ATS
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Author home page(s):
Elaine E. Tseng
Malcolm V. Brock
Michael V. Johnston
William A. Baumgartner
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Tseng, E. E.
Right arrow Articles by Baumgartner, W. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Tseng, E. E.
Right arrow Articles by Baumgartner, W. A.

Ann Thorac Surg 1999;67:371-376
© 1999 The Society of Thoracic Surgeons

Original Articles

Increased intracerebral excitatory amino acids and nitric oxide after hypothermic circulatory arrest

Elaine E. Tseng, MDa, Malcolm V. Brock, MDa, Christopher C. Kwon, MSa, Madhu Annanata, MSa, Mary S. Lange, MAa, Juan C. Troncoso, MDa, Michael V. Johnston, MDa, William A. Baumgartner, MDa

a Division of Cardiac Surgery, Johns Hopkins Medical Institutions and Kennedy-Krieger Research Institute, Baltimore, Maryland, USA

Address reprint requests to Dr Baumgartner, Division of Cardiac Surgery, Johns Hopkins Hospital, Blalock 618, 600 North Wolfe St, Baltimore, MD 21287
e-mail: wbaumgar{at}welchlink.welch.jhu.edu

Presented at the Poster Session of the Thirty-fourth Annual Meeting of The Society of Thoracic Surgeons, New Orleans, LA Jan 26–28, 1998.

Background. Prolonged hypothermic circulatory arrest (HCA) results in neurologic injury, but the mechanism of this injury is unknown. This study was undertaken to measure quantitatively intracerebral excitatory amino acids and citrulline, an equal coproduct of nitric oxide, during HCA. We hypothesized that HCA resulted in higher levels of glutamate, aspartate, glycine, causing increased intracellular calcium, and therefore, nitric oxide and citrulline.

Methods. Ten dogs underwent intracerebral microdialysis and 2 hours of HCA at 18°C. Effluent was analyzed by high performance liquid chromatography with electrochemical detection. Five dogs each were sacrificed at 8 and 20 hours after HCA. Neuronal apoptosis was scored from 0 (no injury) to 100 (severe injury).

Results. Time course of HCA was divided into six periods. Peak levels of amino acids in each period were compared with those at baseline. Glutamate, coagonist glycine, and citrulline, an equal coproduct of nitric oxide, increased significantly over baseline during HCA, cardiopulmonary bypass, and 2 to 8 hours after HCA. Aspartate increased significantly during HCA and 8 to 20 hours after HCA. Apoptosis score was 65.56 ± 5.67 at 8 hours and 30.63 ± 14.96 at 20 hours after HCA.

Conclusions. Our results provide direct evidence that HCA causes increased intracerebral glutamate and aspartate, along with coagonist glycine. We conclude that HCA causes glutamate excitotoxicity with subsequent nitric oxide production resulting in neurologic injury, which begins during arrest and continues until 20 hours after hypothermic circulation arrest. To provide effective cerebral protection, pharmacologic strategies to reduce glutamate excitotoxicity require intervention beyond the initial ischemic insult.




This article has been cited by other articles:


Home page
 J. Thorac. Cardiovasc. Surg.Home page
X. Pan, L. Sun, W. Ma, Y. Tang, C. Long, L. Tian, N. Liu, Z. Feng, and J. Zheng
Overactivation of poly(adenosine phosphate-ribose) polymerase 1 and molecular events in neuronal injury after deep hypothermic circulatory arrest: study in a rabbit model.
J. Thorac. Cardiovasc. Surg., November 1, 2007; 134(5): 1227 - 1233.
[Abstract] [Full Text] [PDF]

Home page
 Ann. Thorac. Surg.Home page
C. J. Barreiro, J. A. Williams, T. P. Fitton, M. S. Lange, M. E. Blue, L. Kratz, P. B. Barker, M. Degaonkar, V. L. Gott, J. C. Troncoso, et al.
Noninvasive Assessment of Brain Injury in a Canine Model of Hypothermic Circulatory Arrest Using Magnetic Resonance Spectroscopy.
Ann. Thorac. Surg., May 1, 2006; 81(5): 1593 - 1598.
[Abstract] [Full Text] [PDF]

