This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a colleague Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Web of Science (2) Citing Articles via Google Scholar Google Scholar Articles by Ho, C.-M. Articles by Su, C.-K. Search for Related Content PubMed PubMed Citation Articles by Ho, C.-M. Articles by Su, C.-K. Related Collections Mechanisms Pharmacology

---

ANESTHETIC PHARMACOLOGY

Ketamine Attenuates Sympathetic Activity Through Mechanisms not Mediated by N-Methyl-d-Aspartate Receptors in the Isolated Spinal Cord of Neonatal Rats

Chiu-Ming Ho, MD, PhD^*, and Chun-Kuei Su, PhD

*Department of Anesthesiology, Taipei Veterans General Hospital and National Yang-Ming University; Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan

Address correspondence and reprint requests to Chiu-Ming Ho, MD, PhD, Department of Anesthesiology, Taipei Veterans General Hospital, No. 201, Sec. 2, Shihpai Rd, Taipei 112, Taiwan. Address e-mail to cmho{at}vghtpe.gov.tw.

Ketamine is believed to have sympathomimetic effects, although the central mechanism remains unclear. Using an in vitro splanchnic nerve-spinal cord preparation from neonatal rats, our previous investigations have demonstrated that tonic sympathetic activity is spontaneously generated from the thoracic spinal cord. We designed this study to investigate whether applications of ketamine to the cord would augment sympathetic activity and whether this action was dependent on N-methyl-d-aspartate receptors. Bath application of ketamine significantly reduced sympathetic activity in a concentration-dependent manner. Ketamine in 10, 20, 40, 80, and 120 µM reduced the sympathetic activity to 82.6% ± 4.4% (P < 0.05), 61.7% ± 5.1%, 42.8% ± 4.2%, 24.9% ± 4.4%, and 9.2% ± 2.7% of the control value, respectively (P < 0.01, n = 8 for each test). The 50% inhibitory concentration of ketamine on sympathetic activity was 32 µM. Pretreatment with DL-2-amino-5-phosphonovaleric acid, a selective competitive N-methyl-d-aspartate receptor antagonist, did not alter ketamine-induced depression of sympathetic activity. These results suggest that ketamine reduces sympathetic activity by mechanisms that are independent of N-methyl-d-aspartate receptor activity.