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Sedative depth on neurological outcomes in a juvenile rat model of cardiopulmonary resuscitation.
Med Hypotheses 2019; 132:109233MH

Abstract

The guidelines for cardiopulmonary resuscitation (CPR) in pediatric advanced life support suggest that midazolam is the preferred agent for sedation in patients with mild hypothermia, whereas children with cardiac arrest (CA) are at a crucial stage regarding their immature nervous system. Studies have shown that midazolam may have a detrimental effect on the developmental of the pediatric nervous system. Our previous study found that midazolam induced neuronal damage after CPR in young rats. It is speculated that: midazolam causes the potential injury of neurons by inhibiting mitochondrial autophagy expression and is an important factor for the poor prognosis in children after successful CPR. This project intends to adopt the modified asphyxiant CPR model in juvenile rats. Survival rate, neurological function and histopathological changes were evaluated to determine the protective effects of appropriate sedation depth on cerebral ischemia-reperfusion injury in juvenile rats after CPR. Combined with cell biology and molecular biology related technologies, the mechanism by which the mitochondrial pinkl-parkin signaling pathway induces autophagy to inhibit neuronal apoptosis may be key factor in the protective effects of sedation depth on the brain. The aim of this study is to provide experimental evidence and elucidate the mechanisms of improvement of cerebral ischemia-reperfusion injury by sedation depth in children after successful CPR and to lay a theoretical and experimental basis for clinical treatment.

Authors+Show Affiliations

The Third People(')s Hospital of Chengdu, The Affiliated Hospital of Southwest Jiaotong University, China.Department of Anesthesiology, Sichuan Academy of Medical Sciences and Sichuan Provincial People's Hospital, Chengdu 610072, Sichuan, China.Department of Anesthesiology, Chengdu Women and Children(')s Central Hospital, Chengdu 610041, Sichuan, China. Electronic address: mengjunwoo@aliyun.com.Department of Orthopedics, Shuangliu First People's Hospital, Chengdu 610200, Sichuan, China. Electronic address: 2014982567@qq.com.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

31606702

Citation

Yuan, Jing, et al. "Sedative Depth On Neurological Outcomes in a Juvenile Rat Model of Cardiopulmonary Resuscitation." Medical Hypotheses, vol. 132, 2019, p. 109233.
Yuan J, Yang MC, Wu MJ, et al. Sedative depth on neurological outcomes in a juvenile rat model of cardiopulmonary resuscitation. Med Hypotheses. 2019;132:109233.
Yuan, J., Yang, M. C., Wu, M. J., & Gou, Y. S. (2019). Sedative depth on neurological outcomes in a juvenile rat model of cardiopulmonary resuscitation. Medical Hypotheses, 132, p. 109233. doi:10.1016/j.mehy.2019.109233.
Yuan J, et al. Sedative Depth On Neurological Outcomes in a Juvenile Rat Model of Cardiopulmonary Resuscitation. Med Hypotheses. 2019;132:109233. PubMed PMID: 31606702.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Sedative depth on neurological outcomes in a juvenile rat model of cardiopulmonary resuscitation. AU - Yuan,Jing, AU - Yang,Meng-Chang, AU - Wu,Meng-Jun, AU - Gou,Yong-Sheng, Y1 - 2019/05/20/ PY - 2019/01/19/received PY - 2019/05/11/revised PY - 2019/05/18/accepted PY - 2019/10/14/pubmed PY - 2019/10/14/medline PY - 2019/10/14/entrez SP - 109233 EP - 109233 JF - Medical hypotheses JO - Med. Hypotheses VL - 132 N2 - The guidelines for cardiopulmonary resuscitation (CPR) in pediatric advanced life support suggest that midazolam is the preferred agent for sedation in patients with mild hypothermia, whereas children with cardiac arrest (CA) are at a crucial stage regarding their immature nervous system. Studies have shown that midazolam may have a detrimental effect on the developmental of the pediatric nervous system. Our previous study found that midazolam induced neuronal damage after CPR in young rats. It is speculated that: midazolam causes the potential injury of neurons by inhibiting mitochondrial autophagy expression and is an important factor for the poor prognosis in children after successful CPR. This project intends to adopt the modified asphyxiant CPR model in juvenile rats. Survival rate, neurological function and histopathological changes were evaluated to determine the protective effects of appropriate sedation depth on cerebral ischemia-reperfusion injury in juvenile rats after CPR. Combined with cell biology and molecular biology related technologies, the mechanism by which the mitochondrial pinkl-parkin signaling pathway induces autophagy to inhibit neuronal apoptosis may be key factor in the protective effects of sedation depth on the brain. The aim of this study is to provide experimental evidence and elucidate the mechanisms of improvement of cerebral ischemia-reperfusion injury by sedation depth in children after successful CPR and to lay a theoretical and experimental basis for clinical treatment. SN - 1532-2777 UR - https://www.unboundmedicine.com/medline/citation/31606702/Sedative_depth_on_neurological_outcomes_in_a_juvenile_rat_model_of_cardiopulmonary_resuscitation L2 - https://linkinghub.elsevier.com/retrieve/pii/S0306-9877(19)30064-7 DB - PRIME DP - Unbound Medicine ER -