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.The force of contraction (34 degrees C, stimulation frequency 1Hz) in the right atrial trabeculae was recorded during 30min of hypoxia followed by 60min of reoxygenation. Desflurane (at 3, 6 and 9%) was administered during the first 5min of reoxygenation. The force of contraction at the end of the 60-min reoxygenation period (FoC(60)) was compared in the study groups (means+/-SD).In the ND group, desflurane at 3, 6 and 9% (FoC(60): respectively 78+/-10%, 84+/-4% and 85+/-12% of baseline) enhanced the recovery of FoC(60) compared with the ND-controls (53+/-7% of baseline; P0.05). In the ID group, desflurane at 3% (61+/-4%) did not modify the recovery of FoC(60) compared with the ID-controls (54+/-6%), whereas desflurane at 6 and 9% (75+/-11% and 81+/-8%, respectively) enhanced the recovery of FoC(60)vs the controls (P0.05). In the NID group, desflurane at 3% (57+/-5%) also failed to modify the recovery of FoC(60) compared with the NID-controls (52+/-10%), while desflurane at 6 and 9% (80+/-10% and 79+/-7%, respectively) enhanced the recovery of FoC(60)vs the controls (P0.05).Desflurane in vitro was able to postcondition diabetic (both ID and NID) human myocardium at 6 and 9%, but not at 3%.
