μ-Opioidergic Stimulation of KATP-Channels as an Approach to Prevention of Reperfusion Damage of the Heart in Experiment

L. N. Maslov, Yu B. Lishmanov, T. V. Lasukova, S. V. Tam

Результат исследований: Материалы для журналаСтатья

Выдержка

In vivo pretreatment with selective μ-opioid receptor agonist DAMCO (0.1 mg/kg intravenously 15 min before heart isolation) increased tolerance of the isolated perfused rat heart to ischemic (45 min) and reperfusion (60 min) damages in vitro. This prior stimulation of μ-opioid receptors led to significant improvement of postreperfusion contractile function, significant prevention of reoxygenation destruction of cardiac cells and a decrease in the incidence of reperfusion arrhythmias. All these cardioprotective effects of μ-receptor activation were completely eliminated by pretreatment with the opioid receptor antagonist naloxone (0.1 mg/kg intravenously 10 min before DAMGO injection) or by pretreatment with the KATP-channel blocker glibenclamide (0.3 mg/kg intravenously 30 min before DAMGO injection). It is concluded that μ-opioid receptor activation can be an approach to prevent ischemic/reperfusion damage of the heart. Cardioprotective effects of μ-receptor activation can be mediated via KATP-channels.

Язык оригиналаАнглийский
Страницы (с-по)39-45
Число страниц7
ЖурналKardiologiya
Том41
Номер выпуска2
СостояниеОпубликовано - 2001

Отпечаток

KATP Channels
Opioid Receptors
Reperfusion Injury
Ala(2)-MePhe(4)-Gly(5)-enkephalin
Reperfusion
Injections
Narcotic Antagonists
Glyburide
Naloxone
Cardiac Arrhythmias
Incidence

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Цитировать

μ-Opioidergic Stimulation of KATP-Channels as an Approach to Prevention of Reperfusion Damage of the Heart in Experiment. / Maslov, L. N.; Lishmanov, Yu B.; Lasukova, T. V.; Tam, S. V.

В: Kardiologiya, Том 41, № 2, 2001, стр. 39-45.

Результат исследований: Материалы для журналаСтатья

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AU - Maslov, L. N.

AU - Lishmanov, Yu B.

AU - Lasukova, T. V.

AU - Tam, S. V.

PY - 2001

Y1 - 2001

N2 - In vivo pretreatment with selective μ-opioid receptor agonist DAMCO (0.1 mg/kg intravenously 15 min before heart isolation) increased tolerance of the isolated perfused rat heart to ischemic (45 min) and reperfusion (60 min) damages in vitro. This prior stimulation of μ-opioid receptors led to significant improvement of postreperfusion contractile function, significant prevention of reoxygenation destruction of cardiac cells and a decrease in the incidence of reperfusion arrhythmias. All these cardioprotective effects of μ-receptor activation were completely eliminated by pretreatment with the opioid receptor antagonist naloxone (0.1 mg/kg intravenously 10 min before DAMGO injection) or by pretreatment with the KATP-channel blocker glibenclamide (0.3 mg/kg intravenously 30 min before DAMGO injection). It is concluded that μ-opioid receptor activation can be an approach to prevent ischemic/reperfusion damage of the heart. Cardioprotective effects of μ-receptor activation can be mediated via KATP-channels.

AB - In vivo pretreatment with selective μ-opioid receptor agonist DAMCO (0.1 mg/kg intravenously 15 min before heart isolation) increased tolerance of the isolated perfused rat heart to ischemic (45 min) and reperfusion (60 min) damages in vitro. This prior stimulation of μ-opioid receptors led to significant improvement of postreperfusion contractile function, significant prevention of reoxygenation destruction of cardiac cells and a decrease in the incidence of reperfusion arrhythmias. All these cardioprotective effects of μ-receptor activation were completely eliminated by pretreatment with the opioid receptor antagonist naloxone (0.1 mg/kg intravenously 10 min before DAMGO injection) or by pretreatment with the KATP-channel blocker glibenclamide (0.3 mg/kg intravenously 30 min before DAMGO injection). It is concluded that μ-opioid receptor activation can be an approach to prevent ischemic/reperfusion damage of the heart. Cardioprotective effects of μ-receptor activation can be mediated via KATP-channels.

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