Changes in histopathology and tumor necrosis factor-α levels in the hearts of rats following asphyxial cardiac arrest

Lee, Jung Hoon; Lee, Tae-Kyeong; Kim, In Hye; Lee, Jae Chul; Won, Moo‐Ho; Park, Joon Ha; Ahn, Ji Hyeon; Shin, Myoung Chul; Ohk, Taek Geun; Moon, Joong Bum; Cho, Jun Hwi; Park, Chan Woo; Tae, Hyun‐Jin

doi:10.15441/ceem.17.220

Cited by 10 publications

(10 citation statements)

References 22 publications

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“…In CA patients, the survival rate accounted for 4 to 39% in out-of-hospital CA patients with their CPR done by the ambulance staff, and they survived via admission. The death of more than half of them occurred within the first 24 hours in the hospital 4 , 14 . In this study, the survival rate decreased time-dependently and reached to 25.8% at two days post-CA, what shows similarity with the survival rate of the CA patients.…”

Section: Discussionmentioning

confidence: 99%

Changes of renal histopathology and the role of Nrf2/HO-1 in asphyxial cardiac arrest model in rats

et al. 2021

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To investigate the role of Nrf2/HO-1 in renal histopathological ailments time-dependently in asphyxial cardiac arrest (CA) rat model. Methods: Eighty-eight Sprague Dawley male rats were divided into five groups of eight rats each. Asphyxial CA was induced in all the experimental rats except for the sham group. The rats were sacrificed at 6 hours, 12 hours, one day and two days post-CA. Serum blood urea nitrogen (BUN), creatinine (Crtn) and malondialdehyde from the renal tissues were evaluated. Hematoxylin and eosin and periodic acid-Schiff staining were done to evaluate the renal histopathological changes in the renal cortex. Furthermore, Nrf2/HO-1 immunohistochemistry (ihc) and western blot analysis were performed after CA. Results: The survival rate of rats decreased in a time-dependent manner: 66.6% at 6 hours, 50% at 12 hours, 38.1% in one day, and 25.8% in two days. BUN and serum Crtn markedly increased in CA-operated groups. Histopathological ailments of the renal cortical tissues increased significantly from 6 hours until two days post-CA. Furthermore, Nrf2/HO-1 expression level significantly increased at 6 hours, 12 hours, and one day. Conclusion: The survival rate decreased time-dependently, and Nrf/HO-1 expression increased from 6 hours with the peak times at 12 hours, and one day post-CA.

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Section: Discussionmentioning

confidence: 99%

Changes of renal histopathology and the role of Nrf2/HO-1 in asphyxial cardiac arrest model in rats

et al. 2021

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“…ACA induction was performed according to published protocols [12][13][14]. In short, rats in each group were anesthetized with a mixture of 2.5% isoflurane in 33% oxygen and 67% nitrous oxide.…”

Section: Induction Of Aca and Cprmentioning

confidence: 99%

“…After 5 min of ACA, CPR was initiated according to published protocols [12][13][14]. In short, the ventilator was reconnected with 100% oxygen, and epinephrine (0.005 mg/kg) (Dai Han Pharm, Seoul, Republic of Korea) and sodium bicarbonate (1 meq/kg, Daewon Pham, Seoul, Republic of Korea) was intravenously administered.…”

Section: Induction Of Aca and Cprmentioning

confidence: 99%

Therapeutic Hypothermia Improves Hind Limb Motor Outcome and Attenuates Oxidative Stress and Neuronal Damage in the Lumbar Spinal Cord Following Cardiac Arrest

