Changes in Sympathetic Innervation of Rat Caudal Artery in Experimental Myocardial Infarction. Effect of Semax Peptide.
Gorbacheva. A M AM; Berdalin. A B AB; Stulova. A N AN; Nikogosova. A D AD; Lin. M D MD; Buravkov. S V SV; Gavrilova. S A SA; Koshelev. V B VB
Key Findings
- Semax reduced the increase in sympathetic nerve density in the caudal artery after myocardial infarction or ischemia/reperfusion.
- The peptide lowered the density of alpha‑adrenoreceptors in the same artery, without affecting beta‑adrenoreceptors.
- Rats treated with Semax showed weaker vascular responses to electrical stimulation and norepinephrine after ischemia/reperfusion injury.
Practical Outcomes
- The results hint that Semax might help blunt harmful sympathetic over‑activation after a heart attack, potentially protecting blood‑vessel function. However, the study was done in rats, not humans, and no dosing or safety data for people are provided, so it isn’t ready for direct self‑experimentation or clinical use by biohackers.
Summary
In rats that had a heart attack, the peptide Semax lowered the growth of nerve endings that boost the sympathetic (fight‑or‑flight) system in a leg artery, reduced the number of alpha‑adrenergic receptors there, and made the blood vessels less reactive to electrical signals and norepinephrine. These effects were seen up to 28 days after the injury.
Abstract
Activation of the sympathetic nervous system aggravates the course of myocardial infarction. Semax peptide moderated the degree of this activation and prevented the increase in the density of sympathetic endings in rat caudal artery in 28 days after ischemia or ischemia/reperfusion. The peptide reduced the density of α-adrenoreceptors in the caudal artery of rats with myocardial infarction. Semax produced no effect on β-adrenoreceptors in both experimental models. The experiments on isolated segments of the caudal artery revealed reduced vascular responsiveness to electrical stimulation and norepinephrine infusion in rats treated with Semax after ischemia/reperfusion injury.
Study Information
pubmed
2016
2016-09-03T00:00:00.000Z
10.1007/s10517-016-3442-y