POTASSIUM CURRENTS IN ATRIAL AND VENTRICULAR MYOCYTES FROM A RAT MODEL OF CIRRHOSIS

The underlying mechanisms for the electrophysiological abnormalities t hat develop as a consequence of cirrhosis of the liver have been studi ed by recording three different K+ currents in mammalian heart tissue. Single myocytes from the atria and ventricles of sham-operated and bi le duct-ligated (BDL) cirrhotic adult rats were current and voltage cl amped using standard whole cell methods. In ventricular myocytes from cirrhotic animals, measurements of the current-voltage relationships, voltage dependence of inactivation, and reactivation kinetics of K+ cu rrents showed that the only significant functional changes (within the physiological range of membrane potentials) were decreases in the den sity of expression of 1) I-t, a Ca2+-independent transient outward Kcurrent, and 2) I-sus, a delayed rectifier K+ current. The decreases i n I-t and I-sus contribute to the prolonged Q-T interval of the electr ocardiogram that has been described in cirrhotic patients. Measurement of K+ currents in atrial myocytes demonstrated that there were no sig nificant differences in any of the K+ current densities between sham a nd BDL animals, although reactivation kinetics of I-t were slowed some what.