scholarly journals Cardioprotection by post-conditioning with exogenous triiodothyronine in isolated perfused rat hearts and isolated adult rat cardiomyocytes

2021 ◽  
Vol 116 (1) ◽  
Author(s):  
Helmut Raphael Lieder ◽  
Felix Braczko ◽  
Nilgün Gedik ◽  
Merlin Stroetges ◽  
Gerd Heusch ◽  
...  
Keyword(s):  
Infarct Size ◽  
Ischemia Reperfusion ◽  
Retention Capacity ◽  
Tetrazolium Chloride ◽  
Rat Cardiomyocytes ◽  
Early Reperfusion ◽  
Adult Rat ◽  
Risk Pathway ◽  
Rat Hearts ◽  
Perfused Rat Hearts

AbstractIschemic post-conditioning (iPoCo) by coronary re-occlusion/reperfusion during immediate reperfusion after prolonged myocardial ischemia reduces infarct size. Mechanical manipulation of culprit lesions, however, carries the risk of coronary microembolization which may obscure iPoCo’s cardioprotection. Pharmacological post-conditioning with exogenous triiodothyronine (T3) could serve as an alternative conditioning strategy. Similar to iPoCo, T3 may activate cardioprotective prosurvival pathways. We aimed to study T3’s impact on infarct size and its underlying signal transduction. Hearts were isolated from male Lewis rats (200–380 g), buffer-perfused and subjected to 30 min/120 min global zero-flow ischemia/reperfusion (I/R). In additional hearts, either iPoCo (2 × 30 s/30 s I/R) was performed or T3 (100–500 µg/L) infused at reperfusion. Infarct size was demarcated with triphenyl tetrazolium chloride staining and calculated as percent of ventricular mass. Infarct size was reduced with iPoCo to 16 ± 7% vs. 36 ± 4% with I/R only. The maximum infarct size reduction was observed with 300 µg/L T3 (14 ± 2%). T3 increased the phosphorylation of protein kinase B and mitogen extracellular-regulated-kinase 1/2, both key enzymes of the reperfusion injury salvage kinase (RISK) pathway. Pharmacological RISK blockade (RISK-BL) during reperfusion abrogated T3’s cardioprotection (35 ± 10%). Adult ventricular cardiomyocytes were isolated from buffer-perfused rat hearts and exposed to 30 min/5 min hypoxia/reoxygenation (H/R); reoxygenation was initiated without or with T3, respectively, and without or with RISK-BL, respectively. Maximal preservation of viability was observed with 500 µg/L T3 after H/R (27 ± 4% of all cells vs. 5 ± 3% in time-matched controls). Again, RISK-BL abrogated protection (11 ± 3%). Mitochondria were isolated at early reperfusion from buffer-perfused rat hearts without or with iPoCo or 300 µg/L T3, respectively, at reperfusion. T3 improved mitochondrial function (i.e.: increased respiration, adenosine triphosphate production, calcium retention capacity, and decreased reactive oxygen species formation) to a similar extent as iPoCo. T3 at reperfusion reduces infarct size by activation of the RISK pathway. T3’s protection is a cardiomyocyte phenomenon and targets mitochondria.

scholarly journals Autophagy and protein kinase C are required for cardioprotection by sulfaphenazole

2010 ◽  
Vol 298 (2) ◽  
pp. H570-H579 ◽  
Author(s):  
Chengqun Huang ◽  
Wayne Liu ◽  
Cynthia N. Perry ◽  
Smadar Yitzhaki ◽  
Youngil Lee ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Enhanced Recovery ◽  
Ischemia Reperfusion ◽  
Dominant Negative ◽  
Rat Cardiomyocytes ◽  
Adult Rat ◽  
Kinase C ◽  
Rat Hearts

