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Role of Endogenous Opioid System in Ischemic-Induced Late Preconditioning.

Fraessdorf J, Hollmann MW, Hanschmann I, Heinen A, Weber NC, Preckel B, Huhn R - PLoS ONE (2015)

Bottom Line: We investigated whether 1) OR are involved in the trigger and/or mediation phase of LPC and 2) a time course effect on the expression of different opioid receptors and their endogenous ligands exists.LPC reduced infarct size from 61±10% in controls to 25±9% (P<0.001).Expression of δ-OR and plasma levels of endogenous opioid peptides are increased after ischemic LPC.

View Article: PubMed Central - PubMed

Affiliation: Department of Anesthesiology, University Hospital Duesseldorf, Duesseldorf, Germany; Department of Anesthesiology, Laboratory of Experimental Intensive Care and Anesthesiology (L.E.I.C.A.), Academic Medical Center (AMC), University of Amsterdam, Amsterdam, The Netherlands.

ABSTRACT

Background: Opioid receptors (OR) are involved in myocardial late preconditioning (LPC) induced by morphine and δ1-opioid receptor (δ1-OR) agonists. The role of OR in ischemic-induced LPC is unknown. We investigated whether 1) OR are involved in the trigger and/or mediation phase of LPC and 2) a time course effect on the expression of different opioid receptors and their endogenous ligands exists.

Methods: Male Wistar rats were randomly allocated to four groups (each group n = 8). Awake animals were ischemic preconditioned by a 5 minutes coronary occlusion. 24 hours later, anesthetized animals underwent 25 minutes coronary occlusion followed by 2 hours of reperfusion. The role of OR was investigated by treatment with intraperitoneal naloxone (Nal) 10 minutes prior to LPC (Nal-LPC; trigger phase) or 10 min prior to sustained ischemia (LPC-Nal; mediation phase).

Results: LPC reduced infarct size from 61±10% in controls to 25±9% (P<0.001). Naloxone during trigger or mediation phase completely abolished LPC-induced cardioprotection (59±9% and 62±9%; P<0.001 vs. LPC). 8, 12 and 24 hours after the ischemic stimulus, expression of δ-OR in the heart was increased, whereas μ-opioid receptor (μ-OR) and κ-opioid receptor (κ-OR) were not. Plasma concentrations of β-endorphin and leu-enkephalin but not dynorphin were increased by LPC.

Conclusion: Ischemic LPC is triggererd and mediated by OR. Expression of δ-OR and plasma levels of endogenous opioid peptides are increased after ischemic LPC.

No MeSH data available.


Related in: MedlinePlus

DOR, KOR and MOR expression in rat myocardium upon ischemic late preconditioning (LPC).Representative western blot analysis experiments of a time course (Sham, 0, 2, 4, 8, 12 and 24 hours after the ischemic stimulus was initiated). Summarized data presenting AVI (arbitray units of average light intensity) are shown. Data are presented as mean±SD, *P<0.05 vs. 0 hours.
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pone.0134283.g003: DOR, KOR and MOR expression in rat myocardium upon ischemic late preconditioning (LPC).Representative western blot analysis experiments of a time course (Sham, 0, 2, 4, 8, 12 and 24 hours after the ischemic stimulus was initiated). Summarized data presenting AVI (arbitray units of average light intensity) are shown. Data are presented as mean±SD, *P<0.05 vs. 0 hours.

Mentions: 8 hours following ischemic LPC, expression of δ-OR was increased and expression remained elevated up to 24 hours in myocardial samples (Fig 3). We could not observe any changes in the expression of κ-OR or μ-OR at any of the measured time points (Fig 3).


Role of Endogenous Opioid System in Ischemic-Induced Late Preconditioning.

Fraessdorf J, Hollmann MW, Hanschmann I, Heinen A, Weber NC, Preckel B, Huhn R - PLoS ONE (2015)

DOR, KOR and MOR expression in rat myocardium upon ischemic late preconditioning (LPC).Representative western blot analysis experiments of a time course (Sham, 0, 2, 4, 8, 12 and 24 hours after the ischemic stimulus was initiated). Summarized data presenting AVI (arbitray units of average light intensity) are shown. Data are presented as mean±SD, *P<0.05 vs. 0 hours.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4520665&req=5

pone.0134283.g003: DOR, KOR and MOR expression in rat myocardium upon ischemic late preconditioning (LPC).Representative western blot analysis experiments of a time course (Sham, 0, 2, 4, 8, 12 and 24 hours after the ischemic stimulus was initiated). Summarized data presenting AVI (arbitray units of average light intensity) are shown. Data are presented as mean±SD, *P<0.05 vs. 0 hours.
Mentions: 8 hours following ischemic LPC, expression of δ-OR was increased and expression remained elevated up to 24 hours in myocardial samples (Fig 3). We could not observe any changes in the expression of κ-OR or μ-OR at any of the measured time points (Fig 3).

Bottom Line: We investigated whether 1) OR are involved in the trigger and/or mediation phase of LPC and 2) a time course effect on the expression of different opioid receptors and their endogenous ligands exists.LPC reduced infarct size from 61±10% in controls to 25±9% (P<0.001).Expression of δ-OR and plasma levels of endogenous opioid peptides are increased after ischemic LPC.

View Article: PubMed Central - PubMed

Affiliation: Department of Anesthesiology, University Hospital Duesseldorf, Duesseldorf, Germany; Department of Anesthesiology, Laboratory of Experimental Intensive Care and Anesthesiology (L.E.I.C.A.), Academic Medical Center (AMC), University of Amsterdam, Amsterdam, The Netherlands.

ABSTRACT

Background: Opioid receptors (OR) are involved in myocardial late preconditioning (LPC) induced by morphine and δ1-opioid receptor (δ1-OR) agonists. The role of OR in ischemic-induced LPC is unknown. We investigated whether 1) OR are involved in the trigger and/or mediation phase of LPC and 2) a time course effect on the expression of different opioid receptors and their endogenous ligands exists.

Methods: Male Wistar rats were randomly allocated to four groups (each group n = 8). Awake animals were ischemic preconditioned by a 5 minutes coronary occlusion. 24 hours later, anesthetized animals underwent 25 minutes coronary occlusion followed by 2 hours of reperfusion. The role of OR was investigated by treatment with intraperitoneal naloxone (Nal) 10 minutes prior to LPC (Nal-LPC; trigger phase) or 10 min prior to sustained ischemia (LPC-Nal; mediation phase).

Results: LPC reduced infarct size from 61±10% in controls to 25±9% (P<0.001). Naloxone during trigger or mediation phase completely abolished LPC-induced cardioprotection (59±9% and 62±9%; P<0.001 vs. LPC). 8, 12 and 24 hours after the ischemic stimulus, expression of δ-OR in the heart was increased, whereas μ-opioid receptor (μ-OR) and κ-opioid receptor (κ-OR) were not. Plasma concentrations of β-endorphin and leu-enkephalin but not dynorphin were increased by LPC.

Conclusion: Ischemic LPC is triggererd and mediated by OR. Expression of δ-OR and plasma levels of endogenous opioid peptides are increased after ischemic LPC.

No MeSH data available.


Related in: MedlinePlus