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1 otocol may decrease the rates of devastating spinal cord ischemia.
2 sion with subsequent reperfusion to generate spinal cord ischemia.
3 arteries are effective for the treatment of spinal cord ischemia.
4 on systemic blood pressure in a rat model of spinal cord ischemia.
5 onstrated to be neuroprotective in brain and spinal cord ischemia.
6 microl/day for 7 days prior to induction of spinal cord ischemia.
9 orta for 60 minutes results in high rates of spinal cord ischemia, an effect mitigated by limiting ba
11 azoxide improves neurological function after spinal cord ischemia and reperfusion by diminishing leve
14 otection protocol could decrease the risk of spinal cord ischemia and/or paraplegia and consists of p
15 a critical determinant of outcome following spinal cord ischemia, and controlled peri-operative bloo
16 y matter involvement similar to that seen in spinal cord ischemia, and three (16%) had isolated white
19 y early detection and immediate treatment of spinal cord ischemia before it evolves to infarction.
22 es the potential catastrophic consequence of spinal cord ischemia from an unexpectedly prolonged aort
23 ctors and interventions to prevent and treat spinal cord ischemia has the potential to prevent spinal
24 ive events associated with increased IM were spinal cord ischemia (HR = 9.46; 95% CI: 3.98-22.47; P <
25 atory complications in 45 patients (22%) and spinal cord ischemia in 22 (11%), of whom 10 (45%) fully
29 are consistent with the idea that transient spinal cord ischemia induces the formation of a death-in
34 Neurologic events included stroke (5.0%) and spinal cord ischemia (permanent 1.7%, temporary 7.9%).
39 ntials (MEPs) monitoring can promptly detect spinal cord ischemia (SCI) from aortic clamping during o
40 ed paralysis with histopathologic changes of spinal cord ischemia (SCI) in 4/8 (50%), with no SCI in
42 has demonstrated low risks of mortality and spinal cord ischemia (SCI), but few large series have be