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Remote preconditioning by infrarenal aortic occlusion is operative via delta1-opioid receptors and free radicals in vivo in the rat heart.
Cardiovasc Res. 2004 Feb 15; 61(3):591-9.CR

Abstract

BACKGROUND

Ischemic preconditioning (PC) is a powerful mechanism in reducing infarct size of the heart. Protection can be performed either by an ischemic stimulus of the heart itself or by ischemia of an organ distant to the heart (remote PC). We have previously shown that remote PC by infrarenal occlusion of the aorta [IOA] in the rat is as powerful as classical ischemic PC. This protection may be transmitted by humoral factors, and protein kinase C is a mediator in the signal transduction mechanism. Focus of the present study was to address the question whether remote preconditioning is dependent on the activation of the delta1-opioid receptor and/or free radicals, the infarct size was determined after either inhibition of the delta1-opioid receptor or scavenging free radicals.

METHODS AND RESULTS

IOA was performed in rats by occlusion of the infrarenal aorta for 15 min followed by a 10-min reperfusion period. Infarction of the heart was induced by 30 min regional ischemia followed by 30 min of reperfusion. The area of infarct was determined by propidium iodide and the risk zone was demarcated by zinc cadmium sulfide fluorescent particles. Control hearts (30 min regional ischemia of the heart followed by 30 min of reperfusion; no IOA) had an infarct size of 54 +/- 3%, whereas classical preconditioning by three ischemia/reperfusion [I/R] cycles, 5 min each, reduced it to 12 +/- 1% of the risk zone (p<0.05). Fifteen minutes IOA with 10 min of reperfusion was highly protective and reduced the infarct size to 20 +/- 5% (p<0.05 vs. control). Inhibition of the delta1-opioid receptors by 7-benzylidenenaltrexone [BNTX] blocked the protection obtained by PC and IOA (41 +/- 4% and 44 +/- 2%, respectively; p<0.05 vs. the group without BNTX). BNTX in control hearts had no influence on infarct size (52 +/- 2%). Inhibition of endogenously released radicals by N-2-mercaptopropionyl glycine [MPG] blocked the infarct size reduction of IOA (46 +/- 3%; p<0.05 vs. IOA), but had no influence on the protection in classically preconditioned hearts protected by three cycles I/R (13 +/- 4%). Only if the number of the preconditioning stimuli was reduced to one was MPG able to overcome the protection (43 +/- 4%, p<0.05 vs. PC with one I/R cycle (21 +/- 4%)).

CONCLUSION

Remote preconditioning using IOA protects the rat heart from infarction. Classical and remote PC share both the delta1-opioid-receptor and free radicals as common elements in their signal transduction pathways. MPG can block protection from IOA and from one, but not from three, classical preconditioning cycles. This indicates that the protection by remote preconditioning is comparable to classical PC with one I/R cycle.

Authors+Show Affiliations

Department of Cardiology, Medical Clinic II, University of Technology Dresden, PO Box 95, Fetscherstr 76 D-01307 Dresden, Germany. cweinbre@web.deNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

