Hydroxyl radical formation during inhalation anesthesia in the reperfused working rat heart

To determine whether isoflurane, sevoflurane and halothane influenced hydroxyl radical production in the ischemic rat heart.

Twenty-four male Wistar rats were divided into four groups; control (C), isoflurane 1.4% (I), sevoflurane 2.5% (S) and halothane 1% (H). The hearts were perfused with modified Krebs-Henseleit bicarbonate buffer by a working heart model for 10 min. Then, whole heart ischemia was induced by severely restricting coronary perfusion for 15 min. Reperfusion of the hearts after this ischemic period lasted for 20 min. The coronary effluent was collected before and during ischemia and at 1, 5, 10, 20 min after reperfusion. At the end of reperfusion, hearts were removed and prepared for measurement. Hydroxyl radicals were identified by their reaction with salicylic acid to yield dihydroxybenzoic acids (DHBAs).

Before and after ischemia, there were no differences in coronary flow and heart rate among the four groups, but cardiac output and LV dP/dt maximum in the anesthetic groups were lower than in the control group. Hydroxyl radical products in the heart were significantly lower in the I group than the other groups (e.g. C vs I, 278.1 +/- 24.3 vs 219.3 +/- 14.4 microM x g(-1), P < 0.05). The concentrations of DHBAs in the coronary effluent at some points in the I and H groups were less than in the C and S groups.

These results indicate that isoflurane and halothane (to a lesser extent), reduce hydroxyl radical production in the ischemic heart, but sevoflurane does not.