Abstract
Nitric oxide (NO), has recently emerged as an important mediator of cellular events which impacts the pathophysiology of cerebral ischemia. Using electrochemical microsensors, we measured the cortical NO concentration within ischemic tissue before and during 3 min. of airway occlusion (asphyxia) and during reperfusion in adult rats (n=6). Baseline concentrations of NO were 1.89 ± 0.33 μM. The maximum concentrations of NO during asphyxia and on reperfusion were 5.15 ± 0.45 μM and 6.50 ± 0.24 μM, respectively. A novel method (cepstral distance) was used to quantify changes in EEG due to brain injury. Our data indicates that excess NO is released in the brain after the onset of ischemia. Its restoration to baseline appears to impact recovery of the brain's electrical function as measured by EEG. Animals (n=2) in which NO did not return to baseline value had isoelectric EEG and showed no sign of recovery.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 2151-2152 |
| Number of pages | 2 |
| Journal | Annual International Conference of the IEEE Engineering in Medicine and Biology - Proceedings |
| Volume | 5 |
| State | Published - Dec 1 1997 |
| Event | Proceedings of the 1997 19th Annual International Conference of the IEEE Engineering in Medicine and Biology Society - Chicago, IL, USA Duration: Oct 30 1997 → Nov 2 1997 |
ASJC Scopus subject areas
- Signal Processing
- Biomedical Engineering
- Computer Vision and Pattern Recognition
- Health Informatics