ABSTRACT
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 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). RESULTS: 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; P<0.05). 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 (P<0.05). 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 (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%.
