Ewha Med J.  1990 Dec;13(4):293-300. 10.12771/emj.1990.13.4.293.

Effect of Naloxone on the Cerebral Ischemia of the Rats

• Lee CH
• Lee GY
• Kim CH
• Pae YS

• KMID: 2170842
• DOI: http://doi.org/10.12771/emj.1990.13.4.293

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.

MeSH Terms

Analgesics, Opioid
Animals
Brain
Brain Ischemia*
Calcium Channels
Carotid Arteries
Carotid Artery, Common
Central Nervous System
Energy Metabolism
Evoked Potentials, Somatosensory
Glucose
Hand
Ischemia
Lactic Acid
Ligation
Metabolism
Naloxone*
Rats*
Rats, Sprague-Dawley
Spinal Injuries
Stroke
Analgesics, Opioid
Calcium Channels
Glucose
Lactic Acid
Naloxone