HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Eliot R. Rosenkranz Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Feng, J. Articles by Rosenkranz, E. R. Search for Related Content PubMed PubMed Citation Articles by Feng, J. Articles by Rosenkranz, E. R.

Ann Thorac Surg 1999;68:1567-1572
© 1999 The Society of Thoracic Surgeons

---

Original Articles

Bradykinin pretreatment improves ischemia tolerance of the rabbit heart by tyrosine kinase mediated pathways

^a Division of Cardiothoracic Surgery, The Children’s Hospital of Buffalo, Buffalo, New York, USA
^b Department of Surgery, The State University of New York at Buffalo, Buffalo, New York, USA

Address reprint requests to Dr Rosenkranz, Division of Cardiothoracic Surgery, The Children’s Hospital of Buffalo, 219 Bryant St, Buffalo, NY 14222
e-mail: erosenkranz{at}chob.edu

Presented at the Thirty-fifth Annual Meeting of The Society of Thoracic Surgeons, San Antonio, TX, Jan 25–27, 1999.

Background. Depressed myocardial performance is an important clinical problem after open-heart surgery. We hypothesized that: (1) pretreating the heart with bradykinin improves postischemic performance, and (2) bradykinin activates protein tyrosine kinase (TK).

Methods. Twenty-seven adult rabbit hearts underwent retrograde perfusion with Krebs-Henseleit buffer (KHB) followed by 50 min 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 µM bradykinin-enriched KHB and cardioplegic arrest with 0.1 µM bradykinin-enriched StTCP. Seven others received 40 µM Genistein (Research Biochemicals, Natick, MA), a selective inhibitor of TK, added to both the 0.1-µM bradykinin-enriched KHB and 0.1-µM bradykinin-enriched StTCP solutions.

Results. Bradykinin pretreatment significantly improved postischemic myocardial performance and coronary flow (CF) compared with control (left ventricular developed pressure: 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). Inhibition of TK with Genistein prevented this improvement in myocardial function, resulting in recovery equivalent to untreated controls.

Conclusions. Bradykinin pretreatment may be an important new strategy for improving myocardial protection during heart surgery. The molecular mechanism of action may be similar to those activated by ischemic preconditioning.

This article has been cited by other articles:

				J. Feng, C. Bianchi, J. L. Sandmeyer, and F. W. Sellke Bradykinin Preconditioning Improves the Profile of Cell Survival Proteins and Limits Apoptosis After Cardioplegic Arrest Circulation, August 30, 2005; 112(9_suppl): I-190 - I-195. [Abstract] [Full Text] [PDF]

				J. Feng, C. Bianchi, J. Li, and F. W. Sellke Bradykinin Preconditioning Preserves Coronary Microvascular Reactivity During Cardioplegia-Reperfusion Ann. Thorac. Surg., March 1, 2005; 79(3): 911 - 916. [Abstract] [Full Text] [PDF]

				M. Wei, X. Wang, P. Kuukasjarvi, J. Laurikka, T. Rinne, E.-L. Honkonen, and M. Tarkka Bradykinin preconditioning in coronary artery bypass grafting Ann. Thorac. Surg., August 1, 2004; 78(2): 492 - 497. [Abstract] [Full Text] [PDF]

				J. Feng, H. Li, and E. R. Rosenkranz Bradykinin protects the rabbit heart after cardioplegic ischemia via NO-dependent pathways Ann. Thorac. Surg., December 1, 2000; 70(6): 2119 - 2124. [Abstract] [Full Text] [PDF]