Abstract
Cardiac arrest (CA) is one of the leading lethal factors. Despite cardiopulmonary resuscitation (CPR) procedure has been consecutively improved and lots of new strategies have been developed, neurological outcome of the patients experienced CPR is still disappointing. Ribonuclease (RNase) has been demonstrated to have neuroprotective effects in acute stroke and postoperative cognitive impairment, possibly through acting against endogenous RNA that released from damaged tissue. However, the role of RNase in post-cardiac arrest cerebral injury is unknown. In the present study, we investigated the role of RNase in neurological outcome of mice undergoing 5 minutes of CA and followed by CPR. RNase or the same dosage of normal saline was administrated. We found that RNase administration could: 1) improve neurologic score on day 1 and day 3 after CA/CPR performance; 2) improve memory and learning ability on day 3 after training in contextual fear-conditioning test; 3) reduce extracellular RNA (exRNA) level in plasma and hippocampus tissue, and hippocampal cytokines mRNA production on day 3 after CA/CPR procedure; 4) attenuate autophagy levels in hippocampus tissue on day 3 after CA/CPR procedure. In conclusion, RNase could improve neurological function by reducing inflammation response and autophagy in mice undergoing CA/CPR.
Highlights
Even though the cardiopulmonary resuscitation (CPR) performance is increasingly perfect, survival rate and neurological function of patients underwent cardiac arrest (CA) and CPR remain poor
We investigated the role of RNase in neurological function after 5 minutes of CA and followed by CPR performance in a mice model
We found that CA and CPR performance could result in severe neurological impairment, which could be significantly reduced by RNase treatment
Summary
Even though the cardiopulmonary resuscitation (CPR) performance is increasingly perfect, survival rate and neurological function of patients underwent cardiac arrest (CA) and CPR remain poor. Most of the patients admitted into intensive care unit (ICU) developed severe neurological defect and other multi-organ dysfunction after return of spontaneous circulation (ROSC), which is defined as post-CA syndrome [2]. Post-cardiac arrest cerebral injury is a crucial factor that results in high mortality and morbidity. Targeted temperature management and organ specific support are acknowledged as the effective approaches to improve neurologic outcome and survival rate of patients underwent CA and CPR [8, 9]. Abella et al proved that intra-arrest hypothermia could improve survival rate and neurological outcome in a mouse model of CA [10]. Effective drug that could attenuate neurological dysfunction and improve cognition of those patients is still lacking
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