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Review
. 2023 Dec 9;24(24):17302.
doi: 10.3390/ijms242417302.

Blood and Brain Metabolites after Cerebral Ischemia

Eva Baranovicova  1 , Dagmar Kalenska  2 , Peter Kaplan  3 , Maria Kovalska  4 , Zuzana Tatarkova  3 , Jan Lehotsky  3
Affiliations
Review

Blood and Brain Metabolites after Cerebral Ischemia

Eva Baranovicova et al. Int J Mol Sci. .

Abstract

The study of an organism's response to cerebral ischemia at different levels is essential to understanding the mechanism of the injury and protection. A great interest is devoted to finding the links between quantitative metabolic changes and post-ischemic damage. This work aims to summarize the outcomes of the most studied metabolites in brain tissue-lactate, glutamine, GABA (4-aminobutyric acid), glutamate, and NAA (N-acetyl aspartate)-regarding their biological function in physiological conditions and their role after cerebral ischemia/reperfusion. We focused on ischemic damage and post-ischemic recovery in both experimental-including our results-as well as clinical studies. We discuss the role of blood glucose in view of the diverse impact of hyperglycemia, whether experimentally induced, caused by insulin resistance, or developed as a stress response to the cerebral ischemic event. Additionally, based on our and other studies, we analyze and critically discuss post-ischemic alterations in energy metabolites and the elevation of blood ketone bodies observed in the studies on rodents. To complete the schema, we discuss alterations in blood plasma circulating amino acids after cerebral ischemia. So far, no fundamental brain or blood metabolite(s) has been recognized as a relevant biological marker with the feasibility to determine the post-ischemic outcome or extent of ischemic damage. However, studies from our group on rats subjected to protective ischemic preconditioning showed that these animals did not develop post-ischemic hyperglycemia and manifested a decreased metabolic infringement and faster metabolomic recovery. The metabolomic approach is an additional tool for understanding damaging and/or restorative processes within the affected brain region reflected in the blood to uncover the response of the whole organism via interorgan metabolic communications to the stressful cerebral ischemic challenge.

Keywords: animal models; blood; cerebral ischemia; cerebral microdialysis; metabolites; stroke; tissues.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Tissue lactate in relation to cerebral ischemia; MCT—monocarboxylate transporters.
Figure 2
Figure 2
Glutamate, glutamine, and GABA (4-aminobutyric acid) cycles and recovery after ischemia.
Figure 3
Figure 3
NAA (N-acetyl aspartate) levels in neurons after ischemia and in the reperfusion period: blue filling as visualization of NAA level, as described in text in detail.
Figure 4
Figure 4
Metabolomic alterations in blood circulation in relation to cerebral ischemia, (BCAAs—branched-chain amino acids, BCKAs—branched-chain ketoacids, BBB-blood–brain barrier).
See this image and copyright information in PMC

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