Inhibition of nonexocytotic norepinephrine release by desipramine reduces myocardial infarction size

2006 ◽  
Vol 84 (11) ◽  
pp. 1185-1189 ◽  
Author(s):  
Doreen Richardt ◽  
Andreas Dendorfer ◽  
Ralph Tölg ◽  
Peter Dominiak ◽  
Gert Richardt
Keyword(s):  
Myocardial Infarction ◽  
Myocardial Ischemia ◽  
Infarct Size ◽  
Coronary Occlusion ◽  
Tricyclic Antidepressant ◽  
In Vivo Model ◽  
Norepinephrine Release ◽  
Area At Risk ◽  
Transport Direction

During myocardial ischemia, a substantial accumulation of norepinephrine occurs in the ischemic zone due to a local nonexocytotic release of norepinephrine. Norepinephrine release is driven by the neuronal monoamine transporter (NET), which reverses its usual transmembrane transport direction. We investigated whether this local accumulation of norepinephrine contributes to irreversible myocardial injury in an in vivo model of myocardial infarction. Male, anaesthetized Wistar rats were subjected to 30 min coronary occlusion and subsequent 120 min reperfusion. Five minutes prior to coronary occlusion, the NET inhibitor desipramine was administered intravenously. Infarct size (IS) was determined by TTC-staining and was related to the area at risk (AAR). The influence of desipramine on cardiac norepinephrine release was investigated in isolated perfused hearts with 30 min of regional ischemia. Norepinephrine was measured in the effluent from the hearts by HPLC and electrochemical detection. Desipramine (0.1–0.8 mg/kg) dose-dependently reduced infarct size (IS/AAR) from 0.54 to 0.21 and suppressed postischemic norepinephrine release from 245 to 108 pg/mL. In summary, the data indicate that nonexocytotic release of norepinephrine in myocardial ischemia exaggerates acute ischemic damage, because suppression of ischemia-induced release of norepinephrine by the tricyclic antidepressant desipramine effectively reduces infarct size in an in vivo model of myocardial ischemia.

scholarly journals Is postconditioning effective in prevention against long-lasting myocardial ischemia in the rabbit?

2009 ◽  
pp. 635-643
Author(s):  
R Létienne ◽  
Y Calmettes ◽  
B Le Grand
Keyword(s):  
Myocardial Infarction ◽  
At Risk ◽  
Myocardial Ischemia ◽  
Infarct Size ◽  
Plasma Levels ◽  
Coronary Occlusion ◽  
Troponin I ◽  
The Other ◽  
Area At Risk ◽  
Triphenyltetrazolium Chloride

The goal of the study was to determine whether postconditioning protects against different ischemia durations in the rabbit. Rabbits were assigned to a 20-, 25-, 45- or 60-min coronary occlusion followed by 24-h of reperfusion. Rabbits received no further intervention (control) or were postconditioned with four cycles of 30-s occlusion and 30-s reperfusion after myocardial infarction. Plasma levels of troponin I were quantified throughout reperfusion. In control conditions, infarct sizes (% area at risk using triphenyltetrazolium chloride) after 20, 25, 45 and 60 min of coronary occlusions were 23±3, 51±4, 70±3 and 81±3 %, respectively. With 20 and 25 min occlusion, postconditioning reduced infarct size by 43±10 and 73±21 %, respectively. On the other hand, with 45 or 60 min occlusion, postconditioning had no significant effects on infarct size (61±3 and 80±2 % of area at risk). Preconditioning protocol was performed with 25- and 60-min coronary occlusion. As expected, preconditioning significantly reduced infarct size. In conclusion, in the rabbit, the cardioprotection afforded by postconditioning is limited to less than 45 min coronary occlusion.

