• A Iguchi, K Haneda, S Sato, and T Horiuchi.
• Tohoku J. Exp. Med. 1986 Jun 1;149(2):191-204.

AbstractTo determine the safe interval of hypothermic total circulatory arrest, the cerebral metabolic state was evaluated in 30 dogs. Surface cooling was achieved by deep ether anesthesia and the animals were assigned to three equal groups. Group I: 30 min circulatory arrest and surface rewarming. Group II: 60 min circulatory arrest and surface rewarming. Group III: 60 min circulatory arrest and perfusion rewarming. Brain tissue gas tension was monitored and cerebral O2 consumption was calculated. Cerebral O2 consumption reduced with cooling, parallel to the decrease in cerebral blood flow. Rapid increase in Po2, elevation of PCO2, and decrease of pH in the brain tissue were observed during circulatory arrest. Brain tissue PO2 increased significantly after circulatory arrest in Group I, but it remained low during rewarming in Groups II and III. Cerebral O2 consumption was at reduced levels in all groups during rewarming and it remained at 29% of the precooling control level in Group II at the end of rewarming, whereas it recovered to 71% and 57% of the precooling levels in Groups I and III, respectively. It was estimated that cerebral metabolism may be recovered after 30 min circulatory arrest, despite a transient reduction in cerebral O2 consumption. On the other hand, after 60 min circulatory arrest, the recovery of cerebral metabolism was delayed in Group II and organic failure might have occurred in this group. However, even after circulatory arrest for 60 min, cerebral metabolism was recovered in Group III. The safe period of circulatory arrest is considered to be prolonged by use of extra-corporeal circulation.

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