Previously, we showed that sulfaphenazole (SUL), an antimicrobial agent that is a potent inhibitor of cytochrome P4502C9, is protective against ischemia-reperfusion (I/R) injury (Ref. 15 ). The mechanism, however, underlying this cardioprotection, is largely unknown. With evidence that activation of autophagy is protective against simulated I/R in HL-1 cells, and evidence that autophagy is upregulated in preconditioned hearts, we hypothesized that SUL-mediated cardioprotection might resemble ischemic preconditioning with respect to activation of protein kinase C and autophagy. We used the Langendorff model of global ischemia to assess the role of autophagy and protein kinase C in myocardial protection by SUL during I/R. We show that SUL enhanced recovery of function, reduced creatine kinase release, decreased infarct size, and induced autophagy. SUL also triggered PKC translocation, whereas inhibition of PKC with chelerythrine blocked the activation of autophagy in adult rat cardiomyocytes. In the Langendorff model, chelerythrine suppressed autophagy and abolished the protection mediated by SUL. SUL increased autophagy in adult rat cardiomyocytes infected with GFP-LC3 adenovirus, in isolated perfused rat hearts, and in mCherry-LC3 transgenic mice. To establish the role of autophagy in cardioprotection, we used the cell-permeable dominant-negative inhibitor of autophagy, Tat-Atg5K130R. Autophagy and cardioprotection were abolished in rat hearts perfused with recombinant Tat-Atg5K130R. Taken together, these studies indicate that cardioprotection mediated by SUL involves a PKC-dependent induction of autophagy. The findings suggest that autophagy may be a fundamental process that enhances the heart's tolerance to ischemia.

Dose-dependent protection of cardiac function by propofol during ischemia and early reperfusion in rats: effects on 15-F2t-isoprostane formation

2003 ◽  
Vol 81 (1) ◽  
pp. 14-21 ◽  
Author(s):  
Zhengyuan Xia ◽  
David V Godin ◽  
Thomas K.H Chang ◽  
David M Ansley
Keyword(s):  
Antioxidant Capacity ◽  
Functional Recovery ◽  
Ischemia Reperfusion ◽  
Oxidant Injury ◽  
Control Groups ◽  
Early Reperfusion ◽  
Rat Hearts ◽  
Perfused Rat Hearts ◽  
Dose Dependent ◽  
Myocardium Ischemia Reperfusion

We examined the effects of propofol (2,6-diisopropylphenol) on functional recovery and 15-F2t-isoprostane generation during ischemia–reperfusion in Langendorff-perfused rat hearts. Before the induction of 40 min of global ischemia, hearts were perfused (10 min) with propofol at 5 (lo-P) or 12 μg/mL (hi-P) in saline or with saline only (control). During ischemia, saline, lo-P, or hi-P was perfused through the aorta at 60 μL/min. During the first 15 min of reperfusion, propofol (5 or 12 μg/mL) was continued, followed by perfusion with 5 μg/mL propofol for 75 min in both propofol-treated groups. After 90 min of reperfusion (Rep-90), heart tissues were harvested for assessment of antioxidant status. In hi-P, we observed increased latency to and greater reduction of ischemic contracture relative to the lo-P or control groups. 15-F2t-Isoprostane concentrations increased during ischemia and were significantly lower in hi-P and lo-P than in control (P < 0.01). At Rep-90, myocardial functional recovery was greater in both propofol-treated groups relative to control, and it correlated positively with tissue antioxidant capacity preservation. Tissue antioxidant capacity was better preserved in hi-P than in lo-P treatment (P < 0.05). We conclude that oxidant injury occurs during ischemia and reperfusion, and propofol provides dose-dependent protection primarily by enhancing tissue antioxidant capacity and reducing lipid peroxidation.Key words: propofol, myocardium, ischemia–reperfusion, 15-F2t-isoprostane.

Abstract 1120: Akt Modified MSCs Secrete a Novel Stem Cell Paracrine Factor that Protects Injured Heart, Activates Cyclin Dependent Kinase and Phosphorylates/Activates Akt Signaling Pathway in Adult Rat Cardiomyocytes

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Jian Guo ◽  
Maria Mirotsou ◽  
Jing Huang ◽  
Hui Mu ◽  
Lunan Zhang ◽  
...  
Keyword(s):  
Stem Cell ◽  
Infarct Size ◽  
Ischemia Reperfusion ◽  
Cyclin Dependent Kinase ◽  
Paracrine Factor ◽  
Traditional Concept ◽  
Rat Cardiomyocytes ◽  
Intramyocardial Injection ◽  
Adult Rat ◽  
Novel Protein

