Abstract | OBJECTIVE: Brief reversible ischemic episodes (ischemic preconditioning, IPC) protect the heart against arrhythmias during a subsequent prolonged low-flow ischemia. We have recently shown that this protection involves release of bradykinin, activation of bradykinin B2 receptors followed by opening of sarcolemmal, but not mitochondrial ATP-sensitive K+ channels. The goal of this study was to clarify a trigger and/or mediator role of bradykinin in the antiarrhythmic effects of IPC during low-flow ischemia. METHODS: Isolated perfused rat hearts underwent 60 minutes of low-flow ischemia induced by reducing perfusion pressure followed by 60 minutes of reperfusion. Preconditioning was induced by 2 x 5 minutes episodes of zero-flow ischemia. In yet other groups, preconditioned or non-preconditioned hearts were treated either with bradykinin (10 nmol/L) or with HOE 140 ( bradykinin B2 receptor antagonist, 100 nmol/L). RESULTS: CONCLUSION:
Bradykinin is a mediator, but unlikely a trigger, of antiarrhythmic effects of IPC during low-flow ischemia.
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Authors | Sergey V Driamov, Mohamed Bellahcene, Silvia Butz, Peter T Buser, Christian E Zaugg |
Journal | Journal of cardiovascular electrophysiology
(J Cardiovasc Electrophysiol)
Vol. 18
Issue 1
Pg. 93-9
(Jan 2007)
ISSN: 1540-8167 [Electronic] United States |
PMID | 17229306
(Publication Type: Journal Article)
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Chemical References |
- Bradykinin Receptor Antagonists
- icatibant
- Bradykinin
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Topics |
- Animals
- Bradykinin
(analogs & derivatives, drug effects, metabolism, pharmacology)
- Bradykinin Receptor Antagonists
- Disease Models, Animal
- Disease Progression
- Electrocardiography
- Heart Rate
(physiology)
- Heart Ventricles
(drug effects, metabolism, physiopathology)
- Ischemic Preconditioning, Myocardial
(methods)
- Male
- Pilot Projects
- Prognosis
- Rats
- Rats, Sprague-Dawley
- Tachycardia, Ventricular
(etiology, metabolism, prevention & control)
- Ventricular Fibrillation
(etiology, metabolism, prevention & control)
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