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Ann Thorac Surg 2001;71:1397-1398
© 2001 The Society of Thoracic Surgeons
a The Heart Center, Missouri Baptist Medical Center, St. Louis, Missouri, USA
Address reprint requests to Dr
Kouchoukos, The Heart Center, Missouri Baptist Medical Center, 3009 N
Ballas Rd, Suite 266-C, St. Louis, MO
63131
e-mail: ntkouch@aol.com
As Originally Published in 1994: by Chris K. Rokkas, MD, Loring R. Helfrich, Jr, BS, Douglas C. Lobner, PhD, Dennis W. Choi, MD, PhD, and Nicholas T. Kouchoukos, MD. Division of Cardiothoracic Surgery, Department of Surgery, and Department of Neurology, Washington University School of Medicine, St. Louis, Missouri.
The release of excitatory amino
acids, particularly glutamate, into the extracellular space plays a
causal role in irreversible neuronal damage after central nervous system
ischemia. Dextrorphan, a noncompetitive
N-methyl-D-aspartate receptor antagonist, has been
shown to provide significant protection against cerebral damage after
focal ischemia. We investigated the changes in extracellular
neurotransmitter amino acid concentrations using in vivo microdialysis
in a swine model of spinal cord ischemia. After lumbar laminectomies
were performed, all animals underwent left thoracotomy and right
atrialfemoral cardiopulmonary bypass with additional aortic arch
perfusion. Microdialysis probes were then inserted stereotactically into
the lumbar spinal cord. The probes were perfused with artificial
cerebrospinal fluid and 15-minute samples were assayed using
high-performance liquid chromatography. Group 1 animals (n = 9)
underwent aortic clamping distal to the left subclavian and proximal to
the renal arteries for 60 minutes. Group 2 animals (n = 7) were treated
with dextrorphan before application of aortic clamps, and during aortic
occlusion
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