Previously, we have shown that intracardiac injection of mesenchymal stem cell (MSC) overexpressing Akt (Akt-MSCs) could dramatically reduced infarct size and restored cardiac function in a paracrine manner. Microarray analysis of Akt-MSCs led to the identification of a novel transcript encoding a secreted protein. Cloning of the cDNA encoding this candidate gene into pET15b allowed the purification as a 6×His tagged recombinant protein. Interestingly, a 30 minute pre-incubation of the H9C2 myocytes with this protein (10nM) reduced H 2 O 2 induced apoptosis by 50% as measured by annexin V/PI staining on flow cytometry (n = 3, p<0.001). Moreover, this protein significantly prevent H 2 O 2 induced DNA fragmentation and inhibited Caspase 9 and Caspase 3/7 activities in adult rat cardiomyocytes by ~36% and ~42%, respectively (n=3, p<0.01). Furthermore, this protein dramatically inhibited the mitochondrial release of Cytochrome C and maintained mitochondrial Bcl-2 protein level. Intramyocardial injection of 1 μg of this novel protein dramatically reduced infarct size (−58%, n=10, p<0.001) and TUNEL positive nuclei (−69%, n=10, p<0.001) in a 30 min ischemia/24h reperfusion rat model. Fibrosis evidenced by collagen deposition was greatly reduced (−61%, n=8, p<0.001) 4 weeks after ischemia/reperfusion injury. Signaling studies demonstrated that this novel protein phosphorylated rat adult cardiomyocytes Akt Thr308 but not Akt Ser473 in a time-depended manner peaking at 30 min. Consequently, downstream Akt substrates, GSK3ß Ser9 and Bad Ser128 , are also phosphorylated at 30 min or at a later time point. In contrast to the traditional concept that PDK1 phosphorylates both Akt Thr308 and Akt Ser473 , our mass-spec and in vitro enzymatic analysis of rat cardiomyocytes stimulated with this factor suggests cyclin-dependent kinase 7 as being responsible for phosphorylation of Akt specifically at Thr 308 position. Further studies would be of great interest to interrogate whether this novel factor could activate other cyclin dependent kinase(s) and render the cardiomyocytes re-entering cell cycle. In conclusion, we have identified a novel paracrine factor from Akt-MSCs that mediates cardioprotective effects through activation of novel pathways involving Akt.

scholarly journals Hemidesmus indicusandHibiscus rosa-sinensisAffect Ischemia Reperfusion Injury in Isolated Rat Hearts

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Vinoth Kumar Megraj Khandelwal ◽  
R. Balaraman ◽  
Dezider Pancza ◽  
Táňa Ravingerová
Keyword(s):  
Infarct Size ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Moderate Increase ◽  
Dependent Manner ◽  
Hemidesmus Indicus ◽  
Rat Hearts ◽  
Perfused Rat Hearts ◽  
Developed Pressure

Hemidesmus indicus(L.) R. Br. (HI) andHibiscus rosa-sinensisL. (HRS) are widely used traditional medicine. We investigated cardioprotective effects of these plants applied for 15 min at concentrations of 90, 180, and 360 μg/mL in Langendorff-perfused rat hearts prior to 25-min global ischemia/120-min reperfusion (I/R). Functional recovery (left ventricular developed pressure—LVDP, and rate of development of pressure), reperfusion arrhythmias, and infarct size (TTC staining) served as the endpoints. A transient increase in LVDP (32%–75%) occurred at all concentrations of HI, while coronary flow (CF) was significantly increased after HI 180 and 360. Only a moderate increase in LVDP (21% and 55%) and a tendency to increase CF was observed at HRS 180 and 360. HI and HRS at 180 and 360 significantly improved postischemic recovery of LVDP. Both the drugs dose-dependently reduced the numbers of ectopic beats and duration of ventricular tachycardia. The size of infarction was significantly decreased by HI 360, while HRS significantly reduced the infarct size at all concentrations in a dose-dependent manner. Thus, it can be concluded that HI might cause vasodilation, positive inotropic effect, and cardioprotection, while HRS might cause these effects at higher concentrations. However, further study is needed to elucidate the exact mechanism of their actions.

scholarly journals Inhibition of LINE-1 expression in the heart decreases ischemic damage by activation of Akt/PKB signaling

