The role of the monosialoganglioside, GM1, as a neuroprotectant in an experimental model of cardiopulmonary bypass and hypothermic circulatory arrest

William A. Baumgartner, J. Mark Redmond, Kenton J. Zehr, Malcolm V. Brock, Elaine E. Tseng, Mary E. Blue, Juan C. Troncoso, Michael V. Johnston

Research output: Contribution to journalArticle

Abstract

Twelve male dogs were placed on closed-chest cardiopulmonary bypass, subjected to 2 h of HCA at 18°C, and rewarmed to 37°C on closed-chest cardiopulmonary bypass. All animals were mechanically ventilated and monitored for 20 h before extubation and survived for 3 days. Group 1 dogs (n = 6) were pretreated with GM1, 30 mg/kg/24 h for 3 days before HCA, and received continuous infusion of GM1 during the procedure and 30 mg/kg/24 h for 3 days after HCA. Group 2 dogs (n = 6) received vehicle only. With a species-specific behavior scale that yielded a neurodeficit score ranging from 0% (normal) to 100% (brain dead), all animals were neurologically assessed every 12 h by two observers. After death at 72 h, brains were examined by glutamate receptor autoradiography and by histologic examination for patterns of selective neuronal necrosis and were scored blindly from 0 (normal) to 100 (severe injury). These results provide evidence of a role for GE in the development of HCA-induced brain injury and suggest that monosialogangliosides may have a neuroprotective effect in prolonged periods of HCA.

Original languageEnglish (US)
Pages (from-to)382-390
Number of pages9
JournalAnnals of the New York Academy of Sciences
Volume845
DOIs
StatePublished - Jan 1 1998

ASJC Scopus subject areas

  • Neuroscience(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • History and Philosophy of Science

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