HIGH SPINAL-ANESTHESIA DOES NOT ALTER EXPERIMENTAL MYOCARDIAL-INFARCTION SIZE OR ISCHEMIC PRECONDITIONING

Objective: The role of the central nervous system in the development o f myocardial infarction and ventricular fibrillation in virgin and isc hemically preconditioned myocardium was investigated. Design: Infarct size and ventricular arrhythmias were assessed after regional ischemia -reperfusion. Animals were randomly assigned to four groups: (1) preco nditioned, central nervous system intact; (2) nonpreconditioned, nervo us system intact; (3) preconditioned, nervous system blocked; and (4) nonpreconditioned, nervous system blocked. Differences in hemodynamics and infarct size were assessed with analysis of variance, and differe nces in ventricular fibrillation were assessed with the Kruskal-Wallis test. Setting: Experiments were performed in the Anesthesiology Resea rch Laboratory at a medical center. Participants: Anesthetized open-ch est New Zealand white rabbits were used for these studies. Interventio ns: Rabbits underwent 30 minutes of coronary artery occlusion and 3 ho urs of reperfusion. The central nervous system was blocked with total spinal anesthesia. Ischemic preconditioning was elicited with 5 minute s of coronary artery occlusion and 10 minutes of reperfusion. Infarcti on was assessed with tetrazolium and expressed as a percentage of the risk zone (mean +/- SEM). Measurements and Main Results: Preconditioni ng resulted in infarct size limitation compared with the control (8% /- 4% v 43% +/- 5%; p < 0.001) and delayed the onset of fibrillation ( 15.5 minutes v 11 minutes; p = 0.001). Spinal blockade neither altered nonpreconditioned infarct size nor attenuated preconditioning (32% +/ - 7% v 8% +/- 3%; p = 0.04), but it was associated with ventricular fi brillation in 24/25 rabbits as compared with 6/14 rabbits without bloc kade. In blocked animals, preconditioning resulted in a decreased dura tion of fibrillation (2.5 minutes v 12.5 minutes; p = 0.0004). However , spinal blockade eliminated the preconditioning-induced delay in fibr illation (10 minutes v 22 minutes; p = NS). Conclusions: It is conclud ed that (1) activation of efferent sympathetic nerves is not necessary for ischemic preconditioning; (2) preconditioning delays the onset of ventricular arrhythmias; and (3) spinal blockade exacerbates ischemia -induced ventricular arrhythmias. Copyright (C) 1997 by W.B. Saunders Company.