Effect of Naloxone on the Cerebral Ischemia of the Rats

Choon Hi Lee, Guie Yong Lee, Chi Hyo Kim, Young Sook Pae

Copyright ⓒ 1990. Ewha Womans University School of Medicine. This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Published Online: Jul 24, 2015

Abstract

Brain ischemia due to a critical reduction in cerebral blood flow is a common cause of irreversible brain damage. Ischemia is invariably accompanied by an increase in tissue lactate concentration due to anaerobic metabolism of glucose and energy failure.

Despite new insights into the pathophysiologic mechanism of cerebral ischemia, the clinical therapeutics of cerebral ischemia is usually limited to agressive anticoagulation and supportive measures.

But. recently, new pharmacological agents including calcium channel blocking agent, perfluorocarbon, free radical scavenger and opiate antagonist are considered as possible therapeutic application for restoration of blood flow to areas of focal ischemia in both laboratory and clinical trials.

Naloxone, an opiate antagonist, has been reported to improve neurological function, spinal blood flow and somatosensory evoked potentials after spinal injury. Thus, Endogenous opioids might play a role in pathophysiology of central nervous system ischemia and that opiate antagonist might be of benefit in the treatment of experimental stroke.

But, on the other hand. there are many evidences that naloxone is not benefical. So use of naloxone for the treatnebt of ischemia insult is controverial.

Therefore, The present investigation was undertaken to elucidate the effects naloxone on cerebral ischemia by measurement of the cerebral energy metabolites concentration.

Cerebral ischemia was produced in spontaneously hypertensive rat(SHR) by bilateral common carotid artery ligation. Naloxone(1mg/kg) was administered intraperitoneally 30 min after the carotid artery ligation.

The results obtained were as follows :

1) There were no differences in the concentration of APT and lactete between normotensive Sprague-Dawley rats and SHR.

2) In bilateral common carotid artery ligated SHR, the concentration of APT was considerable decreased and that lactate was slightly increased.

3) Naloxon didn'y change the cerebral energy metabolism in ischemic model. These data indicated that naloxone had no benefical effect on cerebral ischemia but for definite conclusion, more controlled experiments must be performed.