Abstract
Adenosine, lidocaine, and magnesium (ALM) are clinically available cardioplegic solutions. We examined the effects of low-dose ALM on ischemic stroke in cell and animal models. Cobalt chloride (CoCl2)-treated SH-SY5Y cells were used as a surrogate model to mimic oxygen-glucose deprivation conditions. The cells were incubated with different dilutions of ALM authentic solution (1.0mM adenosine, 2.0mM lidocaine, and5 mM MgSO4 in Earle's balanced salt solution). At a concentration of 2.5%, ALM significantly reduced CoCl2-induced cell loss. This protective effect persisted even when ALM was administered 1h after the insult. We used transient middle cerebral artery occlusion to investigate the therapeutic effects of ALM in vivo. Rats were randomly assigned to two groups-the experimental (ALM) and control (saline) groups-and infusion was administered during the ischemia for 1h. The infarction area was significantly reduced in the ALM group compared with the control group (5.0% ± 2.0% vs. 23.5% ± 5.5%, p = 0.013). Neurological deficits were reduced in the ALM group compared with the control group (modified Longa score: 0 [0-1] vs. 2 [1-2], p = 0.047). This neuroprotective effect was substantiated by a reduction in the levels of various neuronal injury markers in plasma. These results demonstrate the neuroprotective effects of ALM and may provide a new therapeutic strategy for ischemic stroke.
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