doi: 10.1161/01.STR.0000154868.00502.56
(Stroke. 2005;36:532.)
© 2005 American Heart Association, Inc.
Letters to the Editor |
Glucose Metabolism, Noradrenaline Release, and MK-801 in Intracerebral Hemorrhage
Division of Cardiology, Department of Medicine, Wakayama Medical University, Wakayama, Japan.
To the Editor:
We read with great interest the article by Ardizzone et al1 dealing with the glutamate receptor blockade and glucose metabolism in the experimental intracerebral hemorrhage in rats. The results of their study demonstrated that deoxyglucose uptake was increased in the perihematomal region in rats. In addition, they indicated that the glucose uptake produced by the hemorrhages was blocked by pretreatment of the glutamate receptor antagonists MK-801 and NBQX. The authors proposed that glutamate activation of N-methyl-D-aspartate (NMDA) or 
-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors increased glucose hypermetabolism in perihematomal brain after intracerebral hemorrhage, which may partially contribute to the pathophysiology of this disease.
Several studies have shown the mechanisms for neuroprotective effects of MK-801 in the central nervous system. In a study we presented earlier, changes in noradrenaline (NA) release evoked by L-glutamate was investigated in rat central nervous system.2 In an in vitro study, we showed that L-glutamate increased the release of NA from rat medulla oblongata, and further observed that the facilitative effect of L-glutamate on NA release was more pronounced in spontaneously hypertensive rats than in normotensive rats. In addition, it was demonstrated that MK-801 significantly reserved the increase in NA release evoked by L-glutamate. It might be possible that extracellular glutamate accumulation in the brain after hemorrhage may be attributable to the increased release of NA in the damaged regions. It was already shown that NA might stimulate glycogenolysis, enhance glucose uptake, and increase glucose utilization in the cultured astrocytes.3,4 In this context, it can be speculated that the sympatholytic action might explain, at least in part, the neuroprotective effects of MK-801 in neurotoxic disorders. Therefore, we would like to know the magnitude of the changes in the content or release of catecholamines in the perihematomal brain after intracerebral hemorrhage in the present study of Ardizzone et al. Further studies are necessary to assess more thoroughly the relationships between glucose metabolism and neuroprotective effect of MK-801 in the intracerebral hemorrhage.
References
1. Ardizzone TD, Lu A, Wagner KR, Tang Y, Ran R, Sharp FR. Glutamate receptor blockade attenuates glucose hypermetabolism in perihematomal brain after experimental intracerebral hemorrhage in rat. Stroke. 2004; 35: 2587–2591.
2. Tsuda K, Tsuda S, Nishio I, Masuyama Y, Goldstein M. Glutamatergic regulation of [3H]-noradrenaline release in the medulla oblongata of normotensive and spontaneously hypertensive rats. J Hypertens. 1994; 12: 517–522.[Medline] [Order article via Infotrieve]
3. Magistretti PJ, Sorg O, Yu N, Martin JL, Pellerin L. Neurotransmitters regulate energy metabolism in astrocytes: implications for the metabolic trafficking between neural cells. Dev Neurosci. 1993; 15: 306–312.[Medline] [Order article via Infotrieve]
4. Pellerin L, Sdtolz M, Sorg O, Martin JL, Deschepper CF, Magistretti PJ. Regulation of energy metabolism by neurotransmitters in astrocytes in primary culture and in an immortalized cell line. Glia. 1997; 21: 74–83.[CrossRef][Medline] [Order article via Infotrieve]
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