ISOFLURANE AND HALOTHANE DO NOT ALTER THE ENHANCED AFTERLOAD SENSITIVITY OF LEFT-VENTRICULAR RELAXATION IN DOGS WITH PACING-INDUCED CARDIOMYOPATHY

Background The afterload dependence of left ventricular (LV) relaxatio n is accentuated in the failing heart. The authors tested the hypothes is that isoflurane and halothane alter the afterload sensitivity of LV relaxation in dogs with pacing-induced cardiomyopathy. Methods: Dogs (n = 6) were chronically instrumented for measurement of LV and aortic pressures and subendocardial segment length. Hemodynamics were record ed, and LV relaxation was evaluated with a time constant of isovolumic relaxation (tau) under control conditions and during decreases and in creases in LV load produced by abrupt inferior vena caval (IVC) occlus ion and phenylephrine (intravenous infusion), respectively, in the con scious state and during isoflurane and halothane anesthesia (1.5 MAC) on separate days before and after the development of pacing-induced ca rdiomyopathy. The slope (R) of the tau versus LV end-systolic pressure (P-es) relation was also used to determine the afterload sensitivity of LV relaxation. Results: IVC occlusion and phenylephrine produced si milar or less profound changes in P-es, regional end-systolic force Ca n index of LV afterload), and end-systolic segment length in cardiomyo pathic compared with healthy dogs. However, IVC occlusion and phenylep hrine caused more pronounced alterations in tau in conscious and isofl urane-and halothane-anesthetized dogs after the development of cardiom yopathy. R was also greater in cardiomyopathic compared with healthy d ogs (e.g., 0.32 +/- 0.03 before pacing to 1.00 +/- 0.13 ms/mmHg in con scious dogs). No differences In the load dependence of LV relaxation w ere observed between the conscious and anesthetized states before and after production of LV dysfunction. Conclusions: The results indicate that isoflurane and halothane do not alter the afterload dependence of LV relaxation in the normal and cardiomyopathic heart. The lack of ef fect of the volatile anesthetics is probably related to anesthetic-ind uced reductions in the resistance to LV ejection concomitant with simu ltaneous negative inotropic effects.