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Ann Thorac Surg 2000;70:2119-2124
© 2000 The Society of Thoracic Surgeons

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Original article: cardiovascular

Bradykinin protects the rabbit heart after cardioplegic ischemia via NO-dependent pathways

^a Division of Cardiothoracic Surgery, Daughtry Family Department of Surgery, University of Miami School of Medicine, Miami, Florida, USA

Accepted for publication May 7, 2000.

Address reprint requests to Dr Rosenkranz, Division of Cardiothoracic Surgery, Jackson Memorial Hospital, PO Box 016960 (R-114), Miami, FL 33101
e-mail: erosenkr{at}med.miami.edu

Presented at the Seventy-fourth Annual Meeting of the American Heart Association, Atlanta, GA, November 7–9, 1999.

Background. Depressed myocardial performance is an important clinical problem after open heart surgery. We hypothesized pretreating with bradykinin would pharmacologically precondition the heart and improve postischemic performance, and induce myocardial preconditioning by activating nitric oxide synthase.

Methods. Thirty-three rabbit hearts underwent retrograde perfusion with Krebs-Henseleit buffer (KHB) followed by 50 minutes of 37°C cardioplegic ischemia with St. Thomas’ cardioplegia solution (StTCP). Ten control hearts received no pretreatment. Ten bradykinin-pretreated hearts received a 10-minute infusion of 0.1 µMol/L bradykinin-enriched KHB and cardioplegic arrest with 0.1 µMol/L bradykinin-enriched StTCP. Six other hearts received 0.1 µMol/L HOE 140, a selective B2 receptor antagonist, added to both the 0.1 µMol/L bradykinin-enriched KHB and 0.1 µMol/L bradykinin-enriched StTCP solutions. Finally, six other hearts received 100 µMol/L of N--nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide synthase, added to both the 0.1 µMol/L bradykinin-enriched KHB and 0.1 µMol/L bradykinin-enriched StTCP solutions.

Results. Bradykinin pretreatment significantly improved postischemic performance and coronary flow (CF) compared with control (LVDP: 53 ± 5* vs 27 ± 4 mm Hg; +dP/dt_max: 1,025 ± 93* vs 507 ± 85 mm Hg/s; CF: 31 ± 3* vs 22 ± 2 mL/min; *p < 0.05). Both HOE 140 and L-NAME abolished bradykinin-induced protection, resulting in recovery equivalent to untreated controls.

Conclusions. Bradykinin pretreatment improves recovery of ventricular and coronary vascular function via nitric oxide-dependent mechanisms. Pharmacologic preconditioning by bradykinin pretreatment may be an important new strategy for improving myocardial protection during heart surgery.

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