2006 ◽  
Vol 25 (2) ◽  
pp. 314-324 ◽  
Author(s):  
Eliana Lucchinetti ◽  
Jianhua Feng ◽  
Rafaela da Silva ◽  
Genrich V. Tolstonog ◽  
Marcus C. Schaub ◽  
...  
Keyword(s):  
Infarct Size ◽  
Functional Recovery ◽  
Rat Heart ◽  
Cardiac Tissue ◽  
Ischemia Reperfusion ◽  
Myocardial Damage ◽  
Immunoblot Analysis ◽  
Rat Hearts ◽  
Perfused Rat Hearts ◽  
Antisense Odns

Microarray analyses indicate that ischemic and pharmacological preconditioning suppress overexpression of the non-long terminal repeat retrotransposon long interspersed nuclear element 1 (LINE-1, L1) after ischemia-reperfusion in the rat heart. We tested whether L1 overexpression is mechanistically involved in postischemic myocardial damage. Isolated, perfused rat hearts were treated with antisense or scrambled oligonucleotides (ODNs) against L1 for 60 min and exposed to 40 min of ischemia followed by 60 min of reperfusion. Functional recovery and infarct size were measured. Effective nuclear uptake was determined by FITC-labeled ODNs, and downregulation of L1 transcription was confirmed by RT-PCR. Immunoblot analysis was used to assess changes in expression levels of the L1-encoded proteins ORF1p and ORF2p. Immunohistochemistry was performed to localize ORF1/2 proteins in cardiac tissue. Effects of ODNs on prosurvival protein kinase B (Akt/PKB) expression and activity were also determined. Antisense ODNs against L1 prevented L1 burst after ischemia-reperfusion. Inhibition of L1 increased Akt/PKBβ expression, enhanced phosphorylation of PKB at serine 473, and markedly improved postischemic functional recovery and decreased infarct size. Antisense ODN-mediated protection was abolished by LY-294002, confirming the involvement of the Akt/PKB survival pathway. ORF1p and ORF2p were found to be expressed in rat heart. ORF1p showed a predominantly nuclear localization in cardiomyocytes, whereas ORF2p was exclusively present in endothelial cells. ORF1p levels increased in response to ischemia, which was reversed by antisense ODN treatment. No significant changes in ORF2p were noted. Our results demonstrate that L1 suppression favorably affects postischemic outcome in the heart. Modifying transcriptional activity of L1 may represent a novel anti-ischemic therapeutic strategy.

Abstract 38: A Decoy Peptide Selectively Inhibiting Dephosphorylation of Phospholamban

2012 ◽  
Vol 111 (suppl_1) ◽  
Author(s):  
Woo Jin Park ◽  
Jae Gyun Oh ◽  
Dongtak Jeong ◽  
Roger J Hajjar
Keyword(s):  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Cardiac Sarcoplasmic Reticulum ◽  
Rat Cardiomyocytes ◽  
Adult Rat ◽  
Rat Hearts ◽  
Cell Permeable Peptide ◽  
Phosphorylated Peptide ◽  
Developed Pressure

Cardiac sarcoplasmic reticulum Ca2+ ATPase (SERCA2a) plays a crucial role in Ca2+ handling in cardiomyocytes. Phospholamban (PLB) is an endogenous inhibitor of SERCA2a and its inhibitory activity is enhanced by dephosphorylation by protein phosphatase 1 (PP1). Therefore, blocking PP1-mediated dephosphorylation of PLB would be an efficient strategy for restoration of the reduced SERCA2a activity in failing hearts. We sought to develop a decoy peptide that mimics the phosphorylated PLB and thus competitively inhibits the PP1-mediated dephosphorylation of PLB. The phosphorylation sites, Ser16 and Thr17, are located within the flexible extra-membrane loop (amino acids 14-22) of PLB. We therefore synthesized a 9-mer pseudo-phosphorylated peptide derived from this region with a replacement of Ser16 with Glu (ψ-PLB-SE). Two other 9-mer peptides with wild type PLB sequence (ψ-PLB) or with a replacement of Ser16 with Ala (ψ-PLB-SA) were also synthesized. These peptides were coupled to a cell-permeable peptide TAT to facilitate cellular uptake. Treatment of adult rat cardiomyocytes with TAT-ψ-PLB-SE, but not with TAT-ψ-PLB or TAT-ψ-PLB-SA, significantly elevated the phosphorylation level of PLB, concomitant with an increase in contractile parameters in vitro. Perfusion of isolated rat hearts with TAT-ψ-PLB-SE significantly restored the left ventricular developed pressure that was suppressed by ischemia-reperfusion (Fig. 1). These data indicate that ψ-PLB-SE prevented dephosphorylation of PLB by acting as a decoy for PP1 and it would provide effective modality to regulate SERCA2a activity in failing hearts.

