[Pharmacological treatment of memory disorders caused by hypoxia and cerebral ischemia in rats].
Iasnetsov. V V VV; Krylova. I N IN; Provornova. N A NA
Key Findings
- Semax significantly increased survival after bilateral carotid artery occlusion in rats.
- Semax prevented or reduced memory deficits in rats subjected to cerebral ischemia or hypoxic conditions.
- Other nootropics showed similar benefits, while the NMDA antagonist MK‑801 worsened outcomes.
Practical Outcomes
- For biohackers, the data hint that semax might be useful for protecting brain function during oxygen‑depriving events, but there are no human dosage or safety guidelines yet. Until clinical trials confirm these effects, using semax for this purpose remains experimental and should be approached with caution.
Summary
In rats, the peptide semax (along with several other nootropics) helped the animals survive better and kept their memory intact after their brain blood flow was blocked or they were exposed to low oxygen. The study suggests semax could protect against memory loss caused by hypoxia or stroke‑like conditions, but the work was done only in animals.
Abstract
Experiments with white mongrel rats (both females and males) showed that nootropic substances, i.e. sodium hydroxybutyrate, pyracetam, oxyracetam, aniracetam, centrophinoxine, nooglutyl, mexydol, semax, amide L-pyroglutamyl-D-alanine, and MK-801, a specific noncontesting antagonist of the NMDA-receptor complex, significantly increased survivability of the animals following bilateral occlusion of the common carotid arteries. The nootrops prevented, partly or completely, mnestic disorders in the experimental rats. In contrast, MK-801 profoundly aggravated these disorders. Similar results were obtained with a model of hypoxic amnesia. Except for N-acetylglycine amide and amide L-pyroglutamyl-D-alanine, the nootrops fully or to a considerable extent blocked the development of mnestic disorders in hypoxic rats. The authors recommend novel nootrops (nooglutyl, mexidol, semax and GVS-111) for the pharmacological correction of mnestic disorders consequent to hypoxia or cerebral ischemia.
Study Information
pubmed
1998