J Korean Soc Emerg Med.
2025 Feb;36(1):1-11.
Thoracic spinal cord damage in rat following cardiac arrest: neuronal loss, blood-spinal cord barrier leakage, and astrocyte endfeet disruption
- Affiliations
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- 1Department of Emergency Medicine, Kangwon National University Hospital, Kangwon National University School of Medicine, Chuncheon, Korea
- 2Bio-Safety Research Institute, College of Veterinary Medicine, Jeonbuk National University, Iksan, Korea
- 3Department of Anatomy, College of Korean Medicine, Dongguk University, Gyeongju, Korea
- 4Department of Physical Therapy, College of Health Science, Youngsan University, Yangsan, Korea
- 5Department of Biochemistry and Molecular Biology, and Research Institute of Oral Sciences, College of Dentistry, Gangnung-Wonju National University, Gangneung, Korea
- 6Department of Oral Anatomy and Developmental Biology, College of Dentistry, Kyung Hee University, Seoul, Korea
Abstract
Objective
Cardiac arrest and cardiopulmonary resuscitation (CA/R) lead to whole-body ischemia and reperfusion (IR) injury, causing multiple organ dysfunction, including ischemic spinal cord injury. The thoracic spinal cord levels are crucial for maintaining the sympathetic functions vital for life. This study examined blood-spinal cord barrier (BSCB) leakage and astrocyte endfeet (AEF) disruption and their effects on survival, physiological variables, and neuronal damage/death in the intermediate zone (IMZ) at the seventh thoracic spinal cord level after asphyxial CA/R in rats.
Methods
The rats underwent whole-body IR injury by asphyxial CA/R. Kaplan-Meier analysis was conducted to assess the cumulative survival post-CA/R. The histological changes post-CA/R were evaluated using immunohistochemistry, histofluorescence, and double histofluorescence.
Results
No significant differences in body weight, mean arterial pressure, and heart rate were found between the sham and CA/R groups post-CA/R. The survival rates in the CA/R group at 12, 24, and 48 hours were 62.58%, 36.37%, and 7.8%, respectively. Neuronal loss and BSCB leakage began 12 hours post-CA/R, increasing with time. Reactive astrogliosis appeared at 12 hours and increased, while AEF disruption around blood vessels was evident at 48 hours.
Conclusion
The survival rate declined significantly by 48 hours post-CA/R. Neuronal loss and BSCB leakage in the thoracic spinal cord IMZ was evident at 12 hours and significant by 48 hours, aligning with AEF disruption. Neuronal loss in the thoracic spinal cord IMZ post-CA/R may be related to BSCB leakage and AEF disruption.