Yue-Yi Ren1, Hai-Qing Zhang2, Shu-Hua Duan1, Shi-Duan Wang3,
1Heart Center, Qingdao Women and Children’s Hospital, Qingdao University, Shandong –266011; 2Department of Anaesthiology, Qingdao Women and Children’s Hospital, Qingdao University, Shandong - 266011; 3Department of Anaesthiology, The Affiliated Hospital of Qingdao University, Shandong - 266021, China.For correspondence:- Shi-Duan Wang Email:
Received: 29 October 2014 Accepted: 17 February 2015 Published: 31 March 2015
Citation: Ren Y, Zhang H, Duan S, Wang S, Influence of dexmedetomidine on toxicity of intrathecal ketamine on neonatal rat spinal function. Trop J Pharm Res 2015; 14(3):469-477 doi: 10.4314/tjpr.v14i3.16
© 2015 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..
Purpose: To investigate the influence of dexmedetomidine on the effect of ketamine on developing spinal cord.
Methods: Postnatal day 3 (P3) and postnatal day 7 (P7) rat pups received intrathecal ketamine (10 mg/kg b.wt) and/or dexmedetomidine (10 µg/kg b.wt). Spinal reflex function was assessed by evaluating the sensory stimuli based on mechanical withdrawal threshold. Spinal tissue was analysed for activated caspase-3 using monoclonal anti-activated caspase-3. Apoptosis count of the spinal tissue was also measured by Fluoro-Jade C staining while glial reactivity was assessed by ionized calcium binding adapter molecule 1 on Day 7 day following injection. Long-term spinal function in rat pups on postnatal day 35 (P35) was evaluated by measuring the hindlimb withdrawal threshold and gait analysis.
Results: Exposure to intrathecal ketamine at 10 mg/kg in P3 and P7 pups decreased mechanical withdrawal thresholds and increase apoptosis and microglial activation in the spinal cord. Altered spinal function, as presented by a decrease in mechanical withdrawal threshold and altered static gait, was observed in P35 rats exposed to intrathecal ketamine on P3. Dexmedetomidine administration did not alter the spinal function and histology of spinal tissue. Co-administration of dexmedetomidine and ketamine suggests that the former reduced apoptosis counts, altered glial responses, increased mechanical withdrawal threshold and improved gait.
Conclusion: Dexmedetomidine protects against intrathecal ketamine-induced spinal toxicity in neonatal rats.
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