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Exenatide Reduces Infarct Size and Improves Cardiac Function in a Porcine Model of Ischemia and Reperfusion Injury. / Timmers, Leo; Henriques, José P. S.; de kleijn, Dominique P. V.; DeVries, J. Hans; Kemperman, Hans; Steendijk, Paul; Verlaan, Cees W. J.; Kerver, Marjolein; Piek, Jan J.; Doevendans, Pieter A.; Pasterkamp, Gerard; Hoefer, Imo E.

In: Journal of the American College of Cardiology, Vol. 53, No. 6, 2009, p. 501-510.

Research output: Contribution to journalArticleAcademicpeer-review

Harvard

Timmers, L, Henriques, JPS, de kleijn, DPV, DeVries, JH, Kemperman, H, Steendijk, P, Verlaan, CWJ, Kerver, M, Piek, JJ, Doevendans, PA, Pasterkamp, G & Hoefer, IE 2009, 'Exenatide Reduces Infarct Size and Improves Cardiac Function in a Porcine Model of Ischemia and Reperfusion Injury', Journal of the American College of Cardiology, vol. 53, no. 6, pp. 501-510. https://doi.org/10.1016/j.jacc.2008.10.033

APA

Timmers, L., Henriques, J. P. S., de kleijn, D. P. V., DeVries, J. H., Kemperman, H., Steendijk, P., Verlaan, C. W. J., Kerver, M., Piek, J. J., Doevendans, P. A., Pasterkamp, G., & Hoefer, I. E. (2009). Exenatide Reduces Infarct Size and Improves Cardiac Function in a Porcine Model of Ischemia and Reperfusion Injury. Journal of the American College of Cardiology, 53(6), 501-510. https://doi.org/10.1016/j.jacc.2008.10.033

Vancouver

Timmers L, Henriques JPS, de kleijn DPV, DeVries JH, Kemperman H, Steendijk P et al. Exenatide Reduces Infarct Size and Improves Cardiac Function in a Porcine Model of Ischemia and Reperfusion Injury. Journal of the American College of Cardiology. 2009;53(6):501-510. https://doi.org/10.1016/j.jacc.2008.10.033

Author

Timmers, Leo ; Henriques, José P. S. ; de kleijn, Dominique P. V. ; DeVries, J. Hans ; Kemperman, Hans ; Steendijk, Paul ; Verlaan, Cees W. J. ; Kerver, Marjolein ; Piek, Jan J. ; Doevendans, Pieter A. ; Pasterkamp, Gerard ; Hoefer, Imo E. / Exenatide Reduces Infarct Size and Improves Cardiac Function in a Porcine Model of Ischemia and Reperfusion Injury. In: Journal of the American College of Cardiology. 2009 ; Vol. 53, No. 6. pp. 501-510.

BibTeX

@article{b478ab394a4d4db9b032b367244a62fb,
title = "Exenatide Reduces Infarct Size and Improves Cardiac Function in a Porcine Model of Ischemia and Reperfusion Injury",
abstract = "Objectives This study sought to examine whether exenatide is capable of reducing myocardial infarct size. Background Exenatide is a glucagon-like peptide (GLP)-1 analogue with insulinotropic and insulinomimetic properties. Because insulin and GLP-1 have been described as reducing apoptosis, exenatide might confer cardioprotection after acute myocardial infarction (MI). Methods Pigs were randomized to exenatide or phosphate-buffered saline (PBS) treatment after 75 min of coronary artery ligation and subsequent reperfusion. Infarct size was assessed with Evans Blue (Sigma-Aldrich, St. Louis, Missouri) and triphenyltetrazolium chloride. Cardiac function was measured with epicardial ultrasound and conductance catheter-based pressure-volume loops. Western blotting, histology, and activity assays were performed to determine markers of apoptosis/survival and oxidative stress. Results Exenatide reduced myocardial infarct size (32.7 +/- 6.4% vs. 53.6 +/- 3.9%; p = 0.031) and prevented deterioration of systolic and diastolic cardiac function (systolic wall thickening: 47.3 +/- 6.3% vs. 8.1 +/- 1.9%, p <0.001; myocardial stiffness: 0.12 +/- 0.06 mm Hg/ml vs. 0.22 +/- 0.07 mm Hg/ml; p = 0.004). After exenatide treatment, myocardial phosphorylated Akt and Bcl-2 expression levels were higher compared with those after PBS treatment, and active caspase 3 expression was lower. In addition, fewer cells were terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling-positive. In addition, nuclear oxidative stress as assessed with an 8-hydroxydeoxyguanosine staining was reduced in the exenatide treatment arm, and superoxide dismutase activity and catalase activity were increased. Serum insulin levels increased after exenatide treatment, without affecting glucose levels. Conclusions These data identify exenatide as a potentially effective compound to reduce infarct size in adjunction to reperfusion therapy in patients with acute MI. (J Am Coll Cardiol 2009; 53: 501-10) (C) 2009 by the American College of Cardiology Foundation",
author = "Leo Timmers and Henriques, {Jos{\'e} P. S.} and {de kleijn}, {Dominique P. V.} and DeVries, {J. Hans} and Hans Kemperman and Paul Steendijk and Verlaan, {Cees W. J.} and Marjolein Kerver and Piek, {Jan J.} and Doevendans, {Pieter A.} and Gerard Pasterkamp and Hoefer, {Imo E.}",
year = "2009",
doi = "10.1016/j.jacc.2008.10.033",
language = "English",
volume = "53",
pages = "501--510",
journal = "Journal of the American College of Cardiology",
issn = "0735-1097",
publisher = "Elsevier USA",
number = "6",

}

RIS

TY - JOUR

T1 - Exenatide Reduces Infarct Size and Improves Cardiac Function in a Porcine Model of Ischemia and Reperfusion Injury

AU - Timmers, Leo

AU - Henriques, José P. S.

