The mechanism of
cocaine-related
sudden death is unknown. To test whether
cocaine potentiated changes in sinus cycle length, conduction in the atrioventricular node (AH interval) and ventricular effective refractory period induced by infused
norepinephrine and ansae subclaviae stimulation, the dose-response curves of sinus cycle length, AH interval and ventricular effective refractory period to infused
norepinephrine (0.01 to 0.20 micrograms/kg
body weight per min) and the frequency-response curves to ansae subclaviae stimulation (1 to 4 Hz, 2 to 3
mA, 4 ms pulses) were determined before and after
intravenous injection of
cocaine (5 mg/kg) in 15 anesthetized open chest dogs.
Cocaine potentiated shortening of sinus cycle length, AH interval and ventricular effective refractory period induced by
norepinephrine infusion and shifted dose-response curves of these variables to the left in eight dogs (supersensitivity).
Cocaine did not affect frequency-response curves of sinus cycle length and AH interval to ansae subclaviae stimulation. Ansae subclaviae stimulation shortened the ventricular effective refractory period more after
cocaine injection, but frequency-response curves were not shifted to the left in seven dogs (no supersensitivity).
Cocaine did not enhance electrical induction of
ventricular tachyarrhythmias in 15 dogs without acute
myocardial infarction. Acute
myocardial infarction was produced by coronary artery
ligation in another group of 21 dogs. Of 10 dogs with acute
myocardial infarction, spontaneous or electrically induced
ventricular tachycardia developed in 1 dog without drugs, in 3 dogs given
norepinephrine and in 7 dogs given
norepinephrine and
cocaine (p less than 0.03 versus without drugs).(ABSTRACT TRUNCATED AT 250 WORDS)