Hypertonic saline infusion suppresses apoptosis of hippocampal cells in a rat model of cardiopulmonary resuscitation

Xiang Zhou,Yong Liu,Jian Zhu,Yang Huang,Shuibo Zhu,Rongping Wang

doi:10.1038/s41598-017-05919-4

Xiang Zhou, Yong Liu + Show 4 more

Open Access

https://doi.org/10.1038/s41598-017-05919-4

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Abstract

Hypertonic saline (HS) attenuates cerebral edema, improves microcirculation perfusion and alleviates inflammation. However, whether the beneficial effect of HS on neurological function after cardiopulmonary resuscitation (CPR) in rat model of asphyxial cardiac arrest (CA) is mediated via attenuating apoptosis of neurons is not known. We studied the neuroprotective effect of HS in rats after CA and CPR, and explored the likely underlying mechanisms. Animals were randomly assigned to 4 equal groups (n = 15 each) according to the different infusions administered during resuscitation: control (C), normal saline (NS), hypertonic saline (HS), and hydroxyethyl starch (HES) groups. NDS at 12, 24, 48 and 72 h post-ROSC in the HS group were significantly higher than those in the NS and HES groups. Western blot analysis demonstrated a significant increase in Bcl-2 expression in HS, as compared to that in the NS and HES groups. However, Bax and Caspase-3 expressions in HS were significantly lower than that in the NS and HES groups. The apoptosis rate in HS was significantly lower than that in the NS and HES groups, suggesting HS treatment during resuscitation could effectively suppress neuronal cell apoptosis in hippocampal CA1 post-ROSC and improve neuronal function.

Highlights

An estimated 54.4 million people sustain cardiac arrest (CA) in China each year[1], of which only about 1% people survive[2]
We investigated the neuroprotective effect of 10% hypertonic saline on the rats after CA and cardiopulmonary resuscitation (CPR), and attempted to explore the likely underlying mechanism
After orotracheal intubation using a teleflex of 16G venous indwelling catheter, median incision of neck was made on each rat, and blunt dissection of subcutaneous tissue performed to expose the trachea

Summary

Introduction

An estimated 54.4 million people sustain cardiac arrest (CA) in China each year[1], of which only about 1% people survive[2]. Hypertonic saline is known to reduce intracranial pressure, promote osmotic diuresis and improve brain perfusion[8] It can regulate immune function and has anti-inflammatory effect[9]. Both experimental (animal studies)[10] and clinical research[11] has shown hypertonic saline to increase the survival rates after CA and CPR and to improve neuronal function[12]. Rüdiger et al reported that hypertonic saline hydroxyethyl starch failed to ameliorate the newly generated hippocampal neurons in the survived CA and CPR rat models[17] To date, it is not known whether hypertonic saline improves neurological function by attenuating apoptosis of brain injury after resuscitation in an asphyxial cardiac arrest rat model. We investigated the neuroprotective effect of 10% hypertonic saline on the rats after CA and CPR, and attempted to explore the likely underlying mechanism

Methods

Results

Conclusion