Literature DB >> 3950746

Protection against experimental ischemic spinal cord injury.

C S Robertson, R Foltz, R G Grossman, J C Goodman.   

Abstract

The authors have studied the protection against ischemic damage to rabbit spinal cord by pretreatment with agents that block neuronal activity and directly or indirectly reduce tissue metabolism. Hypothermia, thiopental, magnesium, lidocaine, and naloxone were used to pretreat the spinal cord prior to ischemia. Hypothermia and thiopental provided comparable protection: they each increased the duration of ischemia required to produce neurological deficits in 50% of the animals from 26 to 41 minutes. They also increased from 10 to 30 minutes the time that the postsynaptic waves of the spinal somatosensory evoked potential (SSEP) could be absent and the animal still have neurological recovery. Hypothermia and thiopental, when used together, increased the duration of ischemia required to produce neurological deficits to 57 minutes in 50% of the animals. Naloxone increased the duration of ischemia required to produce neurological deficits to 36 minutes in 50% of the animals, and increased to 20 minutes the time that the postsynaptic waves of the SSEP could be absent and the animal still have neurological recovery. Magnesium pretreatment improved neurological outcome, possibly by improving collateral circulation as the SSEP did not fail completely during aortic occlusion in all animals. Lidocaine was not beneficial, perhaps because of the prolonged hypotension that resulted.

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Year:  1986        PMID: 3950746     DOI: 10.3171/jns.1986.64.4.0633

Source DB:  PubMed          Journal:  J Neurosurg        ISSN: 0022-3085            Impact factor:   5.115


  18 in total

Review 1.  Acute spinal cord injury: monitoring and anaesthetic implications.

Authors:  A M Lam
Journal:  Can J Anaesth       Date:  1991-05       Impact factor: 5.063

2.  Cerebral monitoring in the operating room and the intensive care unit - an introductory for the clinician and a guide for the novice wanting to open a window to the brain. Part II: Sensory-evoked potentials (SSEP, AEP, VEP).

Authors:  Enno Freye
Journal:  J Clin Monit Comput       Date:  2005-04       Impact factor: 2.502

3.  Paraplegia after thoracoabdominal aortic surgery: not just assisted circulation, hypothermic arrest, clamp and sew, or TEVAR.

Authors:  Charles Acher; Martha Wynn
Journal:  Ann Cardiothorac Surg       Date:  2012-09

4.  Neuronal protection with magnesium.

Authors:  G Gathwala
Journal:  Indian J Pediatr       Date:  2001-05       Impact factor: 1.967

Review 5.  Hypothermic treatment for acute spinal cord injury.

Authors:  W Dalton Dietrich; Allan D Levi; Michael Wang; Barth A Green
Journal:  Neurotherapeutics       Date:  2011-04       Impact factor: 7.620

6.  Regional lidocaine infusion reduces postischemic spinal cord injury in rabbits.

Authors:  A Z Apaydin; S Büket
Journal:  Tex Heart Inst J       Date:  2001

7.  Spinal cord infarction: a rare cause of paraplegia.

Authors:  Sonali Patel; Khimara Naidoo; Peter Thomas
Journal:  BMJ Case Rep       Date:  2014-06-25

8.  Magnesium sulfate treatment in experimental spinal cord injury: emphasis on vascular changes and early clinical results.

Authors:  Erkan Kaptanoglu; Etem Beskonakli; Ihsan Solaroglu; Asuman Kilinc; Yamac Taskin
Journal:  Neurosurg Rev       Date:  2003-05-29       Impact factor: 3.042

Review 9.  Application of therapeutic hypothermia in the ICU: opportunities and pitfalls of a promising treatment modality. Part 1: Indications and evidence.

Authors:  Kees H Polderman
Journal:  Intensive Care Med       Date:  2004-02-06       Impact factor: 17.440

10.  Local spinal cord glucose utilization in conscious and halothane-anaesthetized rats.

Authors:  G Crosby; S Atlas
Journal:  Can J Anaesth       Date:  1988-07       Impact factor: 5.063

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