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The Journal of Thoracic and Cardiovascular Surgery, Vol 104, 256-261, Copyright © 1992 by The American Association for Thoracic Surgery and The Western Thoracic Surgical Association
AK Qayumi, MT Janusz, WR Jamieson and DM Lyster
The efficacy of pharmacologic agents for prevention and control of
oxygen-derived free radical damage in ischemia-reperfusion injury of the
spinal cord was assessed in a swine model of thoracic and thoracoabdominal
aortic crossclamping. Animals were exposed to 30 minutes of ischemia that
induced lethal, irreversible injury and paraplegia. The experimental groups
were as follows: group A (n = 7), control group, receiving no pharmacologic
intervention; group B (n = 7), deferoxamine 50 mg/kg/day administered
intravenously over 3 to 4 hours before ischemia; group C (n = 7),
allopurinol pretreatment 50 mg/kg/day for 3 days; and group D (n = 7),
superoxide dismutase 60,000 units administered with 50,000 units before
removal of the aortic crossclamp and 10,000 units over 10 minutes of
reperfusion. Proximal hypertension was controlled with sodium nitroprusside
and volume depletion. The methods of assessment were neurologic by a
modified Tarlov criteria and blood flow by radiolabeled microspheres.
Results of blood flow assessment confirmed a true ischemic episode of 30
minutes for all animals in all groups. The blood flow fell significantly
during ischemia (p less than 0.01) and a hyperemic response was evident in
the early reperfusion period. All animals in control group A were
paraplegic. The group B (deferoxamine) results were superior; 85% had grade
III function on a modified Tarlov scale, with animals in the group standing
and even walking with difficulty. Only one animal in this group had good
movements of hind limbs but was unable to stand or walk. Neurologic
recovery was limited in the allopurinol group (group C), with 85% showing
slight neurologic recovery with limited movement of the hind limbs. The
animals in the superoxide dismutase group (group D) all had good recovery,
with strong motor response of hind limbs, but were not able to stand. In
summary, the results of this experimental protocol confirmed the possible
role of oxygen-derived free radicals in the pathophysiology of spinal cord
injury, induced by aortic crossclamping. Moreover, it proved that
ischemia-reperfusion injury could be altered by pharmacologic
interventions.
ARTICLES
Pharmacologic interventions for prevention of spinal cord injury caused by aortic crossclamping
Department of Surgery, Faculty of Medicine, University of British Columbia, Vancouver, Canada.
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