Abstract

INTRODUCTION: Hypothermia is seen as neuroprotective after brain insult (BI). In acute phase after BI it affects brain metabolism by decreasing oxygen and glucose consumption. Hypothermia affects apoptosis and inflammatory mediators. In the later stage of BI, enzyme activation stimulates protein and lipid breakdown, which can be slowed and decreased with hypothermia. In the latest stage of BI hypothermia has shown positive affect in angiogenesis, neurogenesis, synaptogenesis. Hypothermia also reduces vasogenic oedema and blood brain barrier dysfunction. Despite hypothermia´s neuroprotective effect randomized control trials have demonstrated its benefits only limited scenarios - mainly in global ischemia (post-cardiac infarction and ischemia of new-born). Majority of complications related to hypothermia has been due to systemic hypothermia and selective brain cooling has never been demonstrated in large mammals without changes in core temperature of subject. METHODS: We inserted double lumen external ventricular drainage (EVD) into the lateral ventricle of porcine. We added spinal drainage to accelerate CSF exchange to cooled NaCl solution. Brain parenchymal temperature was measured from the contralateral brain hemisphere and the ipsilateral brain hemisphere. RESULTS: Contralateral brain hemisphere temperature dropped by 3.1C from baseline while core temperature changed only by 0.5C. Ipsilateral temperature cooled by 7.5C from baseline to 30.8C, while core temperature was 37.7C. Total time needed to achieve selective cooling was 1.5h. Porcine started to have arrhythmias when brain temperature approached 30.8C. CONCLUSIONS: We are first to describe that selective brain cooling is possible via CSF exchange with double lumen EVD to achieve significant temperature difference between body core and brain. The timing and rate of selective cooling needs to be established as cause of arrhythmias before starting human trials.

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