Abstract
Cardiac arrest (CA) causes severe spinal cord injury and evokes spinal cord disorders including paraplegia. It has been reported that risperidone, an antipsychotic drug, effectively protects neuronal cell death from transient ischemia injury in gerbil brains. However, until now, studies on the effects of risperidone on spinal cord injury after asphyxial CA (ACA) and cardiopulmonary resuscitation (CPR) are not sufficient. Therefore, this study investigated the effect of risperidone on hind limb motor deficits and neuronal damage/death in the lumbar part of the spinal cord following ACA in rats. Mortality, severe motor deficits in the hind limbs, and the damage/death (loss) of motor neurons located in the anterior horn were observed two days after ACA/CPR. These symptoms were significantly alleviated by risperidone (an atypical antipsychotic) treatment after ACA. In vehicle-treated rats, the immunoreactivities of tumor necrosis factor-alpha (TNF-α) and interleukin 1-beta (IL-1β), as pro-inflammatory cytokines, were increased, and the immunoreactivities of IL-4 and IL-13, as anti-inflammatory cytokines, were reduced with time after ACA/CPR. In contrast, in risperidone-treated rats, the immunoreactivity of the pro-inflammatory cytokines was significantly decreased, and the anti-inflammatory cytokines were enhanced compared to vehicle-treated rats. In brief, risperidone treatment after ACA/CPR in rats significantly improved the survival rate and attenuated paralysis, the damage/death (loss) of motor neurons, and inflammation in the lumbar anterior horn. Thus, risperidone might be a therapeutic agent for paraplegia by attenuation of the damage/death (loss) of spinal motor neurons and neuroinflammation after ACA/CPR.
Highlights
Cardiac arrest (CA) abruptly ceases blood circulation and oxygen delivery to the entire body, induces ischemia in the whole body, and develops high mortality after CA/cardiopulmonary resuscitation (CPR) [1,2]
Before asphyxial CA (ACA), mean arterial pressure (MAP) and body temperature were similar to the baselines observed in the Sham+vehicle group
We found that ventral motor neurons at the level of the lumbar spinal cord were dead at two days after ACA/CPR in rats
Summary
CA abruptly ceases blood circulation and oxygen delivery to the entire body, induces ischemia in the whole body, and develops high mortality after CA/CPR [1,2]. Studies on CA have concentrated on the improvement in the rate of the return of spontaneous circulation (ROSC) after CPR [3,4]. It has been reported that CA is one of the causes of severe spinal cord injuries including paraplegia, which negatively affects the quality of life in patients [5,6,7]. It is well known that motor neurons located in the ventral horn of the spinal cord are very vulnerable to ischemia-reperfusion injury [8,9,10]. The factors protecting or attenuating the damage of spinal motor neurons following ischemic insults have been insufficiently reported yet. Hypothermia has been applied to increase the ROSC in order to improve the survival rate of patients with CA. Data using experimental animals indicate that early cooling after the ROSC provides neurological recovery, but delayed hypothermia after ROSC limits these beneficial effects [15,16]
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