Morphine Enhances Pharmacological Preconditioning by Isoflurane

2003 ◽  
Vol 98 (3) ◽  
pp. 705-711 ◽  
Author(s):  
Lynda M. Ludwig ◽  
Hemal H. Patel ◽  
Garrett J. Gross ◽  
Judy R. Kersten ◽  
Paul S. Pagel ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Potassium Channels ◽  
Infarct Size ◽  
Adenosine Triphosphate ◽  
Opioid Receptors ◽  
Myocardial Infarct ◽  
Coronary Artery Occlusion ◽  
Myocardial Infarct Size ◽  
Area At Risk

Background Adenosine triphosphate-regulated potassium channels mediate protection against myocardial infarction produced by volatile anesthetics and opioids. We tested the hypothesis that morphine enhances the protective effect of isoflurane by activating mitochondrial adenosine triphosphate-regulated potassium channels and opioid receptors. Methods Barbiturate-anesthetized rats (n = 131) were instrumented for measurement of hemodynamics and subjected to a 30 min coronary artery occlusion followed by 2 h of reperfusion. Myocardial infarct size was determined using triphenyltetrazolium staining. Rats were randomly assigned to receive 0.9% saline, isoflurane (0.5 and 1.0 minimum alveolar concentration [MAC]), morphine (0.1 and 0.3 mg/kg), or morphine (0.3 mg/kg) plus isoflurane (1.0 MAC). Isoflurane was administered for 30 min and discontinued 15 min before coronary occlusion. In eight additional groups of experiments, rats received 5-hydroxydecanoic acid (5-HD; 10 mg/kg) or naloxone (6 mg/kg) in the presence or absence of isoflurane, morphine, and morphine plus isoflurane. Results Isoflurane (1.0 MAC) and morphine (0.3 mg/kg) reduced infarct size (41 +/- 3%; n = 13 and 38 +/- 2% of the area at risk; n = 10, respectively) as compared to control experiments (59 +/- 2%; n = 10). Morphine plus isoflurane further decreased infarct size to 26 +/- 3% (n = 11). 5-HD and naloxone alone did not affect infarct size, but abolished cardioprotection produced by isoflurane, morphine, and morphine plus isoflurane. Conclusions Combined administration of isoflurane and morphine enhances the protection against myocardial infarction to a greater extent than either drug alone. This beneficial effect is mediated by mitochondrial adenosine triphosphate-regulated potassium channels and opioid receptors in vivo.

Long-term infusion of Met5-enkephalin fails to protect murine hearts against ischemia-reperfusion injury

2005 ◽  
Vol 288 (4) ◽  
pp. H1717-H1723 ◽  
Author(s):  
Koh Kuzume ◽  
Kazuyo Kuzume ◽  
Zhiping Cao ◽  
Lijuan Liu ◽  
Donna M. Van Winkle
Keyword(s):  
Myocardial Ischemia ◽  
Infarct Size ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Opioid Peptide ◽  
Area At Risk ◽  
Regional Myocardial Ischemia ◽  
Chronic Infusion ◽  
Myocardial Ischemia Reperfusion

Recently, we reported that exogenous administration of Met5-enkephalin (ME) for 24 h reduces infarct size after ischemia-reperfusion in rabbits. In the present study, we tested whether ME-induced cardioprotection is exhibited in murine hearts and whether chronic infusion of this peptide can render hearts tolerant to ischemia. Barbiturate-anesthetized open-chest mice (C57BL/6J) were subjected to regional myocardial ischemia-reperfusion (45 min of occlusion and 20 min of reperfusion). Mice received saline vehicle or ME for 24 h or 2 wk before undergoing regional myocardial ischemia-reperfusion or for 24 h followed by a 24-h delay before regional myocardial ischemia-reperfusion. Infarct size was measured with propidium iodide and is expressed as a percentage of the area at risk. Infarcts were smaller after infusion of ME for 24 h than with vehicle control: 49.2 ± 9.0% vs. 22.2 ± 3.2% ( P < 0.01). In contrast, administration of ME for 2 wk failed to elicit cardioprotection: 36.5 ± 9.1% and 41.4 ± 8.2% for control and ME, respectively ( P = not significant). When a 24-h delay was imposed between the end of drug treatment and the onset of the ischemic insult, cardioprotection was lost: 38.5 ± 6.1% and 42.8 ± 6.6% for control and ME, respectively ( P = not significant). Chronic sustained exogenous infusion of the endogenously produced opioid peptide ME is associated with loss of the cardioprotection that is observed with 24 h of infusion. Furthermore, in this in vivo murine model, ME failed to induce delayed tolerance to myocardial ischemia-reperfusion.