Home page
 Ann. Thorac. Surg.Home page
G. Amir, C. Ramamoorthy, R. K. Riemer, V. M. Reddy, and F. L. Hanley
Neonatal Brain Protection and Deep Hypothermic Circulatory Arrest: Pathophysiology of Ischemic Neuronal Injury and Protective Strategies
Ann. Thorac. Surg., November 1, 2005; 80(5): 1955 - 1964.
[Abstract] [Full Text] [PDF]

Home page
 StrokeHome page
Y. Teshima, M. Akao, R. A. Li, T. H. Chong, W. A. Baumgartner, M. V. Johnston, and E. Marban
Mitochondrial ATP-Sensitive Potassium Channel Activation Protects Cerebellar Granule Neurons From Apoptosis Induced by Oxidative Stress
Stroke, July 1, 2003; 34(7): 1796 - 1802.
[Abstract] [Full Text] [PDF]

Home page
 J. Thorac. Cardiovasc. Surg.Home page
T.-A. Miyamoto and K.-J. Miyamoto
Alpha-stat strategy: Cause of ischemia in brains with old cerebral infarction despite selective cerebral hypothermic antegrade perfusion
J. Thorac. Cardiovasc. Surg., December 1, 2002; 124(6): 1260 - 1261.
[Full Text]

Home page
 J. Thorac. Cardiovasc. Surg.Home page
R. S. Bonser, C. H. Wong, D. Harrington, D. Pagano, M. Wilkes, T. Clutton-Brock, and M. Faroqui
Failure of retrograde cerebral perfusion to attenuate metabolic changes associated with hypothermic circulatory arrest
J. Thorac. Cardiovasc. Surg., May 1, 2002; 123(5): 943 - 950.
[Abstract] [Full Text] [PDF]

Home page
 Ann. Thorac. Surg.Home page
J. G. Shake, E. A. Peck, E. Marban, V. L. Gott, M. V. Johnston, J. C. Troncoso, J. M. Redmond, and W. A. Baumgartner
Pharmacologically induced preconditioning with diazoxide: a novel approach to brain protection
Ann. Thorac. Surg., December 1, 2001; 72(6): 1849 - 1854.
[Abstract] [Full Text] [PDF]

Home page
 J. Thorac. Cardiovasc. Surg.Home page
M. P. Ehrlich, J. McCullough, D. Wolfe, N. Zhang, H. Shiang, D. Weisz, C. Bodian, and R. B. Griepp
Cerebral effects of cold reperfusion after hypothermic circulatory arrest
J. Thorac. Cardiovasc. Surg., May 1, 2001; 121(5): 923 - 931.
[Abstract] [Full Text] [PDF]

Home page
 Ann. Thorac. Surg.Home page
Y. Cho, T. Ueda, A. Mori, T. Nakamichi, H. Shimizu, Y. Inoue, and S. Kawada
Exogenous aspartate neurotoxicity in the spinal cord under metabolic stress in vivo
Ann. Thorac. Surg., November 1, 2000; 70(5): 1496 - 1500.
[Abstract] [Full Text] [PDF]

Home page
 Ann. Thorac. Surg.Home page
T.-A. Miyamoto and K.-J. Miyamoto
Bohr effect during cooling to and rewarming from 20{degrees}C cannot be ignored
Ann. Thorac. Surg., August 1, 2000; 70(2): 690 - 690.
[Full Text] [PDF]

Home page
 Ann. Thorac. Surg.Home page
T.-A. Miyamoto and K.-J. Miyamoto
Monitoring adequacy of brain oxygenation
Ann. Thorac. Surg., July 1, 2000; 70(1): 336 - 337.
[Full Text] [PDF]

Home page
 Ann. Thorac. Surg.Home page
T.-A. Miyamoto and K.-J. Miyamoto
Is it justified to disregard the Bohr effect during alpha-stat hypothermia?
Ann. Thorac. Surg., March 1, 2000; 69(3): 973 - 974.
[Full Text] [PDF]

Home page
 Ann. Thorac. Surg.Home page
T. A. Miyamoto and K.-J. Miyamoto
Would pH-stat strategy generate nitric oxide during hypothermic perfusion?
Ann. Thorac. Surg., January 1, 2000; 69(1): 312 - 313.
[Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
ANN THORAC SURG ASIAN CARDIOVASC THORAC ANN EUR J CARDIOTHORAC SURG
J THORAC CARDIOVASC SURG ICVTS ALL CTSNet JOURNALS
Copyright © 1999 by The Society of Thoracic Surgeons.