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.

Objective We hypothesized that by actively exchanging cerebrospinal fluid (CSF) to cooled NaCl and ringer acetate solution we can reduce selectively brain temperature without changes in core temperature of porcine body.

Methods We inserted double lumen external ventricular drainage (EVD) into the lateral ventricle of four porcines. We added spinal drainage to accelerate CSF exchange to cooled NaCl (one porcine)/ringer acetate (three porcine) solutions. Brain parenchymal temperature was measured from the contralateral brain hemisphere and the ipsilateral brain hemisphere. We exchanged CSF to cooled solution in 4 porcine with rates of 180ml-720ml/h. Two of porcine were induced global stroke via endovascular method by closing brains main arteries for 20 min.

Results Contralateral brain hemisphere temperature dropped by 2.2-3.1C from baseline while core temperature changed only by 0.5C. Ipsilateral temperature cooled by 4.5-7.5C from baseline to 29.9-33.8C, while core temperature was on average 37.7C. Total time needed to achieve selective cooling was highly dependent on CSF rate from 10min to 1.5h. One porcine started to have arrhythmias when brain temperature approached 30.8C, in this case CSF exchange was done with NaCl solution, other 3 porcine did not have similar adverse events with ringer acetate. In two stroke induced porcine selective brain cooling was achieved despite 140 mmHg median arterial pressure after stroke.

Conclusion 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.

Disclosures B. Rezai Jahromi: 1; C; IRRAS. 2; C; Neurovascular Innovations. 4; C; Neurovascular Innovations. 6; C; Helsinki Surgical Instruments. N. Järveläinen: None. J. Kauhanen: None. V. Zamotin: None. N. Brandmeir: 1; C; IRRAS. 2; C; IRRAS. M. Niemelä: None. S. Ylä-Herttuala: None.