14962489

Citation

Weinbrenner, Christof, et al. "Remote Preconditioning By Infrarenal Aortic Occlusion Is Operative Via Delta1-opioid Receptors and Free Radicals in Vivo in the Rat Heart." Cardiovascular Research, vol. 61, no. 3, 2004, pp. 591-9.
Weinbrenner C, Schulze F, Sárváry L, et al. Remote preconditioning by infrarenal aortic occlusion is operative via delta1-opioid receptors and free radicals in vivo in the rat heart. Cardiovasc Res. 2004;61(3):591-9.
Weinbrenner, C., Schulze, F., Sárváry, L., & Strasser, R. H. (2004). Remote preconditioning by infrarenal aortic occlusion is operative via delta1-opioid receptors and free radicals in vivo in the rat heart. Cardiovascular Research, 61(3), 591-9.
Weinbrenner C, et al. Remote Preconditioning By Infrarenal Aortic Occlusion Is Operative Via Delta1-opioid Receptors and Free Radicals in Vivo in the Rat Heart. Cardiovasc Res. 2004 Feb 15;61(3):591-9. PubMed PMID: 14962489.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Remote preconditioning by infrarenal aortic occlusion is operative via delta1-opioid receptors and free radicals in vivo in the rat heart. AU - Weinbrenner,Christof, AU - Schulze,Falk, AU - Sárváry,László, AU - Strasser,Ruth H, PY - 2003/04/02/received PY - 2003/09/26/revised PY - 2003/10/05/accepted PY - 2004/2/14/pubmed PY - 2004/6/5/medline PY - 2004/2/14/entrez SP - 591 EP - 9 JF - Cardiovascular research JO - Cardiovasc Res VL - 61 IS - 3 N2 - BACKGROUND: Ischemic preconditioning (PC) is a powerful mechanism in reducing infarct size of the heart. Protection can be performed either by an ischemic stimulus of the heart itself or by ischemia of an organ distant to the heart (remote PC). We have previously shown that remote PC by infrarenal occlusion of the aorta [IOA] in the rat is as powerful as classical ischemic PC. This protection may be transmitted by humoral factors, and protein kinase C is a mediator in the signal transduction mechanism. Focus of the present study was to address the question whether remote preconditioning is dependent on the activation of the delta1-opioid receptor and/or free radicals, the infarct size was determined after either inhibition of the delta1-opioid receptor or scavenging free radicals. METHODS AND RESULTS: IOA was performed in rats by occlusion of the infrarenal aorta for 15 min followed by a 10-min reperfusion period. Infarction of the heart was induced by 30 min regional ischemia followed by 30 min of reperfusion. The area of infarct was determined by propidium iodide and the risk zone was demarcated by zinc cadmium sulfide fluorescent particles. Control hearts (30 min regional ischemia of the heart followed by 30 min of reperfusion; no IOA) had an infarct size of 54 +/- 3%, whereas classical preconditioning by three ischemia/reperfusion [I/R] cycles, 5 min each, reduced it to 12 +/- 1% of the risk zone (p<0.05). Fifteen minutes IOA with 10 min of reperfusion was highly protective and reduced the infarct size to 20 +/- 5% (p<0.05 vs. control). Inhibition of the delta1-opioid receptors by 7-benzylidenenaltrexone [BNTX] blocked the protection obtained by PC and IOA (41 +/- 4% and 44 +/- 2%, respectively; p<0.05 vs. the group without BNTX). BNTX in control hearts had no influence on infarct size (52 +/- 2%). Inhibition of endogenously released radicals by N-2-mercaptopropionyl glycine [MPG] blocked the infarct size reduction of IOA (46 +/- 3%; p<0.05 vs. IOA), but had no influence on the protection in classically preconditioned hearts protected by three cycles I/R (13 +/- 4%). Only if the number of the preconditioning stimuli was reduced to one was MPG able to overcome the protection (43 +/- 4%, p<0.05 vs. PC with one I/R cycle (21 +/- 4%)). CONCLUSION: Remote preconditioning using IOA protects the rat heart from infarction. Classical and remote PC share both the delta1-opioid-receptor and free radicals as common elements in their signal transduction pathways. MPG can block protection from IOA and from one, but not from three, classical preconditioning cycles. This indicates that the protection by remote preconditioning is comparable to classical PC with one I/R cycle. SN - 0008-6363 UR - https://www.unboundmedicine.com/medline/citation/14962489/Remote_preconditioning_by_infrarenal_aortic_occlusion_is_operative_via_delta1_opioid_receptors_and_free_radicals_in_vivo_in_the_rat_heart_ L2 - https://academic.oup.com/cardiovascres/article-lookup/doi/10.1016/j.cardiores.2003.10.008 DB - PRIME DP - Unbound Medicine ER -