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Application of a novel rectal cooling device in hypothermia therapy after cerebral hypoxia-ischemia in rats

BACKGROUND: A new rectal cooling device for therapeutic hypothermia (TH) therapy is designed and is applied in TH treatment of SD rats with ischemic-hypoxic brain damage. METHODS: Healthy adult SD rats (n = 45) were randomly assigned into four groups: the healthy control group (n = 5), the ischemia...

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Detalles Bibliográficos
Autores principales: Liu, Peng, Yang, Rui, Zuo, Zelan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5017120/
https://www.ncbi.nlm.nih.gov/pubmed/27613331
http://dx.doi.org/10.1186/s12871-016-0239-5
Descripción
Sumario:BACKGROUND: A new rectal cooling device for therapeutic hypothermia (TH) therapy is designed and is applied in TH treatment of SD rats with ischemic-hypoxic brain damage. METHODS: Healthy adult SD rats (n = 45) were randomly assigned into four groups: the healthy control group (n = 5), the ischemia and hypoxia group (n = 10), the rectal TH cooling group (n = 18), and the ice blanket TH cooling group (n = 11). The rats in the rectal cooling and ice blanket TH groups received 12 h treatment after hypoxic-ischemic brain damage had been established, while those in the ischemia and hypoxia group did not. Taking the start of TH as the zero point, rats were sacrificed after 24 h and the brain and rectum tissues were sampled for histological analysis. RESULTS: The TH induction time (37.3 ± 14.7 min) in the rectal cooling group was significantly shorter (F = 4.937, P < 0.05) than that in the ice blanket cooling group (75.6 ± 27.2 min). The HE and NISSL staining results showed that rats in the rectal TH cooling group had significantly decreased (P < 0.01) positive neurons cell count compared to those in ischemia and hypoxia group. In addition, TUNEL staining indicated that the number of apoptotic cells (3.9 ± 1.8 cells / × 400 field) and the apoptosis index (4.4 % ± 1.5) were significantly lower in rectal TH cooling group (P < 0.05) than in ischemia and hypoxia group (23.2 ± 12.1 cells / × 400 field, 26.6 % ± 12.1). Also, no rectal frostbite or inflammatory infiltration was observed in rats in the rectal TH treatment groups. CONCLUSION: Our new cooling device realized rapid TH induction in SD rats with ischemic-hypoxic brain damage, inhibited the apoptosis of cells in the hippocampal CAl region, and did not cause histological damage to the rectal tissues. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12871-016-0239-5) contains supplementary material, which is available to authorized users.