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 language | English (US) |
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Pages (from-to) | 382-390 |
Number of pages | 9 |
Journal | Annals of the New York Academy of Sciences |
Volume | 845 |
DOIs | |
State | Published - 1998 |
ASJC Scopus subject areas
- Neuroscience(all)
- Biochemistry, Genetics and Molecular Biology(all)
- History and Philosophy of Science