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Ann Thorac Surg 2000;70:2186
© 2000 The Society of Thoracic Surgeons

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Correspondence

Mechanisms of acute ischemic preconditioning

^a Research Department, Kokura Memorial Hospital, 1-1 Kifune-cho, Kokura-kitaku, Kitakyushu-shi, Fukuoka, 802-8555, Japan
^b Department of Physiology, The University of the Ryukyus School of Medicine, Okinawa, Japan

To the Editor

Zvara and colleagues are to be congratulated for their article [1]. We agree with the view that acute ischemic preconditioning (IPC) is probably different from that ascribable to heat shock protein.

We would like to propose that the effector of acute IPC is taurine, released by the outpouring of adenosine during the brief ischemic conditioning episode, which occurs both in the central nervous system (CNS) and myocardium, locations where the role of adenosine in triggering IPC is well established.

Flooding of interstitial fluid of all areas of the ischemic CNS regardless of whether rich in adenosine A₁ or A₂ receptors with potentially harmful (glutamate) as well as protective (gamma aminobutyric acid and taurine) amino acids is well known.

The inhibitory and protective ß-amino acid taurine (2-aminoethane sulfonic acid, chemically and metabolically stable) is released by activation of (a) ß-receptors and A₂ receptors via cyclic adenosine monophosphate intracellular accumulation secondary to adenylate cyclase activation [2, 3] or (b) receptors for N-methyl-D-aspartate, quinolinic acid or kainate, kappa-opiate, and serotonin [2–4]. However, in cultured glial cells, A₁ agonists also release taurine via unknown mechanisms but apparently not involving A₁ receptors or cyclic adenosine monophosphate [2, 5].

We demonstrated release of taurine in a dose-dependent manner in the hippocampus, rich in A₁ receptors but poor in A₂ receptors, of nonischemic rabbit brain using intracerebral microdialysis [6]. We hypothesized that taurine is released universally in all tissues; therefore, if given systemically, it would be protective for all areas, which was confirmed in the spinal cord ischemic rabbit model [7].

Taurine released locally at the spinal cord level must have been the taurine most responsible for IPC. However, given the fact that taurine crosses the blood-brain barrier in about 20 minutes (unpublished personal data obtained using intracerebral microdialysis), it is possible that taurine released by tissues other than the spinal cord had some role in conferring protection to the second episode of ischemia, because 30 minutes was allowed between the first brief ischemic conditioning episode and the second longer ischemic period. Also, evidence of systemic effects (different hemodynamic profile) was present.

Although the authors conjectured about the possible role adenosine might have played in inducing the differing hemodynamic profiles between the IPC group and the control group, that would only explain the short-lived acute changes immediately after reperfusion following the brief ischemic conditioning. The half-life of adenosine, being less than 8 seconds, could not explain the long-lasting hemodynamic difference. Because similar hemodynamic changes in taurine-treated animals were observed [6], we believe differing profiles during the ensuing 30 minutes of reperfusion were caused by taurine, whose effects last for more than 30 minutes, rather than adenosine.

Inducing IPC of the CNS (spinal cord or brain) to test and evaluate the protective hypothesis is only possible in experimental animals. Clinically, it would be impractical and unacceptable, but could be mimicked by the administration of exogenous taurine and be utilized as a basal protective strategy.

References

1. Zvara D.A., Colonna D.M., Deal D.D., Vernon J.S., Gowda M., Lundell J.C. Ischemic preconditioning reduces neurologic injury in a rat model of spinal cord ischemia. Ann Thorac Surg 1999;68:874-880.[Abstract/Free Full Text]
2. Madelian V., Silliman S., Shain W. Adenosine stimulates cAMP-mediated taurine release from LRM55 glial cells. J Neurosci Res 1988;20:176-181.[Medline]
3. Shain W.G., Martin D.L. Activation of ß-adrenergic receptors stimulates taurine release from glial cells. Cell Mol Neurobiol 1984;4:191-196.[Medline]
4. Vezzani A.-M., Ungerstedt U., French E.D., Schwarcz R. In vivo brain dialysis of amino acids and simultaneous EEG measurements following intrahippocampal quinolinic acid injection: evidence for a dissociation between neurochemical changes and seizures. J Neurochem 1985;45:335-344.[Medline]
5. Huxtable R.J. Taurine in the central nervous system and the mammalian actions of taurine. Prog Neurobiol 1989;22:471-533.
6. Miyamoto T.A., Miyamoto K.J. Does adenosine release taurine in A₁ receptors rich hippocampus?. J Anesthesia 1999;13:94-98.
7. Ohno N., Miyamoto K.J., Miyamoto T.A. Taurine potentiates the efficacy of hypothermia. Asian Cardiovasc Thorac Surg Ann 1999;7:267-271.

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