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Eur J Cardiothorac Surg 2005;28:467-472
© 2005 Elsevier Science NL

Original articles

Heat stress increases the effectiveness of early ischemic preconditioning in spinal cord protection

^a Department of Cardiovascular Surgery, Istanbul University, GATA, Haydarpasa Military Training Hospital, Istanbul 84390, Turkey
^b Department of Cardiovascular Surgery, Gata Military Training Hospital, Ankara, Turkey
^c Department of Neuropathology, Istanbul University, Istanbul, Turkey

Received 12 April 2005; received in revised form 8 June 2005; accepted 13 June 2005.

^* Corresponding author. Tel.: +90 212 534 00 00; fax: +90 212 534 22 32. (Email: dr_murat_basaran{at}yahoo.com).

Abstract

Objective: This study was aimed to test the hypothesis that the combination of heat stress and early ischemic preconditioning (IP) applied before aortic occlusion would be protective against spinal cord ischemic injury. Methods: Thirty Whister–Albino rats were randomly divided into three groups. In group 1 (n=10), aorta was clamped just distal to the left renal artery and above the iliac bifurcation for 45min. Group 2 (n=10) had 5min of transient aortic occlusion and 30min later underwent an additional 45min. In group 3 (n=10), animals were heated to 41°C and maintained at this temperature for 15min. Twenty-four hours later, this hyperthermia pretreated group underwent the same early IP model of aortic occlusion. Neurologic status was assessed on postoperative 24 and 48h by using the 15-point neurologic performance scale. Spinal cords were harvested for histopathological grading (1–4) and evaluated for the presence of heat shock protein-ubiquitin staining. Results: At 24 and 48h, the mean neurologic performance scores of the group 1 were found to be significantly lower than those of groups 2 and 3. Although the neurologic assessment of rats performed on the 24h did not reveal statistically significant difference between groups 2 and 3 (P=0.069); on 48h, the mean neurologic scores of the group 3 were significantly higher than those of group 2 (P=0.005). At 48h, a delayed neurologic deterioration was seen in groups 1 and 2 when compared to the results obtained at 24h. Histologic evaluation correlated well with the neurologic outcome with the least cellular damage in group 3. There were six rats with ubiquitin expression and this was detected only in animals pretreated with sublethal heat stress. Conclusions: An early IP model with a short reperfusion interval does not give the minimal required time for the HSPs expression and is associated with a delayed neurologic deterioration. Neuroprotection provided by heat stress combined with an early IP model lasts up to 48h and heat shock protein-ubiquitin induction may be responsible in this phenomenon.

Key Words: Hyperthermic ischemic preconditioning • Spinal cord ischemic injury • Early ischemic preconditioning