Xenon attenuates cardiopulmonary bypass-induced neurologic and neurocognitive dysfunction in the rat.

Published

Journal Article

BACKGROUND: With clinical data suggesting a role for excitatory amino acid neurotransmission in the pathogenesis of cardiopulmonary bypass (CPB)-associated brain injury, the current study was designed to determine whether xenon, an N-methyl-D-aspartate receptor antagonist, would attenuate CPB-induced neurologic and neurocognitive dysfunction in the rat. METHODS: Following surgical preparation, rats were randomly divided into four groups: (1) sham rats were cannulated but did not undergo CPB; (2) CPB rats were subjected to 60 min of CPB using a membrane oxygenator receiving a gas mixture of 30% O2, 65% N2, and 5% CO2; (3) CPB + MK801 rats received MK801 (0.15 mg/kg intravenous) 15 min prior to 60 min of CPB with the same gas mixture; and (4) CPB + xenon rats underwent 60 min of CPB using an oxygenator receiving 30% O2, 60% xenon, 5% N2, and 5% CO2. Following CPB, the rats recovered for 12 days, during which they underwent standardized neurologic and neurocognitive testing (Morris water maze). RESULTS: The sham and CPB + xenon groups had significantly better neurologic outcome compared to both the CPB and CPB + MK801 groups on postoperative days 1 and 3 (P < 0.05). Compared to the CPB group, the sham, CPB + MK801, and CPB + xenon groups had better neurocognitive outcome on postoperative days 3 and 4 (P < 0.001). By the 12th day, the neurocognitive outcome remained significantly better in the CPB + xenon group compared to the CPB group (P < 0.01). CONCLUSION: These data indicate that CPB-induced neurologic and neurocognitive dysfunction can be attenuated by the administration of xenon, potentially related to its neuroprotective effect via N-methyl-D-aspartate receptor antagonism.

Full Text

Duke Authors

Cited Authors

  • Ma, D; Yang, H; Lynch, J; Franks, NP; Maze, M; Grocott, HP

Published Date

  • March 2003

Published In

Volume / Issue

  • 98 / 3

Start / End Page

  • 690 - 698

PubMed ID

  • 12606913

Pubmed Central ID

  • 12606913

International Standard Serial Number (ISSN)

  • 0003-3022

Digital Object Identifier (DOI)

  • 10.1097/00000542-200303000-00017

Language

  • eng

Conference Location

  • United States