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J Thorac Cardiovasc Surg 2000;120:513-519
© 2000 The American Association for Thoracic Surgery


Surgery for Acquired Cardiovascular Disease

Effect of ischemic pretreatment on heat shock protein 72, neurologic outcome, and histopathologic outcome in a rabbit model of spinal cord ischemia

Peter de Haan, MD, PhDa, Ivo Vanicky, DVMb, Michael J. H. M. Jacobs, MD, PhDc, Onno Bakker, PhDd, Jeroen Lips, MSa, Sven A.G. Meylaerts, MDc, Cor J. Kalkman, MD, PhDa

From the Departments of Anesthesiology,a Vascular Surgery,c and Endocrinology,d Academic Hospital, University of Amsterdam, Academic Medical Center, Amsterdam, The Netherlands, and the Institute of Neurobiology,b Slovak Academy of Sciences, Kosice, Slovakia. The work was performed at the Department of Experimental and Vascular Surgery, Academic Medical Center, Amsterdam, The Netherlands.

This study was supported by the Dutch Heart Association (grant 97.193).

Address for reprints: P. de Haan, MD, Department of Anesthesiology, Academic Hospital, University of Amsterdam, Postbus 22660, 1100 DD Amsterdam, The Netherlands (E-mail: P.deHaan{at}amc.uva.nl ).

Objective: In the present study, we investigated the effect of ischemic pretreatment on heat shock protein 72 concentration and neurologic and histopathologic outcome after transient spinal cord ischemia.
Methods: In 28 New Zealand White rabbits, an aortic occlusion device was placed infrarenally. The animals were randomly assigned to 2 groups: ischemic pretreatment (n = 14 animals) and control (n = 14 animals). The duration of ischemic pretreatment was 6 minutes. After 24 hours, the aorta was occluded for 26 minutes in both groups of animals. Neurologic function was assessed 24 and 48 hours after the definite ischemic insult. At 48 hours, the animals were killed for histopathologic evaluation of the spinal cord. In a separate set of animals, heat shock protein 72 levels were determined in the lumbar spinal cord after both a 6- and 10-minute ischemic period, with the use of a Western blot analysis.
Results: No significant difference in neurologic outcome between the groups was observed at 24 and 48 hours. The incidence of paraplegia and severe paresis at 48 hours was 79% in the control group and 92% in the ischemic pretreatment group. There was no difference in histopathologic scores between the groups. Heat shock protein 72 could be clearly detected 1 and 2 days after 6- or 10-minute periods of spinal cord ischemia.
Conclusions: In the present rabbit study, ischemic pretreatment could not induce tolerance against a moderately severe spinal cord ischemic insult, despite increased heat shock protein 72 levels after the preconditioning stimulus.




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