Coronary endothelial P-selectin in pathogenesis of myocardial ischemia-reperfusion injury

1998 ◽  
Vol 275 (5) ◽  
pp. H1865-H1872 ◽  
Author(s):  
Anthony J. Palazzo ◽  
Steven P. Jones ◽  
Donald C. Anderson ◽  
D. Neil Granger ◽  
David J. Lefer
Keyword(s):  
Myocardial Ischemia ◽  
Infarct Size ◽  
Ischemia Reperfusion Injury ◽  
Myocardial Infarct ◽  
Ischemia Reperfusion ◽  
Myocardial Infarct Size ◽  
Wild Type ◽  
Area At Risk ◽  
Myocardial Ischemia Reperfusion

We investigated in vivo coronary P-selectin expression and its pathophysiological consequences in a murine model of myocardial ischemia-reperfusion (MI/R) using wild-type and P-selectin deficient (−/−) mice. Coronary P-selectin expression [μg monoclonal antibody (MAb)/g tissue] was measured using a radiolabeled MAb method after 30 min of myocardial ischemia and 20 min of reperfusion. P-selectin expression in wild-type mice was significantly ( P< 0.01) elevated in the ischemic zone (0.070 ± 0.010) compared with the nonischemic zone (0.037 ± 0.008). Myocardial P-selectin expression was nearly undetectable in P-selectin −/− mice after MI/R. Furthermore, myocardial infarct size (% of area at risk) after 30 min of myocardial ischemia and 120 min of reperfusion was 42.5 ± 4.4 in wild-type mice and 24.4 ± 4.0 in P-selectin −/− mice ( P < 0.05). In additional experiments of prolonged myocardial ischemia (60 min) and reperfusion (120 min), myocardial infarct size was similar in P-selectin −/− mice and wild-type mice. Our results clearly demonstrate the involvement of coronary P-selectin in the development of myocardial infarction after MI/R.

Anesthetic-induced Preconditioning 

1997 ◽  
Vol 87 (5) ◽  
pp. 1182-1190 ◽  
Author(s):  
Brian A. Cason ◽  
A. Kurt Gamperl ◽  
Robert E. Slocum ◽  
Robert F. Hickey
Keyword(s):  
At Risk ◽  
Myocardial Ischemia ◽  
Infarct Size ◽  
Ischemic Preconditioning ◽  
Coronary Occlusion ◽  
Myocardial Infarct ◽  
Group Analysis ◽  
Myocardial Infarct Size ◽  
Area At Risk ◽  
Myocardial Preconditioning

Background Experimental evidence suggests that ATP-sensitive potassium channels are involved in myocardial ischemic preconditioning. Because some pharmacologic effects of isoflurane are mediated by K(ATP) channels, the authors tested the hypothesis: Isoflurane administration, before myocardial ischemia, can induce or mimic myocardial preconditioning. Methods Myocardial infarct size was measured in three groups of propofol-anesthetized rabbits, each subjected to 30 min of anterolateral coronary occlusion followed by 3 h of reperfusion. Groups differed in their pretreatment: Group 1 (control, N = 13) no pretreatment, Group 2 (ischemic preconditioning, N = 8), 5 min of coronary occlusion and 15 min of reperfusion; Group 3 (isoflurane pretreatment; N = 15), 15 min of isoflurane (1.1% end-tidal) and 15 min of washout. Hemodynamics were monitored serially. Myocardial infarct size and the area at risk were defined using triphenyltetrazolium chloride staining and fluorescent microspheres, respectively, and both were measured using computerized planimetry. Results Infarct size expressed as a percentage of area at risk was 23.4 +/- 8.5% (mean +/- SD) in the isoflurane group compared with 33.1 +/- 13.3% in controls, and 8.7 +/- 6.2% in the ischemia-preconditioned group. Analysis for coincidental regressions, followed by tests for equality of slope and elevation, showed that the linear relationship between infarct size and area at risk was significantly (P &lt; 0.05) different in all three groups because of differences in line elevation. Minor differences in hemodynamic variables were found between groups, which were unlikely to account for the significant differences in infarct size. Conclusion Preadministration of isoflurane, before myocardial ischemia, reduces myocardial infarct size, and mimics myocardial preconditioning.

