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J Thorac Cardiovasc Surg 2004;128:203-210
© 2004 The American Association for Thoracic Surgery

Cardiopulmonary support and physiology

Ischemic preconditioning or heat shock pretreatment ameliorates neuronal apoptosis following hypothermic circulatory arrest

^a Division of Thoracic and Cardiovascular Surgery, Chang Gung Memorial Hospital, Keelung, Taiwan

Received for publication July 9, 2003; revisions received November 26, 2003; accepted for publication December 11, 2003.

^* Address for reprints: Chi-Hsiao Yeh, MD, Division of Thoracic and Cardiovascular Surgery, Chang Gung Memorial Hospital, 222 Mai-Chin Road, Keelung, Taiwan 204
yehccl{at}cgmh.org.tw

OBJECTIVE: Hypothermic circulatory arrest has been widely used in complex cardiac and aortic surgery. Stroke and/or neurologic injury can occur after prolonged hypothermic circulatory arrest, possibly due to apoptosis. Ischemic preconditioning has been widely used as a neuroprotective tool, but its application in neuronal injury under hypothermic circulatory arrest has never been studied.

METHODS: Forty male New Zealand white rabbits were placed on closed-chest cardiopulmonary bypass, subjected to hypothermic circulatory arrest, and rewarmed to normothermia. Experimental groups were treated with heat shock or ischemic preconditioning before hypothermic circulatory arrest. Hippocampal CA1 neurons were analyzed histopathologically. Apoptosis was confirmed by TUNEL assay and Western blot analysis, and serum S-100ß levels, c-Fos and Bcl-2 antibodies, and caspase-3 and heat shock protein 70 levels were measured.

RESULTS: After 2-hour hypothermic circulatory arrest and 4-hour reperfusion, apoptosis was observed in hippocampal CA1 neurons with elevation of serum S-100ß levels, which could be ameliorated by ischemic preconditioning or heat shock manipulations. TUNEL-positive nuclear expression of caspase-3 increased after hypothermic circulatory arrest (3.08% ± 0.71%, P < .001) and was diminished with ischemic preconditioning (1.61% ± 0.42%) and heat shock (1.72% ± 0.38%) manipulations. Ischemic preconditioning or heat shock manipulations produced diverse patterns of heat shock protein 70, c-Fos, and Bcl-2 protein expression, suggesting that these manipulations provide neuroprotection via different pathways.

CONCLUSIONS: Ischemic preconditioning and heat shock can attenuate hippocampal CA1 neuronal apoptosis after prolonged hypothermic circulatory arrest under cardiopulmonary bypass. The expression of heat shock protein 70 may not play a major role in the first window of ischemic preconditioning-induced neuroprotection.

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