scholarly journals Ischemic preconditioning in pigs: a causal role for signal transducer and activator of transcription 3

2017 ◽  
Vol 312 (3) ◽  
pp. H478-H484 ◽  
Author(s):  
Sabine Gent ◽  
Andreas Skyschally ◽  
Petra Kleinbongard ◽  
Gerd Heusch
Keyword(s):  
Signal Transduction ◽  
At Risk ◽  
Infarct Size ◽  
Ischemic Preconditioning ◽  
Ischemia Reperfusion ◽  
Coronary Artery Occlusion ◽  
Area At Risk ◽  
Tetrazolium Chloride ◽  
Early Reperfusion ◽  
Stat3 Phosphorylation

Ischemic preconditioning (IPC), i.e., brief episodes of nonlethal myocardial ischemia-reperfusion (I/R) before sustained ischemia with subsequent reperfusion, reduces infarct size in all species tested so far, including humans. In rodents, the cardioprotective signal transduction causally involves an activation of Akt, ERK1/2, and STAT3. However, there are apparent species differences in the signal transduction between rodents and larger mammals such as pigs, where data on IPC's signal transduction are inconsistent for Akt and ERK1/2. The role of STAT3 has not yet been analyzed. Pigs were subjected to 60 min of left anterior descending coronary artery occlusion and 180 min of reperfusion without or with IPC (2 cycles of 3-min occlusion separated by 2 min of reperfusion 15 min before sustained I/R). Infarct size was analyzed by triphenyl tetrazolium chloride staining, and Akt, ERK1/2, and STAT3 phosphorylation was quantified in myocardial biopsies taken at baseline and early reperfusion. AG490 was used to block the STAT3 signaling pathway. IPC reduced infarct size (%area at risk; mean ± SE, I/R, 45 ± 3 vs. IPC, 18 ± 3, P < 0.05). Akt and ERK1/2 phosphorylation was increased at early reperfusion without and with IPC. In contrast, STAT3 phosphorylation at early reperfusion was only increased with IPC (%baseline; mean ± SE, I/R, 126 ± 29 vs. IPC, 408 ± 147, P < 0.05). AG490 prevented the IPC-related increase of STAT3 phosphorylation at reperfusion (%baseline; mean ± SE, 82 ± 12) and abolished IPC's cardioprotection (%area at risk; mean ± SE, 35 ± 4). In pigs, increased phosphorylation of STAT3 is causally involved, whereas Akt and ERK1/2 seem to play no role in IPC's cardioprotection. NEW & NOTEWORTHY In pig hearts in situ, ischemic preconditioning (IPC) causally involves increased phosphorylation of STAT3, whereas Akt and ERK1/2 play no role for cardioprotection. The cardioprotective signal transduction of IPC is similar to that of ischemic postconditioning and remote IPC in pigs.

scholarly journals IP3R1 regulates Ca2+ transport and pyroptosis through the NLRP3/Caspase-1 pathway in myocardial ischemia/reperfusion injury

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Guixi Mo ◽  
Xin Liu ◽  
Yiyue Zhong ◽  
Jian Mo ◽  
Zhiyi Li ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Ischemia Reperfusion Injury ◽  
Cell Model ◽  
Ischemia Reperfusion ◽  
Inflammatory Factors ◽  
Rat Cardiomyocytes ◽  
Adult Rat ◽  
Caspase 1 ◽  
Intracellular Ca ◽  
Myocardial Ischemia Reperfusion

