Dynamic changes in cerebral oxygenation related to deep hypothermia and circulatory arrest evaluated by near-infrared spectroscopy

Background: Total circulatory arrest in deep hypothermia, which is used in corrective surgery of complex cardiovascular malformations, has been said to cause brain injury. Near-infrared spectroscopy (NIRS) is a new non-invasive method that potentially monitors changes in cerebral oxygenation and tissue oxygen utilisation. The aim of this experimental study in rabbits was to evaluate the change in intravascular and intracellular oxygenation patterns during cooling, deep hypothermic circulatory arrest and rewarming using a commercially available NIRS-cerebral oximeter. Methods: Ten New Zealand White male rabbits (weight, 3.1 +/-0.25 kg BW) were included in this study. All animals underwent cardiopulmonary bypass (CPB), cooling to a rectal temperature below 15 degreesC, 60 min of deep hypothermic circulatory arrest (DHCA) followed by reperfusion and rewarming. Cerebral oxyhaemoglobin (HbO(2)), deoxyhaemoglobin (HHb) and cytochrome oxidase aa(3) (CytOxaa(3)) concentrations were continuously measured during the entire procedure using the Cerebral RedOx (TM) Monitor 2020 (Criticon cerebral redox monitor 2020, Johnson & Johnson Medical). Total haemoglobin concentration (tHb) and regional cerebral oxygen saturation (rSO(2)) values were calculated by integrated algorithm. Results: In all animals an initial increase of oxygenated haemoglobin (HbO(2), rSO(2)) and a fall in deoxygenated haemoglobin (HHb) were found during cooling on bypass. A slight decrease in CytOxaa3 signal was observed in response to initial cooling. Variation in intravascular haemoglobin oxygenation parameters (HbO(2), HHb) were related to haemodynamic changes associated with fluid loading, initiation and termination of CPB, bypass flow rate and cooling and rewarming. When the pump flow was stopped all NIRS parameters, except the HHb value, decreased precipitously during the DHCA-pcriod (P<0.01). After reperfusion and rewarming, all haemoglobin oxygen saturation readings returned nearly to pre-CPB levels (P=0.09), but the CytO-xaa(3) was still significantly lower than the pre-CrB levels (P<less than>0.05). Conclusion: The change in the NIRS-derived haemoglobin oxygenation parameters may reflect physiological changes in systemic and cerebral haemodynamics. CytOxaa(3) values may represent related effects on cellular oxygenation. Thus, continuous, real-time NIRS-monitoring may identify critical periods with inadequate brain tissue oxygenation, particularly during DHCA. The neurological implications of the observed changes in NIRS oxygenation parameters, however, require further quantitative morphological evaluation of the brain in animals surviving a longer reperfusion and observation period.