Model of cardiac arrest in rats by transcutaneous electrical epicardium stimulation

Lin, Jia Wei; Liao, Xianghai; Li, Hui; H, Wei; Liu, Rong; Hu, Chunlin; Huang, Gailing; Dai, Gang; Li, Xin

doi:10.1016/j.resuscitation.2010.05.019

Cited by 26 publications

(26 citation statements)

References 35 publications

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“…15 This stimulator (Isostim, World Precision Instruments Inc) was used to perform direct and constant electric stimulation of the epicardium with crude current, continuous single stimulation, a delay of 100 milliseconds, a wave width of 1 millisecond, a frequency of 50 Hz, an intensity of 1 mA, and a stimulation duration of 3 minutes. The mechanical ventilation was stopped and disconnected from the tracheal tube after the onset of VF.…”

Section: Ventricular Fibrillation and Cpr Modelmentioning

confidence: 99%

Hydrogen Inhalation During Normoxic Resuscitation Improves Neurological Outcome in a Rat Model of Cardiac Arrest Independently of Targeted Temperature Management

et al. 2014

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Background-We have previously shown that hydrogen (H 2 ) inhalation, begun at the start of hyperoxic cardiopulmonary resuscitation, significantly improves brain and cardiac function in a rat model of cardiac arrest. Here, we examine the effectiveness of this therapeutic approach when H 2 inhalation is begun on the return of spontaneous circulation (ROSC) under normoxic conditions, either alone or in combination with targeted temperature management (TTM). Methods and Results-Rats were subjected to 6 minutes of ventricular fibrillation cardiac arrest followed by cardiopulmonary resuscitation. Five minutes after achieving ROSC, post-cardiac arrest rats were randomized into 4 groups: mechanically ventilated with 26% O 2 and normothermia (control); mechanically ventilated with 26% O 2 , 1.3% H 2 , and normothermia (H 2 ); mechanically ventilated with 26% O 2 and TTM (TTM); and mechanically ventilated with 26% O 2 , 1.3% H 2 , and TTM (TTM+H 2 ). Animal survival rate at 7 days after ROSC was 38.4% in the control group, 71.4% in the H 2 and TTM groups, and 85.7% in the TTM+H 2 group. Combined therapy of TTM and H 2 inhalation was superior to TTM alone in terms of neurological deficit scores at 24, 48, and 72 hours after ROSC, and motor activity at 7 days after ROSC. Neuronal degeneration and microglial activation in a vulnerable brain region was suppressed by both TTM alone and H 2 inhalation alone, with the combined therapy of TTM and H 2 inhalation being most effective. Conclusions-H 2 inhalation was beneficial when begun after ROSC, even when delivered in the absence of hyperoxia.Combined TTM and H 2 inhalation was more effective than TTM alone. (Circulation. 2014;130:2173-2180.)

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Section: Ventricular Fibrillation and Cpr Modelmentioning

confidence: 99%

Hydrogen Inhalation During Normoxic Resuscitation Improves Neurological Outcome in a Rat Model of Cardiac Arrest Independently of Targeted Temperature Management

et al. 2014

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“…Cardiac arrest was induced in this rat model by transcutaneous electrical epicardium, which was described previously (Lin et al, 2010). Briefly, 2 disposable acupuncture needles were inserted into the visceral pericardium between the fourth rib of the left sternal border and the third rib of the right sternal border.…”

Section: Animal Preparation and Cardiac Arrest Proceduresmentioning

confidence: 99%

Mild hypothermia attenuates post-resuscitation brain injury through a V-ATPase mechanism in a rat model of cardiac arrest

Zhang

Xie

et al. 2016

Genet. Mol. Res.

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ABSTRACT. Although therapeutic hypothermia is an effective treatment for post-resuscitation brain injury after cardiac arrest (CA), the underlying mechanism remains unclear. Vacuolar H + -ATPase (V-ATPase) plays a key role in cellular adaption to a hypoxic environment. This study sought to evaluate the effect of mild hypothermia on V-ATPase and its involvement in neuroprotection after CA. Male Sprague-Dawley rats were subjected to a 6-min CA, resuscitated successfully, and then assigned to either the normothermia (NT) group or the hypothermia (HT) group. Rats were further divided into 2 subgroups based on the time of euthanasia, either 3 or 24 h after CA (NT-3 h, HT-3 h; NT-24 h, HT-24 h). Mild hypothermia was induced following CA and maintained at 33°C for 2 h. Neurologic deficit scores were used to determine the status of neurological function. Brain specimens were analyzed by TUNEL assay, western blotting, and immunohistochemistry. V-ATPase activity was estimated by subtracting total ATP hydrolysis from the bafilomycin-sensitive activity. Mild hypothermia improved the neurological outcome (HT-24 h: 34.3 ± 16.4 vs NT-24 h: 50.3 ± 17.4) and significantly decreased neurocyte apoptosis 24 h after resuscitation. Mild hypothermia significantly increased V0a1 compared to NT-3 h; V0a1 expression was associated with a decrease in the cleaved caspase 3 expression. These findings suggested that mild hypothermia inhibits CA-induced apoptosis in the hippocampus, which may be associated with reduced V-ATPase impairment. These data provide new insights into the protective effects of hypothermia in vivo.

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“…For example, a sustained transesophageal alternating current stimulation (50 Hz, 18 V) during 60 seconds has been shown to induce VF in mice [38]. In rats and rabbits, VF can be induced with a 50-60 Hz current of 1-5 mA during 3 minutes [40, 43,44]. In another study, a rapid pacing with three periods of 5 seconds of transesophageal stimulation at 30 Hz efficiently induces VF in rats [45].…”

Section: Models Of Shockable Cardiac Arrestmentioning

confidence: 99%

How Can we Study Cardiopulmonary Resuscitation and Cardiac Arrest in Animals: a Review

Blondel¹,

Kohlhauer²,

Zilberstein³

et al. 2016

JDVAR

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Animal research is essential to propose new therapeutic approaches limiting the sequels of cardiac arrest in human and veterinary medicine. The ultimate goal is to improve the long term prognosis and neurological recovery. For such investigations, the use of animal models seems unavoidable as cardiac arrest provokes multiple visceral consequences as well as inflammatory response and coagulopathy. These models allow not only a better understanding of the pathophysiology but also the investigation of new treatment strategies to improve basic life support efficiency or prevent multi-organ failure. In this review, we are summarizing the characteristics of the main animal models used in resuscitation sciences. The choice of the species and methods of evaluation of cardiac arrest is crucial. These studies often concern human medicine but they can also address fundamental questions for veterinary research as they are mostly based on animal research.

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Model of cardiac arrest in rats by transcutaneous electrical epicardium stimulation

Cited by 26 publications

References 35 publications

Hydrogen Inhalation During Normoxic Resuscitation Improves Neurological Outcome in a Rat Model of Cardiac Arrest Independently of Targeted Temperature Management

Hydrogen Inhalation During Normoxic Resuscitation Improves Neurological Outcome in a Rat Model of Cardiac Arrest Independently of Targeted Temperature Management

Mild hypothermia attenuates post-resuscitation brain injury through a V-ATPase mechanism in a rat model of cardiac arrest

How Can we Study Cardiopulmonary Resuscitation and Cardiac Arrest in Animals: a Review

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