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This Article Full Text Full Text (PDF) All Versions of this Article: 289/4/H1366    most recent 00042.2005v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (7) Citing Articles via Google Scholar Google Scholar Articles by Xia, Z. Articles by Ansley, D. M. Search for Related Content PubMed PubMed Citation Articles by Xia, Z. Articles by Ansley, D. M.

15-F_2t-isoprostane exacerbates myocardial ischemia-reperfusion injury of isolated rat hearts

¹Centre for Anesthesia and Analgesia, Department of Anesthesiology, Pharmacology, and Therapeutics, University of British Columbia, Vancouver; ³Department of Anatomy and Histology, University of Northern British Columbia, Prince George, British Columbia, Canada; and ²Anesthesiology Research Laboratory, Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, China

Submitted 14 January 2005 ; accepted in final form 17 May 2005

Reactive oxygen species induce formation of 15-F_2t-isoprostane (15-F_2t-IsoP), a specific marker of in vivo lipid peroxidation, which is increased after myocardial ischemia and during the subsequent reperfusion. 15-F_2t-IsoP possesses potent bioactivity under pathophysiological conditions. However, it remains unknown whether 15-F_2t-IsoP, by itself, can influence myocardial ischemia-reperfusion injury (IRI). Adult rat hearts were perfused by the Langendorff technique with Krebs-Henseleit (KH) solution at a constant flow rate of 10 ml/min. 15-F_2t-IsoP (100 nM), SQ-29548 (1 µM, SQ), a thromboxane receptor antagonist that can abolish the vasoconstrictor effect of 15-F_2t-IsoP, 15-F_2t-IsoP + SQ in KH, or KH alone (vehicle control) was applied for 10 min before induction of 40 min of global ischemia followed by 60 min of reperfusion. During ischemia, saline (control), 15-F_2t-IsoP, 15-F_2t-IsoP + SQ, or SQ in saline was perfused through the aorta at 60 µl/min. 15-F_2t-IsoP, 15-F_2t-IsoP + SQ, or SQ in KH was infused during the first 15 min of reperfusion. Coronary effluent endothelin-1 concentrations were significantly higher in the group treated with 15-F_2t-IsoP than in the control group during ischemia and also in the later phase of reperfusion (P < 0.05). Infusion of 15-F_2t-IsoP increased release of cardiac-specific creatine kinase, reduced cardiac contractility during reperfusion, and increased myocardial infarct size relative to the control group. SQ abolished the deleterious effects of 15-F_2t-IsoP. 15-F_2t-IsoP exacerbates myocardial IRI and may, therefore, act as a mediator of IRI. 15-F_2t-IsoP-induced endothelin-1 production during cardiac reperfusion may represent a mechanism underlying the deleterious actions of 15-F_2t-IsoP.

ischemia-reperfusion injury; SQ-29548; endothelin-1

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