Neuronal injury and tumor necrosis factor-alpha immunoreactivity in the rat hippocampus in the early period of asphyxia-induced cardiac arrest under normothermia

• Main Authors: Hyun-Jin Tae, Il Jun Kang, Tae-Kyeong Lee, Jeong Hwi Cho, Jae-Chul Lee, Myoung Cheol Shin, Yoon Sung Kim, Jun Hwi Cho, Jong-Dai Kim, Ji Hyeon Ahn, Joon Ha Park, In-Shik Kim, Hyang-Ah Lee, Yang Hee Kim, Moo-Ho Won, Young Joo Lee
• Format: Article
• Language: English
• Published: Wolters Kluwer Medknow Publications 2017-01-01
• Series: Neural Regeneration Research
• Subjects: nerve regeneration; post-cardiac arrest syndrome; normothermia; neuronal damage; gliosis; tumor necrosis factor-alpha; neural regeneration
• Online Access: http://www.nrronline.org/article.asp?issn=1673-5374;year=2017;volume=12;issue=12;spage=2007;epage=2013;aulast=Tae

Low survival rate occurs in patients who initially experience a spontaneous return of circulation after cardiac arrest (CA). In this study, we induced asphyxial CA in adult male Sprague-Daley rats, maintained their body temperature at 37 ± 0.5°C, and then observed the survival rate during the post-resuscitation phase. We examined neuronal damage in the hippocampus using cresyl violet (CV) and Fluore-Jade B (F-J B) staining, and pro-inflammatory response using ionized calcium-binding adapter molecule 1 (Iba-1), glial fibrillary acidic protein (GFAP), and tumor necrosis factor-alpha (TNF-α) immunohistochemistry in the hippocampus after asphyxial CA in rats under normothermia. Our results show that the survival rate decreased gradually post-CA (about 63% at 6 hours, 37% at 1 day, and 8% at 2 days post-CA). Rats were sacrificed at these points in time post-CA, and no neuronal damage was found in the hippocampus until 1 day post-CA. However, some neurons in the stratum pyramidale of the CA region in the hippocampus were dead 2 days post-CA. Iba-1 immunoreactive microglia in the CA1 region did not change until 1 day post-CA, and they were activated (enlarged cell bodies with short and thicken processes) in all layers 2 days post-CA. Meanwhile, GFAP-immunoreactive astrocytes did not change significantly until 2 days post-CA. TNF-α immunoreactivity decreased significantly in neurons of the stratum pyramidale in the CA1 region 6 hours post-CA, decreased gradually until 1 day post-CA, and increased significantly again 2 days post-CA. These findings suggest that low survival rate of normothermic rats in the early period of asphyxia-induced CA is related to increased TNF-α immunoreactivity, but not to neuronal damage in the hippocampal CA1 region.