[Peptide correction of arrhythmias induced by stimulation of the vagal sympathetic trunk in cats].
The effects of met-enkephalin, leu-enkephalin, D-Ala2-metenkephalin, and somatostatin on Wenckebach arrhythmia and atrioventricular dissociation was investigated in experiments on anesthesized cats. Arrhythmias were induced by stimulation of the vagus with short repetitive bursts of pulses. Enkephalins evoked a protective effect in both arrhythmias whereas somatostatin had no antiarrhythmic properties. The protective effect of enkephalins persisted after blockage of mu-opiate receptors with naloxone (0.2 mg/kg), but in high doses (2 mg/kg), which blocked both mu- and delta-opiate receptors, antiarrhythmic effects was abolished. It is concluded that the protective effect of enkephalins against vagally induced arrhythmias may be due to the stimulation of delta-opiate receptors located on the presynaptic vagal endings. As a results, stimulation-evoked acetylcholine release is diminished, which prevent the arrhythmogenic effect of the vagus nerve.
Osadchiĭ
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OE
Pokrovskiĭ
V M
VM
D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000627:therapeutic use*; D001145:Arrhythmias, Cardiac / Q000188:drug therapy*; D002415:Cats; D004743:Enkephalin, Leucine / Q000627:therapeutic use; D004744:Enkephalin, Methionine / Q000627:therapeutic use; D013004:Somatostatin / Q000627:therapeutic use; D013564:Sympathetic Nervous System / Q000187:drug effects*; D014630:Vagus Nerve / Q000187:drug effects*
D000889:Anti-Arrhythmia Agents; D013004:Somatostatin; D004744:Enkephalin, Methionine; D004743:Enkephalin, Leucine