Halothane Does Have Protective Properties in the Isolated Ischemic Rat Heart

To determine whether halothane has protective effects on the ischemic heart, the influence of various concentrations (0.5%-1.5%) of halothane on metabolic and functional recovery during reperfusion after 60-min hypothermic (20°C) and 40-min normothermic cardioplegic arrest was determined in the isolated rat heart. Halothane was administered either before and after arrest or intermittently during arrest. Hearts not receiving halothane demonstrated a reduction in adenosine triphosphate (ATP) content from a control value of 20.35 ± 1.66 μmol/g dry wt (mean ± SEM) (before arrest) to 9.34 ± 1.12 μmol/g dry wt at the end of arrest (P < 0.001). The myocardial ATP content, when measured 20 min after arrest and during reperfusion, remained decreased (9.57 ± 0.62 μmol/g dry wt). Under these experimental conditions, aortic flow was reduced from 43.62 ± 2.40 mL/min before arrest to 1.80 ± 1.80 mL/min 20 min after arrest and during reperfusion (P < 0.001). The administration of adrenaline after 20 min of reperfusion resulted in partial recovery to 22.01 ± 8.36 mL/min. Administration of halothane (0.5%) before the cardioplegic period was associated with a reduction of ATP at the end of the normothermic arrest (4.02 ± 0.38 μmol/g dry wt; P < 0.01), but the ATP increased significantly (13.45 ± 0.32 μmol/g dry wt) when measured after the arrest and after 20 min of reperfusion and stimulation with adrenaline. The administration of halothane during the control period (before arrest) reduced aortic flow from 43.24 ± 1.11 to 28.70 ± 1.84 mL/min, whereas it averaged 6.08 ± 2.03 (P < 0.001) and 39.65 ± 3.49 mL/min after 20 min of reperfusion without and with adrenaline, respectively. When halothane (0.5%) was given intermittently during the arrest, the postarrest ATP averaged 8.23 ± 0.62 μmol/g dry wt (P < 0.001), which improved to 16.01 ± 0.90 μmol/g dry wt after 20 min of reperfusion and subsequent administration of adrenaline. Under these experimental conditions, aortic flow during reperfusion was 20.17 ± 4.49 mL/min (P < 0.01), and this improved to 37.67 ± 4.49 mL/min on administration of adrenaline. Similar tendencies were observed with 1% and 1.5% halothane. Our results indicate that halothane does not preserve myocardial ATP during normothermic arrest and ischemia. However, the use of halothane was associated with improved recovery of ATP content and systolic reserve after reperfusion. Hearts not receiving halothane did not restore their ATP content and had depressed systolic reserve. These observations cannot be explained by the effect of halothane on global myocardial mechanics, and the beneficial effect of halothane may be related to the prevention of the reperfusion injury.