[The participation of prostanoids in the realization of the cardioprotective, antistressor and anti-arrhythmic effects of enkephalins]. / Uchastie prostanoidov v realizatsii kardioprotektornykh, antistressornykh i antiaritmicheskikh éffektov énkefalinov.

It has been established that preliminary administration of D-Ala2-Leu5-Arg6-enkephalin, D-Met2-Pro5-enkephalinamide, and D-phenylalanine to experimental animals prevents a stress-induced increase of the content of thromboxane in the blood plasma and myocardium and induces a rise of the level of prostacyclin, PGF2 and PGE in the heart and blood plasma. The authors hold that the changes in the level of prostanoids may mediate cardioprotective and anti-stressor rather than antiarrhythmic effects of enkephalins.

[Effects of opioid neuropeptides on the prostaglandin system and lipid peroxidation processes in the myocardium during stress-induced damage]. / Vliianie opioidnykh neiropeptidov na sistemu prostaglandinov i protsessy perekisnogo okisleniia lipidov v miokarde pri ego stressornom povrezhdenii.

The stress was subsequenced by lowering of Thromboxane A2 level and activation of peroxidation of lipids without any changes of prostacyclin content in myocardium. It was found that the pre-increase of the opioid peptides in blood plasma led to the absence of prostacyclin and thromboxane dynamic and myocardial lipids peroxidation inhibition during the subsequent stress.

[The action of an enzymatically stable Leu-enkephalin analog on the prostanoid content in the myocardium under stress- and adrenaline-induced damage]. / Vozdeistvie énzimoustoichivogo analoga lei-énkefalina na soderzhanie prostanoidov v miokarde pri stressornom i adrenalinom povrezhdenii.

The protective action of enzymatically stable analogue of Leu-enkephalin (D-ala-2-leu5-arg6), injected intraperitoneally, in the course of stress- and epinephrine induced myocardial damage was demonstrated in animal (129 white rats) experiments. Two effect of enkephalin were sufficient for the cardiac protection: enkephalin-stimulated prostacyclin biosynthesis and simultaneous inhibition of thromboxane production.