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Volume 128, Issue 4 , Pages 602-608 , October 2004

Reduction of myocardial reperfusion injury by aprotinin after regional ischemia and cardioplegic arrest

Tanveer A. Khan, MD
- Department of Surgery, Division of Cardiothoracic Surgery, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Mass, USA
Cesario Bianchi, MD, PhD
- Department of Surgery, Division of Cardiothoracic Surgery, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Mass, USA
Pierre Voisine, MD
- Department of Surgery, Division of Cardiothoracic Surgery, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Mass, USA
Jun Feng, MD, PhD
- Department of Surgery, Division of Cardiothoracic Surgery, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Mass, USA
Jeralyn Baker, CCP
- Department of Surgery, Division of Cardiothoracic Surgery, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Mass, USA
Melanie Hart, PhD
- Department of Anesthesiology, Center for Experimental Therapeutics and Reperfusion Injury, Brigham and Women's Hospital and Harvard Medical School, Boston, Mass, USA
Minoru Takahashi, PhD
- Department of Anesthesiology, Center for Experimental Therapeutics and Reperfusion Injury, Brigham and Women's Hospital and Harvard Medical School, Boston, Mass, USA
Greg Stahl, PhD
- Department of Anesthesiology, Center for Experimental Therapeutics and Reperfusion Injury, Brigham and Women's Hospital and Harvard Medical School, Boston, Mass, USA
Frank W. Sellke, MD
- Department of Surgery, Division of Cardiothoracic Surgery, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Mass, USA
- Address for reprints: Frank W. Sellke, MD, Division of Cardiothoracic Surgery, Beth Israel Deaconess Medical Center, 110 Francis St, LMOB 2A, Boston, MA 02215, USA

Received 21 October 2003 ,Revised 9 February 2004 ,Accepted 17 March 2004.

Global and regional myocardial function. The LV +dP/dt was similar in both the control and treatment groups at baseline, during regional ischemia, and in the period of post-CPB reperfusion (top). Both

Global and regional myocardial function. The LV +dP/dt was similar in both the control and treatment groups at baseline, during regional ischemia, and in the period of post-CPB reperfusion (top). Both groups showed dyskinesis of the distal LAD territory, as seen by negative percentage segment shortening during regional ischemia and post-CPB reperfusion. Whereas the impairment in regional function was characterized by increasing dyskinesis in the control group, aprotinin treatment resulted in a trend of decreasing dyskinesis, with a significant difference at 90 minutes of post-CPB reperfusion (*P < .05 vs control). BL, Baseline; 15I, 15 minutes of ischemia; 30I, 30 minutes of ischemia; 30R, 30 minutes of reperfusion; 60R, 60 minutes of reperfusion; 90R, 90 minutes of reperfusion.
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Coronary blood flow. No significant differences were observed in coronary blood flow between groups. BL, Baseline; 15I, 15 minutes of ischemia; 30I, 30 minutes of ischemia; 30R, 30 minutes of reperfus

Coronary blood flow. No significant differences were observed in coronary blood flow between groups. BL, Baseline; 15I, 15 minutes of ischemia; 30I, 30 minutes of ischemia; 30R, 30 minutes of reperfusion; 60R, 60 minutes of reperfusion; 90R, 90 minutes of reperfusion.
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Representative image of LV infarct size. Triphenyl tetrazolium chloride staining was used to determine the LV infarct size (arrows), which was markedly decreased in the LV myocardium of aprotinin-trea

Representative image of LV infarct size. Triphenyl tetrazolium chloride staining was used to determine the LV infarct size (arrows), which was markedly decreased in the LV myocardium of aprotinin-treated animals (right) compared with controls (left).
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Quantification of LV infarct size. Infarct size was measured as a percentage of the LV ischemic area. The percent of the LV ischemic area that progressed to infarction was significantly reduced in the

Quantification of LV infarct size. Infarct size was measured as a percentage of the LV ischemic area. The percent of the LV ischemic area that progressed to infarction was significantly reduced in the aprotinin group compared with the LV myocardium from control animals (*P < .05).
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Myocardial nitrotyrosine staining. Aprotinin treatment decreased staining for nitrotyrosine, a measure of tissue peroxynitrite, as shown in the representative myocardial sections from the distal LAD t

Myocardial nitrotyrosine staining. Aprotinin treatment decreased staining for nitrotyrosine, a measure of tissue peroxynitrite, as shown in the representative myocardial sections from the distal LAD territory of aprotinin-treated (right) and control (left) animals.
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Tissue MPO activity. Tissue MPO activity was determined as a measure of neutrophil infiltration. Myocardium from the distal LAD territory had reduced MPO activity with aprotinin therapy compared with

Tissue MPO activity. Tissue MPO activity was determined as a measure of neutrophil infiltration. Myocardium from the distal LAD territory had reduced MPO activity with aprotinin therapy compared with controls (*P < .05).
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Coronary microvascular relaxation. Endothelium-dependent coronary microvessel relaxation responses were markedly increased with adenosine diphosphate (ADP) and also with substance P (SubP) with aproti

Coronary microvascular relaxation. Endothelium-dependent coronary microvessel relaxation responses were markedly increased with adenosine diphosphate (ADP) and also with substance P (SubP) with aprotinin treatment compared with controls. Aprotinin also increased coronary microvessel relaxation in response to the endothelium-independent vasodilator sodium nitroprusside (SNP); *P < .05 and **P < .01 vs control).
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