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Ann Thorac Surg 2005;79:911-916
© 2005 The Society of Thoracic Surgeons
Division of Cardiothoracic Surgery, Department of Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts
Accepted for publication September 2, 2004.
* Address reprint requests to Dr Sellke, Division of Cardiothoracic Surgery, BIDMC, LMOB 2A, 110 Francis Street, Boston, MA 02215 (E-mail: fsellke{at}caregroup.harvard.edu).
BACKGROUND: Alterations of microvascular reactivity reduce myocardial perfusion after ischemic cardioplegia. We hypothesized that bradykinin preconditioning (BKPC) would preserve endothelium-dependent microvascular responses and improve myocardial function after cardioplegic ischemiareperfusion.
METHODS: Rabbit hearts were perfused with Krebs-Henseleit buffer (KHB). The hearts were arrested for 60 minutes with moderately cold (25°C) crystalloid cardioplegia (MCCP, n = 8) or with cold (0° to 4°C) crystalloid cardioplegia (CCCP) (n = 6). The BKPC hearts received a 10-minute coronary infusion of 108 M BK-enriched KHB, followed by a 5-minute recovery period, and then were arrested for 60 minutes with MCCP (BKPC + MCCP, n = 8) or with CCCP (BKPC + CCCP, n = 6). The hearts were reperfused for 30 minutes with KHB. Six control hearts were perfused with KHB for 90 minutes without cardioplegia-ischemia. Left ventricle performance was measured, and in vitro relaxation responses of precontracted coronary arterioles (internal diameter, 80 to 150 µm) were obtained in a pressurized no-flow state.
RESULTS: Ischemic arrest with MCCP or CCCP markedly reduced endothelium-dependent relaxation to adenosine 5'-diphosphate, substance P, and calcium ionophore (A23187
CONCLUSIONS: BKPC preserves endothelium-dependent microvascular responses and prevents the hypercontractility to U46619
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