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

Heat stress increases the effectiveness of early ischemic preconditioning in spinal cord protection 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. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png European Journal of Cardio-Thoracic Surgery Oxford University Press

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

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References (25)

Publisher
Oxford University Press
Copyright
© 2005 Elsevier B.V. All rights reserved.
Subject
Original articles
ISSN
1010-7940
eISSN
1873-734X
DOI
10.1016/j.ejcts.2005.06.014
pmid
16054387
Publisher site
See Article on Publisher Site

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.

Journal

European Journal of Cardio-Thoracic SurgeryOxford University Press

Published: Sep 1, 2005

Keywords: Hyperthermic ischemic preconditioning Spinal cord ischemic injury Early ischemic preconditioning

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