Abstract
Purpose: This prospective, randomized study was performed to investigate the effects of oxygen (O2) treatment during sustained epileptic activity on mortality, subsequent seizure frequency, and neuronal damage. Methods: Status epilepticus (SE) was induced by intraperitoneal injection of 340mg/kg pilocarpine, and terminated by diazepam after 40min. During SE, rats were randomized to O2 treatment (insufflation rate of 1.5l/min O2) during SE or normal air conditions. Outcome measures were SE-related mortality, seizure occurrence, mossy fiber sprouting, neuronal cell loss and expression of 27-kDa heat-shock protein (Hsp27). Results: O2-treated and O2-untreated animals did not differ with respect to SE latency, diazepam dose required to stop SE. While 7/38 rats died during SE in the O2-untreated group, very little mortality (1/38) occurred in the O2-treated group (P2-treated rats died which was not observed in the O2-untreated group indicating no significant difference in overall mortality. There was a tendency towards lower seizure rate in the O2-treated group at one month after pilocarpine-induced SE. Three months after SE, however, seizure rates were no longer different between both groups. Moreover, mossy fiber sprouting, neuronal cell loss and Hsp27 expression did not differ between O2-treated and O2-untreated groups. Conclusion: Our findings indicate that O2 treatment might delay the relative risk of epileptic seizures following an initial brain injury, but it may also lead to a rather unfavorably increased heterogeneity of epileptogenesis in experimental studies.
| Original language | English |
|---|---|
| Pages (from-to) | 90-97 |
| Number of pages | 8 |
| Journal | Epilepsy Research |
| Volume | 108 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - Jan 2014 |
| Externally published | Yes |
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Keywords
- Heat-shock protein
- Oxygen
- Pilocarpine
- Status epilepticus
- Timm stain
ASJC Scopus subject areas
- Clinical Neurology
- Neurology
Cite this
Effects of oxygen insufflation during pilocarpine-induced status epilepticus on mortality, tissue damage and seizures. / Müller, Lorenz; Müller, Steffen; Sellmann, Tina; Groeneweg, Linda; Tokay, Tursonjan; Köhling, Rüdiger; Kirschstein, Timo.
In: Epilepsy Research, Vol. 108, No. 1, 01.2014, p. 90-97.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Effects of oxygen insufflation during pilocarpine-induced status epilepticus on mortality, tissue damage and seizures
AU - Müller, Lorenz
AU - Müller, Steffen
AU - Sellmann, Tina
AU - Groeneweg, Linda
AU - Tokay, Tursonjan
AU - Köhling, Rüdiger
AU - Kirschstein, Timo
PY - 2014/1
Y1 - 2014/1
N2 - Purpose: This prospective, randomized study was performed to investigate the effects of oxygen (O2) treatment during sustained epileptic activity on mortality, subsequent seizure frequency, and neuronal damage. Methods: Status epilepticus (SE) was induced by intraperitoneal injection of 340mg/kg pilocarpine, and terminated by diazepam after 40min. During SE, rats were randomized to O2 treatment (insufflation rate of 1.5l/min O2) during SE or normal air conditions. Outcome measures were SE-related mortality, seizure occurrence, mossy fiber sprouting, neuronal cell loss and expression of 27-kDa heat-shock protein (Hsp27). Results: O2-treated and O2-untreated animals did not differ with respect to SE latency, diazepam dose required to stop SE. While 7/38 rats died during SE in the O2-untreated group, very little mortality (1/38) occurred in the O2-treated group (P2-treated rats died which was not observed in the O2-untreated group indicating no significant difference in overall mortality. There was a tendency towards lower seizure rate in the O2-treated group at one month after pilocarpine-induced SE. Three months after SE, however, seizure rates were no longer different between both groups. Moreover, mossy fiber sprouting, neuronal cell loss and Hsp27 expression did not differ between O2-treated and O2-untreated groups. Conclusion: Our findings indicate that O2 treatment might delay the relative risk of epileptic seizures following an initial brain injury, but it may also lead to a rather unfavorably increased heterogeneity of epileptogenesis in experimental studies.
AB - Purpose: This prospective, randomized study was performed to investigate the effects of oxygen (O2) treatment during sustained epileptic activity on mortality, subsequent seizure frequency, and neuronal damage. Methods: Status epilepticus (SE) was induced by intraperitoneal injection of 340mg/kg pilocarpine, and terminated by diazepam after 40min. During SE, rats were randomized to O2 treatment (insufflation rate of 1.5l/min O2) during SE or normal air conditions. Outcome measures were SE-related mortality, seizure occurrence, mossy fiber sprouting, neuronal cell loss and expression of 27-kDa heat-shock protein (Hsp27). Results: O2-treated and O2-untreated animals did not differ with respect to SE latency, diazepam dose required to stop SE. While 7/38 rats died during SE in the O2-untreated group, very little mortality (1/38) occurred in the O2-treated group (P2-treated rats died which was not observed in the O2-untreated group indicating no significant difference in overall mortality. There was a tendency towards lower seizure rate in the O2-treated group at one month after pilocarpine-induced SE. Three months after SE, however, seizure rates were no longer different between both groups. Moreover, mossy fiber sprouting, neuronal cell loss and Hsp27 expression did not differ between O2-treated and O2-untreated groups. Conclusion: Our findings indicate that O2 treatment might delay the relative risk of epileptic seizures following an initial brain injury, but it may also lead to a rather unfavorably increased heterogeneity of epileptogenesis in experimental studies.
KW - Heat-shock protein
KW - Oxygen
KW - Pilocarpine
KW - Status epilepticus
KW - Timm stain
UR - http://www.scopus.com/inward/record.url?scp=84890791233&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84890791233&partnerID=8YFLogxK
U2 - 10.1016/j.eplepsyres.2013.10.017
DO - 10.1016/j.eplepsyres.2013.10.017
M3 - Article
VL - 108
SP - 90
EP - 97
JO - Epilepsy Research
JF - Epilepsy Research
SN - 0920-1211
IS - 1
ER -