et al. 2020

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Hypothermia enhances outcomes of patients after resuscitation after cardiac arrest (CA). However, the underlying mechanism is not fully understood. In this study, we investigated effects of hypothermic therapy on neuronal damage/death, microglial activation, and changes of endogenous antioxidants in the anterior horn in the lumbar spinal cord in a rat model of asphyxial CA (ACA). A total of 77 adult male Sprague–Dawley rats were randomized into five groups: normal, sham ACA plus (+) normothermia, ACA + normothermia, sham ACA + hypothermia, and ACA + hypothermia. ACA was induced for 5 min by injecting vecuronium bromide. Therapeutic hypothermia was applied after return of spontaneous circulation (ROSC) via rapid cooling with isopropyl alcohol wipes, which was maintained at 33 ± 0.5 °C for 4 h. Normothermia groups were maintained at 37 ± 0.2 °C for 4 h. Neuronal protection, microgliosis, oxidative stress, and changes of endogenous antioxidants were evaluated at 12 h, 1 day, and 2 days after ROSC following ACA. ACA resulted in neuronal damage from 12 h after ROSC and evoked obvious degeneration/loss of spinal neurons in the ventral horn at 1 day after ACA, showing motor deficit of the hind limb. In addition, ACA resulted in a gradual increase in microgliosis with time after ACA. Therapeutic hypothermia significantly reduced neuronal loss and attenuated hind limb dysfunction, showing that hypothermia significantly attenuated microgliosis. Furthermore, hypothermia significantly suppressed ACA-induced increases of superoxide anion production and 8-hydroxyguanine expression, and significantly increased superoxide dismutase 1 (SOD1), SOD2, catalase, and glutathione peroxidase. Taken together, hypothermic therapy was found to have a substantial impact on changes in ACA-induced microglia activation, oxidative stress factors, and antioxidant enzymes in the ventral horn of the lumbar spinal cord, which closely correlate with neuronal protection and neurological performance after ACA.

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“…Asphyxial CA induction was performed according to published protocols [ 14 , 15 , 16 ]. In short, rats were anesthetized with 2.5% isoflurane in oxygen (33%) and nitrous oxide (67%), and the rats were endotracheally intubated with a 14-gauge cannula and ventilated to maintain respiration using a rodent ventilator (Harvard Apparatus, Holliston, MA, USA).…”

Section: Methodsmentioning

confidence: 99%

“…CPR was performed according to published protocols [ 14 , 15 , 16 ]. In short, CPR was performed from 5 min after asphyxial CA as follows.…”

Section: Methodsmentioning

confidence: 99%

Neuronal Death in the CNS Autonomic Control Center Comes Very Early after Cardiac Arrest and Is Not Significantly Attenuated by Prompt Hypothermic Treatment in Rats

Ahn

Lee

Tae

et al. 2021

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Autonomic dysfunction in the central nervous system (CNS) can cause death after recovery from a cardiac arrest (CA). However, few studies on histopathological changes in animal models of CA have been reported. In this study, we investigated the prevalence of neuronal death and damage in various brain regions and the spinal cord at early times after asphyxial CA and we studied the relationship between the mortality rate and neuronal damage following hypothermic treatment after CA. Rats were subjected to 7–8 min of asphyxial CA, followed by resuscitation and prompt hypothermic treatment. Eight regions related to autonomic control (the cingulate cortex, hippocampus, thalamus, hypothalamus, myelencephalon, and spinal cord) were examined using cresyl violet (a marker for Nissl substance) and Fluoro-Jade B (a marker for neuronal death). The survival rate was 44.5% 1 day post-CA, 18.2% 2 days post-CA and 0% 5 days post-CA. Neuronal death started 12 h post-CA in the gigantocellular reticular nucleus and caudoventrolateral reticular nucleus in the myelencephalon and lamina VII in the cervical, thoracic, lumbar, and sacral spinal cord, of which neurons are related to autonomic lower motor neurons. In these regions, Iba-1 immunoreactivity indicating microglial activation (microgliosis) was gradually increased with time after CA. Prompt hypothermic treatment increased the survival rate at 5 days after CA with an attenuation of neuronal damages and death in the damaged regions. However, the survival rate was 0% at 12 days after CA. Taken together, our study suggests that the early damage and death of neurons related to autonomic lower motor neurons was significantly related to the high mortality rate after CA and that prompt hypothermic therapy could increase the survival rate temporarily after CA, but could not ultimately save the animal.

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Changes in histopathology and tumor necrosis factor-α levels in the hearts of rats following asphyxial cardiac arrest

Cited by 10 publications

References 22 publications

Changes of renal histopathology and the role of Nrf2/HO-1 in asphyxial cardiac arrest model in rats

Changes of renal histopathology and the role of Nrf2/HO-1 in asphyxial cardiac arrest model in rats

Therapeutic Hypothermia Improves Hind Limb Motor Outcome and Attenuates Oxidative Stress and Neuronal Damage in the Lumbar Spinal Cord Following Cardiac Arrest

Neuronal Death in the CNS Autonomic Control Center Comes Very Early after Cardiac Arrest and Is Not Significantly Attenuated by Prompt Hypothermic Treatment in Rats

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