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Ann Thorac Surg 2001;72:2180-2181
© 2001 The Society of Thoracic Surgeons
a Department of Cardiovascular Surgery, Institut Mutualiste Montsouris, Paris, France
To the Editor
We read with great interest the recent update by Rokkas and Kouchoukos [1] of the article "Dextrorphan Inhibits the Release of Excitatory Amino Acids During Spinal Cord Ischemia." Their continuing efforts have helped all of us to better understand the pathophysiological mechanisms implicated in spinal cord ischemia related to operations on the thoracoabdominal aorta. There is now compelling evidence that excitatory amino acids are involved in both necrotic and apoptotic death of spinal neurons after transient spinal cord ischemia. Dextrorphan, like most other N-methyl-D-aspartate (NMDA) antagonists, is no longer used clinically because of intolerable side effects [1]. However, other drugs have been found to protect the brain and spinal cord, and some are currently being used in humans [2]. Magnesium sulfate, memantine, and riluzole have demonstrated efficacy in spinal cord ischemia models and are currently prescribed for patients with various neurological disorders [2, 3]. Thus, these drugs are candidates for pilot human studies in the field of thoracoabdominal aortic surgery.
Magnesium salts have demonstrated neuroprotective effects in several models of spinal cord ischemia and are reported to be neuroprotective even when injected 24 hours after ischemia [2, 4, 5]. Because Mg2+ ions cross the blood-brain barrier, intravenous administration significantly raises the Mg2+ levels in cerebrospinal fluid. The combination of intravenous MgCl2 and a 3°C decrease in body temperature can extend the time of spinal cord tolerance to ischemia almost 3-fold [4]. Moreover, magnesium sulfate is reported to improve both neurological recovery and spinal cord histopathology after transient ischemia [2]. The mechanism of magnesium neuroprotection is probably due to a number of factors and may involve noncompetitive blockade of NMDA receptors, blockade of Ca2+ channels, attenuation of endothelial and neuronal reperfusion injuries, and regeneration of adenosine triphosphate after ischemia. Also, Mg2+ ions may be beneficial by vasodilating segmental vessels supplying the spinal cord through the release of endothelial prostacyclin and preventing thrombosis of critical segmental vessels through an inhibition of platelet reactivity [2].
We recently started a pilot study with magnesium sulfate during repair of thoracic and thoracoabdominal aortic aneurysms. Magnesium sulfate (100 mg/kg) was injected intravenously over 15 minutes, starting 30 minutes before aortic clamping. An infusion rate of 40 mg · kg-1 · h-1 was maintained during the entire aortic cross-clamp period. This pharmacological approach was combined with distal bypass, mild permissive hypothermia (33° to 34°C) and cerebrospinal fluid drainage.
We have used this technique in 7 patients (2 patients with a descending thoracic aneurysm and 5 patients with Marfan’s syndrome and type I or II thoracoabdominal aortic aneurysm). In all patients, segmental vessels T8 through L2 were reimplanted routinely. Mean serum magnesium levels were 2.34 ± 0.17 mmol/L at aortic cross-clamping, 2.11 ± 0.43 mmol/L at unclamping, and 1.18 ± 0.23 after 24 hours of reperfusion. All patients but 1 were extubated within 24 hours after operation, and none sustained either immediate or delayed neurological deficits. No patient died, and all were discharged within 15 days postoperatively. None of the patients have experienced potential side effects of magnesium such as neuromuscular blockade, severe hypotension, electrocardiographic changes, or bleeding. This protocol appears safe, and the combination of high magnesium levels with mild hypothermia affords additional protection against spinal cord ischemia-reperfusion injury, thereby extending the period of safe occlusion of the thoracic aorta.
References
This article has been cited by other articles:
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  C. D. Etz, T. M. Homann, K. A. Plestis, N. Zhang, M. Luehr, D. J. Weisz, G. Kleinman, and R. B. Griepp Spinal cord perfusion after extensive segmental artery sacrifice: can paraplegia be prevented? Eur. J. Cardiothorac. Surg., April 1, 2007; 31(4): 643 - 648. [Abstract] [Full Text] [PDF]
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