The purpose of this study was to gain new insights in the role of
succinylcholine in the initiation of
malignant hyperthermia (MH). The intravenous (i.v.) administration of
succinylcholine (2.0 mg/kg) induced
fasciculations and
masseter spasm in both normal swine and those susceptible to MH. However, the amplitudes and durations of generalized
fasciculations were significantly greater in the susceptible animals that subsequently developed a fulminant episode of MH:
succinylcholine induced not only
tachycardia,
hyperthermia,
contractures, and increases in PaCO2 and
lactate, all classic indicators of an episode, but also an initial severe
hypotension. The mean arterial pressure in these swine decreased from 115 +/- 6 mm Hg to 60 +/- 12 mm Hg (mean +/- SD), 1 min after the administration of
succinylcholine. Normal swine developed neither cardiovascular effects nor altered metabolism in response to
succinylcholine. The pretreatment of animals with a nondepolarizing muscle relaxant (
pancuronium 0.1 mg/kg) minimized
fasciculations induced by
succinylcholine, but did not prevent the
hypotension nor episodes of MH in the susceptible swine. In the pretreated and untreated susceptible swine,
dantrolene was an equally effective treatment. Plasma
catecholamine levels after
succinylcholine administration were increased only in the susceptible swine without the
pancuronium pretreatment. We concluded that the effects of
succinylcholine on skeletal muscle and/or on other tissues play a significant role in the initiation of a MH episode in swine with this
genetic disorder, and that these effects are not dependent on an abnormal sensitivity for
succinylcholine-induced
skeletal muscle fasciculations in these animals.