrest remains the leading cause of death in the us and europe , with an out - of - hospital cardiac arrest survival - to - discharge rate of less than 10% . in - hospital cardiac arrest presents a dismal prognosis . according to a large in - hospital registry , the survival - to - discharge rate is 18% , whereas that of a developing country is 6.9% . without prompt care when immediate care is available and victims are successfully resuscitated , the majority of these initial survivors subsequently suffer crippling neurologic injury or die in the few days following the cardiac arrest event . thus , improving survival and brain function after initial resuscitation from cardiac arrest remains a critical challenge . therapeutic hypothermia , introduced more than six decades ago , remains an important neuroprotective factor in cardiac arrest . laboratory studies have demonstrated that cooling after resuscitation from cardiac arrest improves both survival as well as subsequent neurologic and cardiac function and has few side effects . these findings have been reproduced using a variety of cooling techniques in different species , including rats , dogs , and pigs . however , physician use of hypothermia induction in patients resuscitated from cardiac arrest is low . in 2003 , abella and colleagues   reported that 87% of us physicians did not use therapeutic hypothermia following cardiac arrest . various reasons for non - use were cited : 49% felt that there were not enough data , 32% mentioned lack of incorporation of hypothermia into advanced cardiovascular life support protocols , and 28% felt that cooling methods were technically too difficult or too slow . in 2002 , a european group demonstrated an improvement in survival - to - discharge rate with favorable neurologic status in cooled patients , compared with normothermic patients surviving after cardiac arrest ( 53% versus 35% , respectively ) , and with no significant adverse events from cooling ; thereafter , induced hypothermia was considered the best practice for patients following cardiac arrest . in 2005 , the american heart association recommended the consideration of therapeutic hypothermia for unconscious adult patients with return of spontaneous circulation following out - of - hospital cardiac arrest due to ventricular fibrillation . in 2008 , binks and colleagues   reported that 85.6% of intensive care units in the uk were using hypothermia as part of post - cardiac arrest management . clinical observation demonstrated that tumor necrosis factor - alpha ( tnf ) and interleukin-6 ( il-6 ) protein were increased in cerebrospinal fluid following cardiac arrest . animal studies showed that inflammatory markers were unregulated in rats ' hippocampus tissue and pigs ' serum and myocardial tissue after cardiac arrest [ 8 - 10 ] . meybohm and colleagues   go further to demonstrate anti - inflammatory and anti - apoptosis effects of therapeutic hypothermia via the reduction of the upregulation expression of il-1 , il-6 , il-10 , tnf and intercellular adhesion molecule-1 , bcl-2 , and bax mrna and il-1 protein in cerebral cortex after cardiac arrest in a pig model . small reductions in core temperature lead to vaso - constriction and shivering , effectively hindering hypothermia . thus , prevention of vasoconstriction and shivering has become a major goal during induction of therapeutic hypothermia . sevoflurane pre - conditioning and early post - conditioning reduced both cerebral infarct size and neurological defect score , reduced impairment of hippocampus long - term potentiation resulting from myocardial ischemia , and increased nuclear factor inhibitory kappabalpha content in thp-1 cells [ 11 - 13 ] . sevoflurane pre - conditioning preserves myocardial function in patients undergoing coronary artery bypass graft surgery under cardiologic arrest . an in vivo study showed that combination hypothermia with sevoflurane attenuates the inflammatory response during endotoxemia . however , meybohm and colleagues   could not provide evidence to support the view that sevoflurane post - conditioning confers additional anti - inflammatory effects in pigs ' cerebral cortex after cardio - pulmonary resuscitation . in summary , meybohm and colleagues   provide useful evidence to support the clinical use of therapeutic hypothermia for cardiac arrest , but they did not study the anti - inflammatory effects of sevoflurane in this model . it is even possible that in the setting of clinical practice , anesthetics may not provide significant neuroprotection beyond that which is already being produced by therapeutic hypothermia . thus , at this time , it is difficult to recommend anesthetics for the purpose of neuroprotection in cardiac arrest .
in the previous issue of critical care , meybohm and colleagues provide evidence to support hypothermia as a kind of therapeutic option for patients suffering cardiac arrest . 
 although anesthetics had been used to induce hypothermia , sevoflurane post - conditioning fails to confer additional anti - inflammatory effects after cardiac arrest . 
 further research in this area is warranted .