AbstractIntracellular ion channel inositol 1,4,5-triphosphate receptor (IP3R1) releases Ca2+ from endoplasmic reticulum. The disturbance of IP3R1 is related to several neurodegenerative diseases. This study investigated the mechanism of IP3R1 in myocardial ischemia/reperfusion (MI/R). After MI/R modeling, IP3R1 expression was silenced in myocardium of MI/R rats to explore its role in the concentration of myocardial enzymes, infarct area, Ca2+ level, NLRP3/Caspase-1, and pyroptosis markers and inflammatory factors. The adult rat cardiomyocytes were isolated and cultured to establish hypoxia/reperfusion (H/R) cell model. The expression of IP3R1 was downregulated or ERP44 was overexpressed in H/R-induced cells. Nifedipine D6 was added to H/R-induced cells to block Ca2+ channel or Nigericin was added to activate NLRP3. IP3R1 was highly expressed in myocardium of MI/R rats, and silencing IP3R1 alleviated MI/R injury, reduced Ca2+ overload, inflammation and pyroptosis in MI/R rats, and H/R-induced cells. The binding of ERP44 to IP3R1 inhibited Ca2+ overload, alleviated cardiomyocyte inflammation, and pyroptosis. The increase of intracellular Ca2+ level caused H/R-induced cardiomyocyte pyroptosis through the NLRP3/Caspase-1 pathway. Activation of NLRP3 pathway reversed the protection of IP3R1 inhibition/ERP44 overexpression/Nifedipine D6 on H/R-induced cells. Overall, ERP44 binding to IP3R1 inhibits Ca2+ overload, thus alleviating pyroptosis and MI/R injury.

Abstract 13780: Effects of Op2113 on Myocardial Infarct Size and No Reflow in a Rat Myocardial Ischemia/reperfusion Model

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Wangde Dai ◽  
Bruno Le Grand ◽  
Aurelie Boucard ◽  
Juan Carreno ◽  
lifu Zhao ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Infarct Size ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Vehicle Group ◽  
Tetrazolium Chloride ◽  
Early Reperfusion ◽  
Risk Zone ◽  
No Reflow ◽  
No Reflow Phenomenon

Background: Despite advances in early reperfusion therapy for acute ST elevation myocardial infarction (MI), mortality rates and prevention of heart failure after the MI are not optimal. There have been many attempts to further reduce the size of acute MI and to limit the no reflow phenomenon after reperfusion, with mixed results. One promising approach may be to target the mitochondria. The purpose of the present study was to determine whether OP2113 and its active principle ATT (Anethol-TriThione, named also 5-(4-Methoxyphenyl)-3H-1,2-dithiole-3-thione; CAS 532-11-6 ), a pharmaceutical that has been shown to decrease mitochondrial reactive species production from complex I of the mitochondrial respiratory chain, could limit MI size and the no reflow phenomenon in a standardized rat model of 30 minutes of proximal coronary artery occlusion and reperfusion. Methods and Results: Anesthetized rats were exposed to MI and received OP2113 as an intravenous infusion starting either 5 minutes prior to coronary artery occlusion (preventive), or 5 minutes prior to reperfusion (curative), or received vehicle starting 5 minutes prior to coronary artery occlusion. Infusions continued until the end of the study (3 hours of reperfusion). MI size ( triphenyl tetrazolium chloride staining technique) , expressed as a percentage of the ischemic risk zone ( blue dye technique) was significantly lower in the OP2113 treated preventive group at 44.5 ± 2.9% versus 57.0 ± 3.6% ( p<0.05) in the vehicle group, with a nonsignificant trend toward a smaller infarct size in the curative group ( 50.8 ± 3.9%). Area of no reflow ( thioflavin S technique) as a percentage of the risk zone was significantly smaller in both the OP2113 treated preventive (28.8 ± 2.4%; p =0.026 vs vehicle) and curative groups ( 30.1 ± 2.3%; p=0.04 vs vehicle) compared to the vehicle group ( 38.9 ± 3.1%). OP2113 was not associated with any hemodynamic changes. Conclusions: These results suggest that OP2113 is a promising agent to reduce no-reflow as well as to reduce MI size, especially if it is on board early in the course of the MI. It appears to have benefit on no-reflow even when administered relatively late in the course of ischemia.

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