Effects of somatosensory electrical stimulation on neuronal injury after global hypoxia-ischemia.
Electrical stimulation (ES) is used after cardiac arrest (CA) for diagnostic and therapeutic purposes. The effects of ES on brain damage induced by hypoxic-ischemic brain injury (HI) has not been investigated. Stimulation of afferent pathways by ES may increase neural injury by releasing excitatory neurotransmitters (glutamate) and thereby exacerbating excitotoxicity. To test this hypothesis, ES was applied to the median nerve (2 h) of adult male Wistar rats after 5 min of asphyxic CA and cardiopulmonary resuscitation. Control animals received no ES. Assessment of neuronal damage in five regions of interest was performed in survivors (ESn=15, Control n=10, Sham n=3) after 48 h using H&E, Cresyl-Violet, and TUNEL stains, and Caspase-3 and activated ERK 1/2 immunohistochemistry. Ratios of injured to normal cells were calculated. Most injury was found in hippocampus and cerebellum. ES animals showed significantly lower injury ratios in bilateral hippocampus as compared with controls (F=20.8, p<0.00001). TUNEL staining, caspase-3 and activated ERK 1/2 showed no differences between groups. It is concluded that ES during the acute phase of HI does not amplify neuronal damage at 48 h, but may have a protective effect that requires further investigation.
Buitrago
Manuel M
MM
Dept. of Neurology, University of Tübingen, Hoppe-Seyler-Str. 3, 72076 Tübingen, Germany.
Luft
Andreas R
AR
Thakor
Nitish V
NV
Blue
Mary E
ME
Hanley
Daniel F
DF
D000344:Afferent Pathways / Q000378:metabolism / Q000503:physiopathology*; D000818:Animals; D053148:Caspase 3; D020169:Caspases / Q000378:metabolism; D002531:Cerebellum / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D002544:Cerebral Infarction / Q000473:pathology / Q000503:physiopathology* / Q000628:therapy; D004195:Disease Models, Animal; D004599:Electric Stimulation Therapy / Q000009:adverse effects / Q000379:methods; D005073:Evoked Potentials, Somatosensory / Q000502:physiology; D048049:Extracellular Signal-Regulated MAP Kinases / Q000378:metabolism; D007839:Functional Laterality / Q000502:physiology; D018698:Glutamic Acid / Q000378:metabolism; D006624:Hippocampus / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D020925:Hypoxia-Ischemia, Brain / Q000473:pathology / Q000503:physiopathology* / Q000628:therapy; D008297:Male; D008475:Median Nerve / Q000502:physiology; D009410:Nerve Degeneration / Q000473:pathology / Q000503:physiopathology* / Q000628:therapy; D051381:Rats; D017208:Rats, Wistar; D013003:Somatosensory Cortex / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*
D018698:Glutamic Acid; D048049:Extracellular Signal-Regulated MAP Kinases; C505410:Casp3 protein, rat; D053148:Caspase 3; D020169:Caspases