Inhibition of Factor XIIa-Mediated Factor XI Activation Reduces Infarct Size in a Mouse Model of Myocardial Ischemia and Reperfusion

Blood ◽  
2014 ◽  
Vol 124 (21) ◽  
pp. 2873-2873
Author(s):  
Christina U Lorentz ◽  
Norah G Verbout ◽  
Zhiping Cao ◽  
Helen Liu ◽  
Owen J.T. McCarty ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
At Risk ◽  
Myocardial Ischemia ◽  
Infarct Size ◽  
Board Of Directors ◽  
Area At Risk ◽  
Employment Equity ◽  
Advisory Committees ◽  
Factor Xiia ◽  
Equity Ownership

Abstract The role of the intrinsic coagulation pathway in acute myocardial infarction is poorly defined. Both coagulation factors XII (FXII) and XI (FXI) support experimental thrombus propagation in animals. Additionally, humans with FXI deficiency have a lower incidence of thrombosis and stroke, however no such association has been established for FXII. Curiously, the incidence of previously verified myocardial infarction (MI) among 96 surviving FXI deficient subjects that were interviewed in an epidemiologic study was found to be similar to or possibly even higher than the recorded incidence of MI in an age/sex matched dataset from morbidity/mortality statistics of the general Israeli population (Salomon et al. J Thromb Haemost. 2003;1:658). However, the outcome of these coronary events were not reported, except for the fact that all interviewed FXI subjects were alive at the time of the interview. To investigate the contribution of FXI activation by FXIIa in experimental MI, we used a standard mouse model of acute myocardial ischemia (AMI). To inhibit FXI in the mouse, we utilized our monoclonal antibody (14E11) that targets the Apple 2 domain of FXI, and has been shown in vitro to inhibit the activation of FXI by factor XIIa, while not significantly inhibiting activation of FXI by thrombin. To evaluate the efficacy of 14E11 in reducing ischemic injury in mice, the left coronary artery (LCA) of wildtype male mice was reversibly ligated for 40 min, and 14E11 (1 mg/kg; iv) or vehicle was infused during the last 15 min of occlusion. Occlusion was confirmed by sustained S-T elevation, regional cyanosis and wall motion abnormalities. Following occlusion, the ligature was removed and the heart reperfused for 2 hr. To delineate the area of risk and ischemia, the LCA was re-occluded at 2 hr post-reperfusion and fluorescent polymers infused into the apex of the heart. The heart was excised, cut into 1 mm thick transverse slices and photographed under UV light to identify the area at risk. Tissue sections were additionally stained with 2,3,5-triphenyltetrazolium chloride solution and infarcted areas evaluated via morphometric analysis. The area at risk was evaluated as the percent of total heart volume and infarct size was calculated as the percentage of area at risk. Our results indicated that the area of risk did not differ between treatment groups, however treatment with 14E11 reduced infarct volume by 33% (p<0.05, n=10) compared with vehicle control (n=10). These results suggest that FXII-mediated activation of FXI contributes to the pathology of experimental MI in mice. Since FXII has no hemostatic function, we conclude that the data warrant further evaluation of whether systemic anticoagulation by selective inhibition of FXII-mediated FXI activation before interventional reperfusion is safe and reduces infarct size in patients with acute coronary syndrome. Figure 1 Figure 1. Disclosures Lorentz: Aronora, Inc: Employment. Verbout:Aronora, Inc: Employment. Tucker:Aronora, Inc: Employment, Equity Ownership, Membership on an entity's Board of Directors or advisory committees. Gruber:Aronora, Inc: Employment, Equity Ownership, Membership on an entity's Board of Directors or advisory committees.

scholarly journals Isoflurane Protects against Myocardial Infarction during Early Reperfusion by Activation of Phosphatidylinositol-3-Kinase Signal Transduction: Evidence for Anesthetic-induced Postconditioning in Rabbits

2005 ◽  
Vol 102 (1) ◽  
pp. 102-109 ◽  
Author(s):  
Pascal C. Chiari ◽  
Martin W. Bienengraeber ◽  
Paul S. Pagel ◽  
John G. Krolikowski ◽  
Judy R. Kersten ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Infarct Size ◽  
Coronary Occlusion ◽  
Minimum Alveolar Concentration ◽  
Left Ventricular ◽  
Saline Control ◽  
Phosphatidylinositol 3 Kinase ◽  
Area At Risk ◽  
Early Reperfusion ◽  
Phosphatidylinositol 3

