Literature DB >> 20571450

Investigation of the relationship between venticular fibrillation duration and cardiac/neurological damage in a rabbit model of electrically induced arrhythmia.

Chun-Lin Hu1, Hong-Yan Wei, Zi-You Liu, Xing Li, Xiao-Xing Liao, Yu-Jie Li, Hong Zhan, Xiao-Li Jing, Yan Xiong, Yan-Yan Liu, Gui-Fu Wu.   

Abstract

BACKGROUND: To establish a simple, economic, and reliable alternating current (AC)-induced cardiac arrest (ACCA) model in rabbits for cardiopulmonary cerebral resuscitation research.
METHODS: Ventricular fibrillation was induced in 27 New Zealand rabbits by external transthoracic AC, which were randomly divided into three groups according to the duration of untreated ACCA (ACCA-3 minutes, ACCA-5 minutes, and ACCA-8 minutes). After ACCA, all animals received cardiopulmonary resuscitation for 2 minutes and subsequent defibrillation until return of spontaneous circulation (ROSC). The troponin I levels were measured at 4 hours after ROSC. Animals died spontaneously or were killed at 72 hours after ROSC. The hippocampus were removed and fixed in 3% formalin. TdT-mediated dUTP-biotin nick end labeling and Nissl stainings were performed in 10-μm thickness coronal sections. Furthermore, two rabbits (without induction of ventricular fibrillation, cardiopulmonary resuscitation, and defibrillation) served as normal control group.
RESULTS: Mean survival times after ROSC were 48.57 hours ± 24.70 hours, 18.0 hours ± 15.13 hours, and 3.88 hours ± 2.39 hours for groups ACCA-3 minutes, ACCA-5 minutes, and ACCA-8 minutes, respectively. Survival was significantly different between ACCA-3 minutes and other two groups (p = 0.002 and p = 0.01). Neuronal necrosis and apoptosis were found in the hippocampus CA1, CA2, and CA3 areas of group ACCA-3 minutes. In contrast, neuronal necrosis and TdT-mediated dUTP-biotin nick end labeling positive cells were fewer in control animals.
CONCLUSIONS: The rabbits in group ACCA-3 minutes had significant neuronal damage with apoptosis in hippocampus CA1, CA2, and CA3 areas at 72 hours after ROSC and survived longer than those in other groups. The model we describe may be a simple, economic, and reliable model for experimental investigation on cardiopulmonary cerebral resuscitation.

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Year:  2010        PMID: 20571450     DOI: 10.1097/TA.0b013e3181dbbefc

Source DB:  PubMed          Journal:  J Trauma        ISSN: 0022-5282


  4 in total

1.  Pre-arrest hypothermia improved cardiac function of rats by ameliorating the myocardial mitochondrial injury after cardiac arrest.

Authors:  Yuanzheng Lu; Xiaoyun Zeng; Xiaoli Jing; Meixian Yin; Mms Mary P Chang; Hongyan Wei; Yan Yang; Xiaoxing Liao; Gang Dai; Chunlin Hu
Journal:  Exp Biol Med (Maywood)       Date:  2019-09-17

Review 2.  [Post-resuscitation syndrome. Role of inflammation after cardiac arrest].

Authors:  A Schneider; M Albertsmeier; B W Böttiger; P Teschendorf
Journal:  Anaesthesist       Date:  2012-05       Impact factor: 1.041

3.  Ulinastatin attenuates oxidation, inflammation and neural apoptosis in the cerebral cortex of adult rats with ventricular fibrillation after cardiopulmonary resuscitation.

Authors:  Chun Lin Hu; Jin Ming Xia; Jie Cai; Xin Li; Xiao Xing Liao; Hui Li; Hong Zhan; Gang Dai; Xiao Li Jing
Journal:  Clinics (Sao Paulo)       Date:  2013-09       Impact factor: 2.365

4.  Clinical observation of ulinastatin combined with CRRT in the treatment of early cardiopulmonary resuscitation.

Authors:  Qinghong Liu; Jinliang Peng; Yuming Zhou; Weilan Zeng; Shihui Xiao; Hui Cheng; Zhenzhou Zhong; Xiangming Liao; Xiaoliu Xiao; Liang Luo; Xianghong Liu
Journal:  Exp Ther Med       Date:  2017-10-17       Impact factor: 2.447

  4 in total

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