MARINE TOXINS AND VENOMOUS AND POISONOUS MARINE ANIMALS
325
from vagal escape, and normal reflex slowing of the heart in the presence
of an increasing blood pressure might not be observed. While these
suggested activities would certainly explain and simplify the syndrome
of the poisoning, this writer suspects that the mechanisms may not be
quite so simple. Nevertheless, further pharmacological studies with
these activities in mind should be most fruitful.
As previously noted (Russell et al., 1961; Mosher et al., 1964)
tetrodotoxin possesses pharmacological properties very similar to
those of certain local anesthetics, though far more potent. As pointed
out by the latter authors, the toxin appears to differ from procaine
and cocaine in that it acts selectively to prevent or reduce the usual
increase in permeability to the sodium ion without seeming to affect
the permeability to potassium (Narahashi et al., 1964).
In summary, the toxin has a particular effect on the axons of the
preganglionic cholinergic and somatic motor nerves. It blocks the
excitability of directly stimulated muscle fibers. In the frog it blocks
the action potential at concentrations of approximately lpg/l of
bathing solution. The toxin provokes hypotension either through its
effect on vasomotor tone through the preganglionic cholinergic fibers,
or through its action on the heart directly. It depresses respiration by
its effect on the nerve, neuromuscular junction and muscle, and perhaps
by its direct effect on the respiratory centers. It may also depress the
respiratory centers indirectly through the hypotensive crisis, which no
doubt precipitates a cerebral and cerebellar anemia. It might be
concluded that while these-various mechanisms are not yet firmly
established, our present state of knowledge on this, one of the most
toxic non-proteins known, is far more gratifying than on any other of
the fish poisons.
( c ) Clinical problem. Tetraodon poisoning is the most dangerous
form of ichthyosarcotoxism. According to Halstead (1964), Japanese
statistics show a mortality rate of 61.5% for this type of poisoning.
Approximately twenty persons a year die of the poisoning in Japan.
Deaths are also reported from other endemic areas. The clinical case
is characterized by the rapid onset (5-30 min) of weakness, dizziness,
pallor and paresthesia about the lips, tongue and throat. The paresthesia is usually described as ( ( tingling or pricking sensations ”, and is
often noted in the limbs, particularly the fingers and toes, as the
illness develops. While tetrodotoxin is considered by most workers to
be a potent emetic, and nausea is often one of the presenting symptoms,
vomiting does not occur in most cases. In those cases in which it does,
the vomiting develops during the first hour of the illness.
325
from vagal escape, and normal reflex slowing of the heart in the presence
of an increasing blood pressure might not be observed. While these
suggested activities would certainly explain and simplify the syndrome
of the poisoning, this writer suspects that the mechanisms may not be
quite so simple. Nevertheless, further pharmacological studies with
these activities in mind should be most fruitful.
As previously noted (Russell et al., 1961; Mosher et al., 1964)
tetrodotoxin possesses pharmacological properties very similar to
those of certain local anesthetics, though far more potent. As pointed
out by the latter authors, the toxin appears to differ from procaine
and cocaine in that it acts selectively to prevent or reduce the usual
increase in permeability to the sodium ion without seeming to affect
the permeability to potassium (Narahashi et al., 1964).
In summary, the toxin has a particular effect on the axons of the
preganglionic cholinergic and somatic motor nerves. It blocks the
excitability of directly stimulated muscle fibers. In the frog it blocks
the action potential at concentrations of approximately lpg/l of
bathing solution. The toxin provokes hypotension either through its
effect on vasomotor tone through the preganglionic cholinergic fibers,
or through its action on the heart directly. It depresses respiration by
its effect on the nerve, neuromuscular junction and muscle, and perhaps
by its direct effect on the respiratory centers. It may also depress the
respiratory centers indirectly through the hypotensive crisis, which no
doubt precipitates a cerebral and cerebellar anemia. It might be
concluded that while these-various mechanisms are not yet firmly
established, our present state of knowledge on this, one of the most
toxic non-proteins known, is far more gratifying than on any other of
the fish poisons.
( c ) Clinical problem. Tetraodon poisoning is the most dangerous
form of ichthyosarcotoxism. According to Halstead (1964), Japanese
statistics show a mortality rate of 61.5% for this type of poisoning.
Approximately twenty persons a year die of the poisoning in Japan.
Deaths are also reported from other endemic areas. The clinical case
is characterized by the rapid onset (5-30 min) of weakness, dizziness,
pallor and paresthesia about the lips, tongue and throat. The paresthesia is usually described as ( ( tingling or pricking sensations ”, and is
often noted in the limbs, particularly the fingers and toes, as the
illness develops. While tetrodotoxin is considered by most workers to
be a potent emetic, and nausea is often one of the presenting symptoms,
vomiting does not occur in most cases. In those cases in which it does,
the vomiting develops during the first hour of the illness.