Background Brief episodes of ischemia during early reperfusion after coronary occlusion reduce the extent of myocardial infarction. Phosphatidylinositol-3-kinase (PI3K) signaling has been implicated in this "postconditioning" phenomenon. The authors tested the hypothesis that isoflurane produces cardioprotection during early reperfusion after myocardial ischemia by a PI3K-dependent mechanism. Methods Pentobarbital-anesthetized rabbits (n = 80) subjected to a 30-min coronary occlusion followed by 3 h reperfusion were assigned to receive saline (control), three cycles of postconditioning ischemia (10 or 20 s each), isoflurane (0.5 or 1.0 minimum alveolar concentration), or the PI3K inhibitor wortmannin (0.6 mg/kg, intravenously) or its vehicle dimethyl sulfoxide. Additional groups of rabbits were exposed to combined postconditioning ischemia (10 s) and 0.5 minimum alveolar concentration isoflurane in the presence and absence of wortmannin. Phosphorylation of Akt, a downstream target of PI3K, was assessed by Western blotting. Results Postconditioning ischemia for 20 s, but not 10 s, reduced infarct size (P &lt; 0.05) (triphenyltetrazolium staining; 20 +/- 3% and 34 +/- 3% of the left ventricular area at risk, respectively) as compared with control (41 +/- 2%). Exposure to 1.0, but not 0.5, minimum alveolar concentration isoflurane decreased infarct size (21 +/- 2% and 43 +/- 3%, respectively). Wortmannin abolished the protective effects of postconditioning (20 s) and 1.0 minimum alveolar concentration isoflurane. Combined postconditioning (10 s) and 0.5 minimum alveolar concentration isoflurane markedly reduced infarct size (17 +/- 5%). This action was also abolished by wortmannin (44 +/- 2%). Isoflurane (1.0 minimum alveolar concentration) increased Akt phosphorylation after ischemia (32 +/- 6%), and this action was blocked by wortmannin. Conclusions Isoflurane acts during early reperfusion after prolonged ischemia to salvage myocardium from infarction and reduces the threshold of ischemic postconditioning by activating PI3K.

Critical role of angiopoietins/Tie-2 in hyperglycemic exacerbation of myocardial infarction and impaired angiogenesis

2008 ◽  
Vol 294 (6) ◽  
pp. H2547-H2557 ◽  
Author(s):  
Qin-hui Tuo ◽  
Heng Zeng ◽  
Amanda Stinnett ◽  
Heidi Yu ◽  
Judy L. Aschner ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Myocardial Ischemia ◽  
Infarct Size ◽  
Myocardial Infarct ◽  
Critical Role ◽  
Myocardial Infarct Size ◽  
Vascular Integrity ◽  
Impaired Angiogenesis

Angiopoietin-1 (Ang-1) and angiopoietin-2 (Ang-2) are the two ligands of the Tie-2 receptor, a receptor tyrosine kinase that is expressed on the endothelium. A balanced angiopoietin/Tie-2 system is critical for the maintenance of vascular integrity. We investigated the potential role of a disrupted angiopoietin/Tie-2 system on hyperglycemic exacerbation of myocardial infarction and impaired angiogenesis. Using streptozotocin (STZ) mice subjected to myocardial ischemia, we examined the effects of shifting the Ang-2-to-Ang-1 ratio on myocardial infarction size, apoptosis, bone marrow (BM) cell-endothelial progenitor cell (EPC) differentiation, and angiogenesis. In control mice, myocardial ischemia increased expression of both Ang-2 and Tie-2. In STZ mice, Ang-2 expression was elevated, whereas Tie-2 expression was reduced, and neither was significantly altered by ischemia. Myocardial infarct size and apoptosis were increased in STZ compared with control mice. Using in vivo administration of an adenovirus containing Ang-1 or Ang-2, we found that shifting the Ang-2-to-Ang-1 ratio to favor Ang-1 reduced myocardial apoptosis and infarct size in STZ mice, while shifting the Ang-2-to-Ang-1 ratio to favor Ang-2 resulted in a significant increase in myocardial infarct size and apoptosis in control mice. Myocardial ischemia-stimulated BM cell-EPC differentiation was inhibited and myocardial angiogenesis was reduced in STZ mice. Systemic administration of Ad-Ang-1 restored BM cell-EPC differentiation and increased myocardial VEGF expression and angiogenesis in STZ mice. Our data demonstrate that disturbed angiopoietin/Tie-2 signaling contributes to the hyperglycemic exacerbation of myocardial infarction and impaired angiogenesis. Restoration of the Ang-2-to-Ang-1 ratio may be a novel therapeutic strategy for the treatment of diabetic myocardial ischemic diseases.

