European journal of cardio-thoracic surgery : official journal of the European Association for Cardio-thoracic Surgery · 2005
Heat stress increases the effectiveness of early ischemic preconditioning in spinal cord protection.
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Basaran Murat, Kafali Eylul, Sayin Omer, Ugurlucan Murat, Us Melih Hulusi, Bayindir Cicek, Yilmaz Ahmet Turan, Dayioglu Enver
Аннотация
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 45 min. Group 2 (n=10) had 5 min of transient aortic occlusion and 30 min later underwent an additional 45 min. In group 3 (n=10), animals were heated to 41 degrees C and maintained at this temperature for 15 min. 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 48 h 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 48 h, 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 48 h, the mean neurologic scores of the group 3 were significantly higher than those of group 2 (P=0.005). At 48 h, 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 48 h and heat shock protein-ubiquitin induction may be responsible in this phenomenon.
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 45 min. Group 2 (n=10) had 5 min of transient aortic occlusion and 30 min later underwent an additional 45 min. In group 3 (n=10), animals were heated to 41 degrees C and maintained at this temperature for 15 min. 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 48 h 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 48 h, 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 48 h, the mean neurologic scores of the group 3 were significantly higher than those of group 2 (P=0.005). At 48 h, 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 48 h and heat shock protein-ubiquitin induction may be responsible in this phenomenon.