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Therapeutic hypothermia attenuates paraplegia and neuronal damage in the lumbar spinal cord in a rat model of asphyxial cardiac arrest

Author:
Lee, Jae-Chul, Tae, Hyun-Jin, Cho, Jeong Hwi, Kim, In-Shik, Lee, Tae-Kyeong, Park, Cheol Woo, Park, Young Eun, Ahn, Ji Hyeon, Park, Joon Ha, Yan, Bing Chun, Lee, Hyang-Ah, Hong, Seongkweon, Won, Moo-Ho
Source:
Journal of thermal biology 2019 v.83 pp. 1-7
ISSN:
0306-4565
Subject:
animal injuries, animal models, cardiac arrest, cardiopulmonary resuscitation, death, hindlimbs, hypothermia, ischemia, motor neurons, rats, spinal cord
Abstract:
Spinal cord ischemia can result from cardiac arrest. It is an important cause of severe spinal cord injury that can lead to serious spinal cord disorders such as paraplegia. Hypothermia is widely acknowledged as an effective neuroprotective intervention following cardiac arrest injury. However, studies on effects of hypothermia on spinal cord injury following asphyxial cardiac arrest and cardiopulmonary resuscitation (CA/CPR) are insufficient. The objective of this study was to examine effects of hypothermia on motor deficit of hind limbs of rats and vulnerability of their spinal cords following asphyxial CA/CPR. Experimental groups included a sham group, a group subjected to CA/CPR, and a therapeutic hypothermia group. Severe motor deficit of hind limbs was observed in the control group at 1 day after asphyxial CA/CPR. In the hypothermia group, motor deficit of hind limbs was significantly attenuated compared to that in the control group. Damage/death of motor neurons in the lumbar spinal cord was detected in the ventral horn at 1 day after asphyxial CA/CPR. Neuronal damage was significantly attenuated in the hypothermia group compared to that in the control group. These results indicated that therapeutic hypothermia after asphyxial CA/CPR significantly reduced hind limb motor dysfunction and motoneuronal damage/death in the ventral horn of the lumbar spinal cord following asphyxial CA/CPR. Thus, hypothermia might be a therapeutic strategy to decrease motor dysfunction by attenuating damage/death of spinal motor neurons following asphyxial CA/CPR.
Agid:
6393812