AU - de kleijn, Dominique P. V.

AU - DeVries, J. Hans

AU - Kemperman, Hans

AU - Steendijk, Paul

AU - Verlaan, Cees W. J.

AU - Kerver, Marjolein

AU - Piek, Jan J.

AU - Doevendans, Pieter A.

AU - Pasterkamp, Gerard

AU - Hoefer, Imo E.

PY - 2009

Y1 - 2009

N2 - Objectives This study sought to examine whether exenatide is capable of reducing myocardial infarct size. Background Exenatide is a glucagon-like peptide (GLP)-1 analogue with insulinotropic and insulinomimetic properties. Because insulin and GLP-1 have been described as reducing apoptosis, exenatide might confer cardioprotection after acute myocardial infarction (MI). Methods Pigs were randomized to exenatide or phosphate-buffered saline (PBS) treatment after 75 min of coronary artery ligation and subsequent reperfusion. Infarct size was assessed with Evans Blue (Sigma-Aldrich, St. Louis, Missouri) and triphenyltetrazolium chloride. Cardiac function was measured with epicardial ultrasound and conductance catheter-based pressure-volume loops. Western blotting, histology, and activity assays were performed to determine markers of apoptosis/survival and oxidative stress. Results Exenatide reduced myocardial infarct size (32.7 +/- 6.4% vs. 53.6 +/- 3.9%; p = 0.031) and prevented deterioration of systolic and diastolic cardiac function (systolic wall thickening: 47.3 +/- 6.3% vs. 8.1 +/- 1.9%, p <0.001; myocardial stiffness: 0.12 +/- 0.06 mm Hg/ml vs. 0.22 +/- 0.07 mm Hg/ml; p = 0.004). After exenatide treatment, myocardial phosphorylated Akt and Bcl-2 expression levels were higher compared with those after PBS treatment, and active caspase 3 expression was lower. In addition, fewer cells were terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling-positive. In addition, nuclear oxidative stress as assessed with an 8-hydroxydeoxyguanosine staining was reduced in the exenatide treatment arm, and superoxide dismutase activity and catalase activity were increased. Serum insulin levels increased after exenatide treatment, without affecting glucose levels. Conclusions These data identify exenatide as a potentially effective compound to reduce infarct size in adjunction to reperfusion therapy in patients with acute MI. (J Am Coll Cardiol 2009; 53: 501-10) (C) 2009 by the American College of Cardiology Foundation

AB - Objectives This study sought to examine whether exenatide is capable of reducing myocardial infarct size. Background Exenatide is a glucagon-like peptide (GLP)-1 analogue with insulinotropic and insulinomimetic properties. Because insulin and GLP-1 have been described as reducing apoptosis, exenatide might confer cardioprotection after acute myocardial infarction (MI). Methods Pigs were randomized to exenatide or phosphate-buffered saline (PBS) treatment after 75 min of coronary artery ligation and subsequent reperfusion. Infarct size was assessed with Evans Blue (Sigma-Aldrich, St. Louis, Missouri) and triphenyltetrazolium chloride. Cardiac function was measured with epicardial ultrasound and conductance catheter-based pressure-volume loops. Western blotting, histology, and activity assays were performed to determine markers of apoptosis/survival and oxidative stress. Results Exenatide reduced myocardial infarct size (32.7 +/- 6.4% vs. 53.6 +/- 3.9%; p = 0.031) and prevented deterioration of systolic and diastolic cardiac function (systolic wall thickening: 47.3 +/- 6.3% vs. 8.1 +/- 1.9%, p <0.001; myocardial stiffness: 0.12 +/- 0.06 mm Hg/ml vs. 0.22 +/- 0.07 mm Hg/ml; p = 0.004). After exenatide treatment, myocardial phosphorylated Akt and Bcl-2 expression levels were higher compared with those after PBS treatment, and active caspase 3 expression was lower. In addition, fewer cells were terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling-positive. In addition, nuclear oxidative stress as assessed with an 8-hydroxydeoxyguanosine staining was reduced in the exenatide treatment arm, and superoxide dismutase activity and catalase activity were increased. Serum insulin levels increased after exenatide treatment, without affecting glucose levels. Conclusions These data identify exenatide as a potentially effective compound to reduce infarct size in adjunction to reperfusion therapy in patients with acute MI. (J Am Coll Cardiol 2009; 53: 501-10) (C) 2009 by the American College of Cardiology Foundation

U2 - 10.1016/j.jacc.2008.10.033

DO - 10.1016/j.jacc.2008.10.033

M3 - Article

C2 - 19195607

VL - 53

SP - 501

EP - 510

JO - Journal of the American College of Cardiology

JF - Journal of the American College of Cardiology

SN - 0735-1097

IS - 6

ER -

ID: 882976