Preoperative stress conditioning prevents paralysis after experimental aortic surgery: increased heat shock protein content is associated with ischemic tolerance of the spinal cord.
BACKGROUND
All forms of surgical therapy are stressful and injurious. The problems of paralysis, renal dysfunction, and colonic ischemia associated with aortic occlusion are due to acute ischemia-reperfusion injury at the cellular level. Acute-anterior spinal cord ischemia is the most devastating outcome of these iatrogenic-ischemic events. The majority of surgical procedures are performed electively and therefore provide an opportunity to preoperatively condition the patient to minimize these ischemia-related morbidities.


OBJECTIVE
We sought to determine whether acute spinal cord injury associated with aortic occlusion can be prevented by induction of the cellular stress response by means of preoperative administration of whole-body hyperthermia or stannous chloride.


METHODS
The study consisted of an experimental rabbit model of infrarenal aortic occlusion for 20 minutes at normothermic body temperature.


RESULTS
Control rabbits experienced an 88% (7/8) incidence of paralysis after spinal cord ischemia induced by 20 minutes of aortic occlusion, whereas animals treated preoperatively with either whole-body hyperthermia (0/9) or stannous chloride (0/4) never became paralyzed (P <.001 for control vs treated groups). Ischemic protection of the spinal cord was associated with increased content of stress proteins within tissues of pretreated animals.


CONCLUSIONS
Prior induction of the heat shock response in the whole animal will increase the content of stress proteins within the spinal cord and other tissues and result in the prevention of hind-limb paralysis associated with aortic occlusion. We have designated the preoperative induction of the cellular stress response for the prevention of ischemic tissue injury stress conditioning. We suggest that stress-conditioning protocols represent the opportunity to practice preventative medicine at the molecular level.
Perdrizet
George A
GA
Department of Surgery and Trauma, Hartford Hospital and University of Connecticut School of Medicine, Farmington, CT 06102-5037, USA. gperdi@harthosp.org
Lena
Christopher J
CJ
Shapiro
David S
DS
Rewinski
Michael J
MJ
D000818:Animals; D001012:Aorta, Abdominal / Q000601:surgery*; D015153:Blotting, Western; D005260:Female; D006360:Heat-Shock Proteins / Q000235:genetics / Q000378:metabolism*; D006614:Hindlimb; D006979:Hyperthermia, Induced; D019194:Ischemic Preconditioning; D010264:Paraplegia / Q000517:prevention & control*; D011817:Rabbits; D020760:Spinal Cord Ischemia / Q000517:prevention & control*; D013997:Time Factors; D017971:Tin Compounds / Q000494:pharmacology
D006360:Heat-Shock Proteins; D017971:Tin Compounds; C023599:stannous chloride