The Spinal Cord Damage in a Rat Asphyxial Cardiac Arrest/Resuscitation Model
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ORIGINAL WORK
The Spinal Cord Damage in a Rat Asphyxial Cardiac Arrest/Resuscitation Model Gerburg Keilhoff1*, Maximilian Titze1, Henning Rathert1, Tue Minh Nguyen Thi1 and Uwe Ebmeyer2 © 2020 Springer Science+Business Media, LLC, part of Springer Nature and Neurocritical Care Society
Abstract Background: After cardiac arrest/resuscitation (CA/R), animals often had massive functional restrictions including spastic paralysis of hind legs, disturbed balance and reflex abnormalities. Patients who have survived CA also develop movement restrictions/disorders. A successful therapy requires detailed knowledge of the intrinsic damage pattern and the respective mechanisms. Beside neurodegenerations in the cerebellum and cortex, neuronal loss in the spinal cord could be a further origin of such movement artifacts. Methods: Thus, we aimed to evaluate the CA/R-induced degeneration pattern of the lumbar medulla spinalis by immunocytochemical expression of SMI 311 (marker of neuronal perikarya and dendrites), IBA1 (microglia marker), GFAP (marker of astroglia), calbindin D28k (marker of the cellular neuroprotective calcium-buffering system), MnSOD (neuroprotective antioxidant), the transcription factor PPARγ and the mitochondrial marker protein PDH after survival times of 7 and 21 days. The CA/R specimens were compared with those from sham-operated and completely naïve rats. Results & Conclusion: The main ACA/R-mediated results were: (1) degeneration of lumbar spinal cord motor neurons, characterized by neuronal pyknotization and peri-neuronal tissue artifacts; (2) attendant activation of microglia in the short-term group; (3) attendant activation of astroglia in the long-term group; (4) degenerative pattern in the intermediate gray matter; (5) activation of the endogenous anti-oxidative defense systems calbindin D28k and MnSOD; (6) activation of the transcription factor PPARγ, especially in glial cells of the gray matter penumbra; and (7) activation of mitochondria. Moreover, marginal signs of anesthesia-induced cell stress were already evident in sham animals when compared with completely naïve spinal cords. A correlation between the NDS and the motor neuronal loss could not be verified. Thus, the NDS appears to be unsuitable as prognostic tool. Keywords: Calbindin D28k, Asphyxial cardiac arrest, Intermediate gray matter, MnSOD, Motor neurons, PPARγ, Pyruvate dehydrogenase, Spinal cord Introduction In previous studies, we detected only limited degeneration in the cortex and cerebellum in our asphyxial cardiac arrest/resuscitation (ACA/R) model of the rat, in contrast to the massive degenerated hippocampal CA1 region [1, 2]. Nevertheless, the animals very often had massive functional restrictions, especially in the hind legs (L3–L5 *Correspondence: [email protected] 1 Institute of Biochemistry and Cell Biology, Medical Faculty, University of Magdeburg, Leipziger Strasse 44, 39120 Magdeburg, Germany Full list of author information is available at the end of the article
dermatomal reflexes). The balance includ
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