Quinteiro R A, Biagetti M O, de Forteza E
Teaching and Research Department, Favaloro Foundation, Buenos Aires, Argentina.
J Cardiovasc Pharmacol. 1990 Jan;15(1):29-36. doi: 10.1097/00005344-199001000-00005.
We evaluated the effect of lidocaine (5 micrograms/ml) on Vmax and conduction velocity during longitudinal and transverse propagation to fiber orientation in strips of uniform anisotropic ventricular muscle from adult canine hearts. Tissues were markedly anisotropic, with conduction velocities 3.2 times faster during longitudinal propagation than during transverse propagation to the long axis of the fibers, and with the greatest values of Vmax associated with the slowest conduction velocities. After addition of lidocaine, Vmax (normalized values with respect to control for each cycle length, expressed as mean +/- SEM) decreased from 0.99 +/- 0.02 at a cycle length of 1,000 ms to 0.86 +/- 0.02 at a cycle length of 300 ms during longitudinal propagation. During transverse propagation, Vmax decreased from 0.99 +/- 0.03 at a cycle length of 1,000 ms to 0.87 +/- 0.03 at a cycle length of 300 ms. The differences in the relative changes between both directions at these cycle lengths, as well as with intermediate values of 500, 400, and 350 ms, were not significant. Similar results were obtained for conduction velocity. We conclude from these findings that under these experimental conditions the effects of lidocaine are characterized by a relative change both in Vmax and conduction velocity that is almost the same during longitudinal and transverse propagation at all cycle lengths explored. Moreover, the rapid binding-rate constants reported for lidocaine may play a significant role in determining the characteristics of Vmax and conduction velocity depressions in both directions.
