• Top
• Objective
• Methods
• Results
• Conclusion

Objective

More recent studies have suggested that deep hypothermic cardiocirculatory arrest (DHCA) results in metabolic abnormalities with detrimental effects on enzyme function and membrane stability after rewarming, which may be associated with an increased risk for neurocellular injury. We evaluated whether brain tissue oxygen pressure (ptiO₂) showed sign of cellular hypoxia during cardiopulmonary bypass (CPB) with 1 h of DHCA and monitored changes in global cerebral blood flow (CBF) in a rabbit model.

Methods

Ten New Zealand white rabbits (body weight 2.5 ± 0.5 kg) were included in this study. Anesthetized and ventilated rabbits were placed on CPB (α-stat strategy) utilizing a membrane oxygenator with nonpulsatile pump flows of 150-200 ml/kg body weight per min for induction of DHCA by active cooling to 15 °C rectal temperature. Rewarming was started after 1 h of complete DHCA. Brain tissue oxymetry with a microsensor catheterprobe (Licox) in the frontoparietal cortex and CBF-measurement using the hydrogen clearance technique were obtained at baseline, during cooling, resumption of CPB and systemic rewarming, and finally while off CPB and with stable hemodynamics.

Results

Under baseline conditions, ptiO₂ was 38 ± 15 mmHg and changed to 40 ± 11 mmHg before the onset of DHCA. The CBF was lower than baseline before DHCA. During circulatory arrest the ptiO₂ decreased within 15 min to 14 ± 5 mmHg, after 30 min to 5 ± 1 mmHg and after 40 min to zero. Neither the ptiO2 nor CBF recovered fully during rewarming. After rewarming and termination of CPB the ptiO₂(25 ± 6 mmHg versus baseline 38 ± 15 mmHg; P < 0.05) and CBF (43 ± 8 versus 68 ± 11 ml/100 g per min; P < 0.05) were significantly reduced compared with pre-CPB values. Arterial and jugular-venous lactate levels increased after rewarming (P < 0.05) and corresponded to the appearance of anaerobic metabolism.

Conclusion

These observations suggest a persistent neurocellular function suppression after rewarming and a generated low-flow situation leading to transient regional cerebral tissue hypoxia events. Delayed brain tissue reoxygenation after DHCA may be attributable to excessive metabolic demand (compensation of an oxygen debt), inadequate tissue blood redistribution with reduced capillary perfusion, or oxygen utilization disturbances (mitochondrial dysfunction, reversibly inhibition of enzyme activity, immunoreactivity for specific proteins and cytochrome oxidase).

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