ENFLURANE AND ISOFLURANE REDUCE REPERFUSION DYSFUNCTION IN THE ISOLATED RAT-HEART

We evaluated the possible cardioprotective effects of enflurane (E) an d isoflurane (I) in isolated rat hearts subjected to 40 min normotherm ic arrest. After reperfusion, hearts were stimulated with adrenaline t o evaluate their systolic reserves. In hearts not receiving I or E, ad enosine triphosphate (ATP) was reduced from 23.0 +/- 0.8 to 9.3 +/- 1. 1 mumol/g dry weight (means +/- SEM; P < 0.001) after arrest. This was associated with a significant reduction in ventricular work (Wt) from 13.6 +/- 0. 7 to 1.6 +/- 0.7 mW (P < 0.001). Adrenaline partially res tored Wt but not the ATP. E and I given only during normothermic arres t (in the cardioplegic solution) resulted in reductions in ATP similar to the hearts not receiving the drugs. However, on reperfusion and su bsequent administration of adrenaline, hearts subjected to the anesthe tic drugs performed as well as hearts before arrest. For example, in h earts not exposed to I or E, the Wt after the elective arrest was 1.55 +/- 0.05% (mean +/- SEM) of the pre-arrest value. This was significan tly less than hearts exposed to either one of the inhalational agents (40.02 +/- 3.49% of the pre-arrest value; P < 0.0001). Adrenaline impr oved function in hearts which did not receive I or E to 55.02 +/- 12.8 0% of the pre-arrest value, but this was significantly less than the W t performed by the hearts exposed to the anesthetic agents (122.67 +/- 7.78% of pre-arrest value; P < 0.001). This beneficial effect of I an d E during reperfusion probably is mediated by the effect of the anest hetic agents on Ca2+ slow channels. The effect could not be ascribed t o depression of global myocardial contractile function associated with I and E.