Journal Article

Myocardial protection with intermittent cross-clamp fibrillation: does preconditioning play a role?

Masahiro Fujii and David J Chambers

in European Journal of Cardio-Thoracic Surgery

Published on behalf of European Association for Cardio-Thoracic Surgery

Volume 28, issue 6, pages 821-831
Published in print December 2005 | ISSN: 1010-7940
Published online December 2005 | e-ISSN: 1873-734X | DOI: https://dx.doi.org/10.1016/j.ejcts.2005.06.048
Myocardial protection with intermittent cross-clamp fibrillation: does preconditioning play a role?

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  • Clinical Pharmacology and Therapeutics
  • Cardiovascular Medicine

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Objective: Previously, we showed intermittent cross-clamp fibrillation afforded equivalent protection to cardioplegia. This study examined whether protection induced by intermittent cross-clamp fibrillation involves an ischemic preconditioning mechanism. Methods: Isolated Langendorff-perfused rat hearts were subjected to three different studies to determine: Study 1, whether a single intermittent cross-clamp fibrillation episode (10 min) and reperfusion (10 min) before prolonged ischemia acts as a preconditioning trigger for protection; Study 2, whether cardioprotection induced by intermittent cross-clamp fibrillation alone (no prolonged ischemia) involves a preconditioning mechanism; Study 3, whether intermittent cross-clamp fibrillation cardioprotection can be prevented by targeting putative components of the preconditioning mechanism (protein kinase C or the mitochondrial ATP-sensitive potassium (KATP) channel). Hearts were reperfused (60 min) and recovery of function (left ventricular developed pressure measured using an intraventricular balloon) and myocardial injury (creatine kinase leakage) were measured. Results: In Study 1, recovery of function in the single intermittent cross-clamp fibrillation hearts was 61 ± 3% (mean ± SEM) (p < 0.05) compared to 41 ± 2% in control group; glibenclamide (a non-specific ATP-sensitive potassium (KATP)-channel blocker) prevented this preconditioning protection (37 ± 4%). In Study 2, recovery of function in intermittent cross-clamp fibrillation hearts (62 ± 3%) was significantly (p < 0.05) higher than intermittent cross-clamp fibrillation hearts treated with glibenclamide (33 ± 2%) and ischemia hearts (30 ± 5%). In Study 3, protection by intermittent cross-clamp fibrillation (60 ± 3%; p < 0.05) was attenuated by protein kinase C inhibition (chelerythrine, 34 ± 3%) and mitochondrial KATP-channel blockade (5-hydroxydecanoate, 27 ± 4%) to levels not significantly different from that of ischemia hearts (25 ± 4%). Conclusions: The cardioprotective efficacy of intermittent cross-clamp fibrillation was attenuated by protein kinase C inhibition or KATP-channel blockade. Involvement of these putative preconditioning cascade components in association with cardioprotection induced by intermittent cross-clamp fibrillation, suggests a role for the ischemic preconditioning mechanism.

Keywords: Research; Ischemia; Preconditioning; Left ventricular function; Heart preservation

Journal Article.  7006 words.  Illustrated.

Subjects: Clinical Pharmacology and Therapeutics ; Cardiovascular Medicine

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