Cardioprotective effects of the serine protease inhibitor aprotinin after regional ischemia and reperfusion on the beating heart Diethard Pruefer, MDa*,

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Presentation transcript:

Cardioprotective effects of the serine protease inhibitor aprotinin after regional ischemia and reperfusion on the beating heart Diethard Pruefer, MDa*, Ute Buerke, MDb*, Markus Khalil, MDb, Manfred Dahm, MDa, Harald Darius, MDb, Hellmut Oelert, MDa, Michael Buerke, MDb The Journal of Thoracic and Cardiovascular Surgery Volume 124, Issue 5, Pages 942-949 (November 2002) DOI: 10.1067/mtc.2002.123703 Copyright © 2002 American Association for Thoracic Surgery Terms and Conditions

Fig. 1 Effect of single administration of aprotinin on myocardial injury after reperfusion of ischemic myocardium. CK activity is calculated as the difference between IVS and LVFW expressed in international units per 100 mg. All values are means ± SEM. The Journal of Thoracic and Cardiovascular Surgery 2002 124, 942-949DOI: (10.1067/mtc.2002.123703) Copyright © 2002 American Association for Thoracic Surgery Terms and Conditions

Fig. 2 Effect of single administration of aprotinin on neutrophil accumulation after reperfusion of ischemic myocardium. Cardiac MPO as a marker for leukocyte infiltration is expressed as the difference between LVFW and IVS activity. All values are means ± SEM. The Journal of Thoracic and Cardiovascular Surgery 2002 124, 942-949DOI: (10.1067/mtc.2002.123703) Copyright © 2002 American Association for Thoracic Surgery Terms and Conditions

Fig. 3 Photomicrographs of ischemic-reperfused (20 minutes of ischemia and 24 hours of reperfusion) myocardium of rats treated either with vehicle (A) or 20,000 U/kg aprotinin (B). A, Ischemic-reperfused myocardial tissue exhibits numerous leukocytes sequestered inside the coronary vasculature and transmigrated PMNs into the myocardium. Cardiac myocytes are severely injured (ie, necrotic). B, Ischemic-reperfused myocardial tissue after aprotinin treatment exhibits significant reduced PMN adhesion and PMN transmigration. In addition, there were almost no visible signs of cardiac injury. (Original magnification 100×.) C, Photomicrograph of rat heart tissue after 20 minutes of ischemia and 24 hours of reperfusion incubated with terminal deoxynucleotidyltransferase to add residues of digoxigenin nucleotide catalytically to the 3′-OH end of DNA and labeled with peroxidase substrate solution. (Original magnification 400×.) Brown reaction product is clearly present in nuclei of apoptotic myocytes in vehicle-treated rats. D, Ischemic-reperfused myocardial tissue of rats treated with aprotinin demonstrated remarkably diminished immunostaining, indicating reduced occurrence of myocardial apoptosis after aprotinin treatment. (Original magnification 400×.) The Journal of Thoracic and Cardiovascular Surgery 2002 124, 942-949DOI: (10.1067/mtc.2002.123703) Copyright © 2002 American Association for Thoracic Surgery Terms and Conditions

Fig. 4 Percentage of apoptotic cardiac myocytes in sham-operated MI rats, MI/R rats treated with vehicle (n = 5), and MI/R rats treated with 20,000 U/kg aprotinin (n = 5). Apoptosis was determined with the TUNEL reaction. Values are means ± SEM. The Journal of Thoracic and Cardiovascular Surgery 2002 124, 942-949DOI: (10.1067/mtc.2002.123703) Copyright © 2002 American Association for Thoracic Surgery Terms and Conditions