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Lemoine S.,Institute Federatif Of Recherche Icore 146 | Durand C.,Institute Federatif Of Recherche Icore 146 | Zhu L.,Institute Federatif Of Recherche Icore 146 | Zhu L.,Caen University Hospital Center | And 9 more authors.
Diabetes and Metabolism | Year: 2010

Aim: We tested the hypothesis that brief exposure to desflurane at the time of reoxygenation might be able to protect against hypoxia-reoxygenation injury in human myocardium from diabetic (insulin-dependent, ID; and non-insulin-dependent, NID) patients and non-diabetic (ND) subjects. Methods: The force of contraction (34°C, stimulation frequency 1 Hz) in the right atrial trabeculae was recorded during 30 min of hypoxia followed by 60 min of reoxygenation. Desflurane (at 3, 6 and 9%) was administered during the first 5 min of reoxygenation. The force of contraction at the end of the 60-min reoxygenation period (FoC60) was compared in the study groups (means ± SD). Results: In the ND group, desflurane at 3, 6 and 9% (FoC60: respectively 78 ± 10%, 84 ± 4% and 85 ± 12% of baseline) enhanced the recovery of FoC60 compared with the ND-controls (53 ± 7% of baseline; P < 0.05). In the ID group, desflurane at 3% (61 ± 4%) did not modify the recovery of FoC60 compared with the ID-controls (54 ± 6%), whereas desflurane at 6 and 9% (75 ± 11% and 81 ± 8%, respectively) enhanced the recovery of FoC60 vs the controls (P < 0.05). In the NID group, desflurane at 3% (57 ± 5%) also failed to modify the recovery of FoC60 compared with the NID-controls (52 ± 10%), while desflurane at 6 and 9% (80 ± 10% and 79 ± 7%, respectively) enhanced the recovery of FoC60 vs the controls (P < 0.05). Conclusion: Desflurane in vitro was able to postcondition diabetic (both ID and NID) human myocardium at 6 and 9%, but not at 3%. © 2009 Elsevier Masson SAS. All rights reserved.

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