THE EFFECTS OF KETAMINE ON CONDUCTION-VELOCITY AND MAXIMUM RATE OF RISE OF ACTION-POTENTIAL UPSTROKE IN GUINEA-PIG PAPILLARY-MUSCLES - COMPARISON WITH QUINIDINE
Y. Hara et al., THE EFFECTS OF KETAMINE ON CONDUCTION-VELOCITY AND MAXIMUM RATE OF RISE OF ACTION-POTENTIAL UPSTROKE IN GUINEA-PIG PAPILLARY-MUSCLES - COMPARISON WITH QUINIDINE, Anesthesia and analgesia, 79(4), 1994, pp. 687-693
Using standard microelectrode techniques, the effects of ketamine on t
he maximum rate of rise of action potential upstroke (V-max) and the c
onduction velocity were examined and compared with the effects of quin
idine, a sodium channel blocker, in isolated guinea pig papillary musc
les. Both ketamine and quinidine decreased V-max and the square of the
conduction velocity in a concentration-dependent manner. The conducti
on slowing paralleled the decreases in V-max, suggesting that the sodi
um current inhibition produced by these drugs is responsible for the c
onduction slowing. In the presence of quinidine, a train of stimulatio
n after a quiescent period produced an exponential decline in V-max an
d the decrease in V-max was enhanced by increasing stimulation frequen
cy (i.e., use-dependent block). Ketamine significantly depressed V-max
of the first action potential after a long quiescent period (tonic bl
ock), and failed to produce a further decrease in V-max during the sub
sequent train of stimulation. The decrease in V-max was enhanced by si
multaneous administration of ketamine and quinidine. Thus, ketamine de
creases conduction velocity by inhibiting the sodium current. The mode
of action on cardiac conduction is similar to that of quinidine, but
different from that of volatile anesthetics which produce conduction s
lowing by impairing cell-to-cell coupling. However, ketamine produces
a tonic block of the sodium channel while quinidine produces a use-dep
endent block. We conclude that ketamine should be administered with ca
ution to patients receiving Class I antiarrhythmic drugs.