caffeinol has been researched along with Brain-Ischemia* in 2 studies
1 review(s) available for caffeinol and Brain-Ischemia
Article | Year |
---|---|
[Caffeinol: a neuroprotective action in ischemic brain damage].
Caffeinol--a combination of ethanol and caffeine in appropriate concentrations--exerts neuroprotective and anticonvulsive action. Research conducted on rats in models of ischemic brain damage have shown that caffeinol decreases the size of cortical damage by about 80%, improves motional coordination and memory. The sooner caffeinol was administered, the better were beneficial therapeutic effects. What is more, the medicine may be safely combined with other methods used in stroke treatment, such as hypothermia and thrombolysis, what additionally increases its neuroprotective influence. Research on people have shown that caffeinol is less effective as neuroprotective agent in patients abusing alcohol, while chronic intake of caffeine does not influence its activity. Mechanism of its activity is not known yet, however, it is assumed that it bases on an antagonism of NMDA receptors. Regarding the fact that the most of strokes in humans concern subcortical areas, it is justified to conduct further research on caffeinol, which would involve other brain structures, thus allowing to define its use in clinical practice. Topics: Animals; Brain Ischemia; Caffeine; Combined Modality Therapy; Drug Combinations; Ethanol; Humans; Neuroprotective Agents; Rats; Receptors, N-Methyl-D-Aspartate; Thrombolytic Therapy | 2015 |
1 other study(ies) available for caffeinol and Brain-Ischemia
Article | Year |
---|---|
Caffeinol at the receptor level: anti-ischemic effect of N-methyl-D-aspartate receptor blockade is potentiated by caffeine.
Although caffeinol (a combination of a low dose of caffeine and ethanol) was shown to robustly reduce stroke damage in experimental models and is now in clinical evaluation for treatment of ischemic stroke, little is known about the potential mechanism of its action.. We used an in vivo excitotoxicity model based on intracortical infusion of N-methyl-D-aspartate (NMDA) and a model of reversible focal ischemia to demonstrate NMDA receptor inhibition as a potential mechanism of caffeinol anti-ischemic activity.. Caffeinol reduced the size of excitotoxic lesion, and substitution of ethanol in caffeinol with the NMDA antagonists CNS-1102 and MK-801 but not with MgSO(4) produced treatment with strong synergistic effect that was at least as robust in reducing ischemic damage as caffeinol. This NMDA receptor antagonist and caffeine combination demonstrated a long window of opportunity, activity in spontaneously hypertensive rats, and, unlike caffeinol, was fully effective in animals chronically pretreated with ethanol.. Our study suggests that antiexcitotoxic properties may underlie some of the anti-ischemic effect of caffeinol. This study provides strong evidence that the anti-ischemic effect of NMDA receptor blockers in general can be dramatically augmented by caffeine, thus opening a possibility for new use of NMDA-based pharmacology in the treatment of stroke. Topics: Animals; Brain Ischemia; Caffeine; Disease Models, Animal; Dizocilpine Maleate; Dose-Response Relationship, Drug; Drug Combinations; Drug Synergism; Ethanol; Excitatory Amino Acid Agonists; Excitatory Amino Acid Antagonists; Guanidines; Male; N-Methylaspartate; Nerve Degeneration; Neuroprotective Agents; Neurotoxins; Phosphodiesterase Inhibitors; Rats; Rats, Inbred SHR; Rats, Sprague-Dawley; Receptors, N-Methyl-D-Aspartate; Time Factors; Treatment Outcome | 2010 |