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It is unclear whether nitrous oxide (N(2)O) has a protective effect on cardiac function in vitro. In addition, little is known about the cardioprotective effect of anesthesia administered during hypoxia or ischemia. We therefore studied the cardioprotective effects of N(2)O and sevoflurane administered before or during hypoxia in isolated rat hearts. Rat hearts were excised and perfused using the Langendorff technique. For hypoxia-reoxygenation, hearts were made hypoxic (95% N(2), 5% CO(2)) for 45 min and then reoxygenated (95% O(2), 5% CO(2)) for 40 min (control: CT group). Preconditioning was achieved through three cycles of application of 4% sevoflurane (sevo-pre group) or 50% N(2)O (N(2)O-pre group) for 5 min with 5-min washouts in between. Hypoxic conditions were achieved by administering the 4% sevoflurane (sevo-hypo group) or 50% N(2)O (N(2)O-hypo group) during the 45-min hypoxic period. L-type calcium channel currents (I(Ca,L)) were recorded on rabbit myocytes. (1) Both 4% sevoflurane and 50% N(2)O significantly reduced left ventricular developed pressure (LVDP). Sevoflurane also increased left ventricular end-diastolic pressure, though N(2)O did not. (2) The recoveries of LVDP and pressure-rate product (PRP) after hypoxia-reoxygenation were better in the sevo-pre group than in the CT or N(2)O-pre group. (3) Application of either sevoflurane or N(2)O during hypoxia improved recovery of LVDP and PRP, and GOT release was significantly lower than in the CT group. (4) Sevoflurane and N(2)O reduced I(Ca,L) to similar extents. Although sevoflurane administered before or during hypoxia exerts a cardioprotective effect, while N(2)O shows a cardioprotective effect only when administered during hypoxia.

Sevoflurane and nitrous oxide exert cardioprotective effects against hypoxia-reoxygenation injury in the isolated rat heart