Medroxyprogesterone acetate prevents the cardioprotective and anti-inflammatory effects of 17β-estradiol in an in vivo model of myocardial ischemia and reperfusion

2007 ◽  
Vol 293 (3) ◽  
pp. H1408-H1415 ◽  
Author(s):  
Erin A. Booth ◽  
Benedict R. Lucchesi
Keyword(s):  
Myocardial Ischemia ◽  
Infarct Size ◽  
Medroxyprogesterone Acetate ◽  
Troponin I ◽  
Hormone Replacement ◽  
In Vivo Model ◽  
Ischemia And Reperfusion ◽  
Area At Risk ◽  
Myocardial Ischemia And Reperfusion ◽  
17Β Estradiol

Previous studies demonstrated the protective effects of estrogen administration in models of cardiovascular disease. However, there is a discrepancy between these data and those from the recent clinical trials with hormone replacement therapy in menopausal women. One possible explanation for the divergent results is the addition of progestin to the hormone regimen in the Women's Health Initiative and the Heart and Estrogen/Progestin Replacement Study trials. The aim of the present study was to examine the effects of a combination of 17β-estradiol (E2, 20 μg) and medroxyprogesterone acetate (MPA, 80 μg) on infarct size in New Zealand White rabbits. Infarct size as a percentage of the area at risk was significantly reduced by administration of E2 30 min before induction of myocardial ischemia compared with vehicle (19.5 ± 3.1 vs. 55.7 ± 2.6%, P < 0.001). However, E2 + MPA failed to elicit a reduction in infarct size (52.5 ± 4.6%), and MPA had no effect (50.8 ± 2.6%). E2 also reduced serum levels of cardiac troponin I, immune complex deposition in myocardial tissue, activation of the complement system, and lipid peroxidation. All these effects were reversed by MPA. The results suggest that MPA antagonizes the infarct-sparing effects of E2, possibly through modulation of the immune response after ischemia and reperfusion.

scholarly journals Platelet-Activating Factor Acetylhydrolase Prevents Myocardial Ischemia-Reperfusion Injury

Circulation ◽  
1999 ◽  
Vol 100 (suppl_2) ◽  
Author(s):  
Elizabeth N. Morgan ◽  
Edward M. Boyle ◽  
Wang Yun ◽  
John C. Kovacich ◽  
Timothy G. Canty ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Ischemia Reperfusion Injury ◽  
Tissue Injury ◽  
Ischemia Reperfusion ◽  
Platelet Activating Factor ◽  
Neutrophil Infiltration ◽  
In Vivo Model ◽  
Area At Risk ◽  
Myocardial Ischemia Reperfusion

Background —Platelet-activating factor (PAF) is one of the most potent biological mediators of tissue injury. PAF acetylhydrolase (PAF-AH) is a recently isolated naturally occurring enzyme that hydrolyzes PAF and renders it inactive. We hypothesize that inhibition of PAF with PAF-AH will reduce myocardial ischemia-reperfusion (I/R) injury in vivo. Methods and Results —The coronary ligation model was used in New Zealand white rabbits. The large branch of the marginal coronary artery was occluded for 45 minutes, followed by 2 hours of reperfusion. Fifteen minutes before reperfusion, animals were given either 2 mg/kg of vehicle or of PAF-AH. At the completion of 120 minutes of reperfusion, percentage of necrosis, degree of neutrophil infiltration, and measurements of regional contractility were assessed. Data are expressed as the mean±SEM and compared by Student’s t test or Mann-Whitney ANOVA. Both groups of animals showed an equivalent area at risk; however, 46.7±11% was necrotic in the animal treated with vehicle. In contrast, 20.9±7.0% was necrotic in the animals treated with PAF-AH ( P <0.05). Systolic shortening and wall thickness were significantly greater in those animals treated with PAF-AH at 15, 30, 60, and 120 minutes of reperfusion ( P <0.05). Quantification of neutrophil infiltration showed a 62% reduction in the PAF-AH treated animals compared with those treated with vehicle alone. Conclusions —PAF-AH is a potent cardioprotective agent in an in vivo model of I/R injury.

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