Changes in Sympathetic Innervation of Rat Caudal Artery in Experimental Myocardial Infarction. Effect of Semax Peptide.

Bulletin of experimental biology and medicine2016PMID: 27591879

View on PubMed DOI: 10.1007/s10517-016-3442-y

Animal StudySemax

Plain Language Summary

Showed Semax prevented increased sympathetic nerve ending density in rat caudal artery after experimental myocardial infarction. The peptide moderated sympathetic nervous system activation that aggravates MI course, demonstrating cardiovascular protective effects.

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.

Authors

Gorbacheva, A M; Berdalin, A B; Stulova, A N; Nikogosova, A D; Lin, M D; Buravkov, S V; Gavrilova, S A; Koshelev, V B

Keywords

Semaxautonomic nervous systemcardioprotectionmyocardial infarctionrat