Hypothermic properties of dexmedetomidine provide neuroprotection in rats following cerebral ischemia‑reperfusion injury

  • Authors:
    • Jian Lu
    • Li‑Jun Liu
    • Jian‑Liang Zhu
    • Yi Shen
    • Zhi‑Wei Zhuang
    • Chang‑Lai Zhu
  • View Affiliations

  • Published online on: May 24, 2019     https://doi.org/10.3892/etm.2019.7613
  • Pages: 817-825
Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

Dexmedetomidine (Dex) is a sedative and analgesic agent that is widely administered to patients admitted to the intensive care unit, and has been demonstrated to result in hypothermia. Many patients have been revealed to benefit from therapeutic hypothermia, which can mitigate cerebral ischemia/reperfusion (I/R) injury following successful cardiopulmonary resuscitation. However, studies investigating the efficacy of Dex in I/R treatment is lacking. The present study aimed to investigate the efficacy of Dex in mitigating neuronal damage, and to determine the possible mechanism of its effects in a rat model of cardiac arrest (CA). CA was induced in Sprague‑Dawley rats by asphyxiation for 5 min. Following successful resuscitation, the surviving rats were randomly divided into two treatment groups; one group was intraperitoneally administered with Dex (D group), whereas the control group was treated with normal saline (N group). Critical parameters, including core temperature and blood pressure were monitored following return of spontaneous circulation (ROSC). Arterial blood samples were collected at 10 min after surgery (baseline) 30 and 120 min post‑ROSC; and neurological deficit scores (NDS) of the rats were taken 12 or 24 h after ROSC prior to euthanasia. The hippocampal tissue was then removed for analysis by histology, electron microscopy and western blotting. Rats in the D group exhibited a lower core temperature and higher NDS scores compared with the N group (P<0.05). In addition, Dex injection resulted in reduced expression of apoptotic and autophagy‑associated factors in the hippocampus (P<0.05). Dex treatment induced hypothermia and improved neurological function in rats after ROSC following resuscitation from CA by inhibiting neuronal apoptosis and reducing autophagy, which suggested that Dex may be a potential therapy option for patients with CA.
View Figures
View References

Related Articles

Journal Cover

July-2019
Volume 18 Issue 1

Print ISSN: 1792-0981
Online ISSN:1792-1015

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Lu J, Liu LJ, Zhu JL, Shen Y, Zhuang ZW and Zhu CL: Hypothermic properties of dexmedetomidine provide neuroprotection in rats following cerebral ischemia‑reperfusion injury. Exp Ther Med 18: 817-825, 2019.
APA
Lu, J., Liu, L., Zhu, J., Shen, Y., Zhuang, Z., & Zhu, C. (2019). Hypothermic properties of dexmedetomidine provide neuroprotection in rats following cerebral ischemia‑reperfusion injury. Experimental and Therapeutic Medicine, 18, 817-825. https://doi.org/10.3892/etm.2019.7613
MLA
Lu, J., Liu, L., Zhu, J., Shen, Y., Zhuang, Z., Zhu, C."Hypothermic properties of dexmedetomidine provide neuroprotection in rats following cerebral ischemia‑reperfusion injury". Experimental and Therapeutic Medicine 18.1 (2019): 817-825.
Chicago
Lu, J., Liu, L., Zhu, J., Shen, Y., Zhuang, Z., Zhu, C."Hypothermic properties of dexmedetomidine provide neuroprotection in rats following cerebral ischemia‑reperfusion injury". Experimental and Therapeutic Medicine 18, no. 1 (2019): 817-825. https://doi.org/10.3892/etm.2019.7613