W I N E TOXINS AND VENOMOUS AND POISONOUS MARINE ANIMALS
269
cardioinhibitory and vasomotor centers, and conduction in the myocardium. The rabbit and mouse seemed more susceptible to the toxin
than the dog ; the frog appeared quite resistant. Using the same poison,
Kellaway (1935) demonstrated further actions on the nervous and
cardiovascular systems. He suggested that the venom had a direct
effect on both the central nervous system, particularly the respiratory
and cardiovascular centers, and on the peripheral nervous system,
particularly the neuromuscular junction and the sensory nerve endings.
The poison caused a rapid fall in systemic arterial pressure and a
slowing of respiration. The latter Kellaway attributed to the central
effects of the toxin.
Fingerman and associates (1963) found that in the frog the toxin
had a marked effect on peripheral nerve and skeletal muscle. The
“ curare-like ” action was attributed to some mechanism which prevented the muscle from responding to acetylcholine. Subsequently,
Bolton et al. (1969) obtained somewhat similar results; they demonstrated a progressive diminution in the amplitude of the end plate
potential of the frog nerve-muscle preparation exposed to the toxin.
The toxin also modified the contraction of the directly stimulated
muscle, a change which was in part reversible. Attempts to detect
cytological or histochemical changes at the neuromuscular junction
were unsuccessful.
On the basis of their observations, Pepler and Loubser (1960)
concluded that the toxin had a very marked specific acetylcholinesterase inhibitory effect similar to the organo-phosphorus compounds.
This point, however, is open to considerable question. Schantz (1960)
indicated that the contraction of isolated muscle fibers in the presence
of ATP and magnesium ions is not inhibited by the poison, nor does
the toxin alter the rate of oxygen consumption in the respiring
diaphragm of the mouse.
Murtha’s work (1960) not only confirms many of the findings and
impressions of the earlier workers but it gives us considerable insight
into the various modes of action for the poison. The poison has a direct
effect on the heart and its conduction system. It produces changes
which range from a slight decrease in heart rate and contractile force
with simple P-R interval prolongation or S-T segment change, to severe
bradycardia and bundle-branch block or complete cardiac failure.
These changes are not unlike those provoked by other marine toxins
(Russell and van Harreveld, 1954 ; Russell and Emery, 1960 ; Saunders
et al. 1962), although this should not be interpreted to imply that these
toxins are indeed related. On the isolated cat papillary muscle the
toxin provokes a prompt but reversible depression in contractility.
269
cardioinhibitory and vasomotor centers, and conduction in the myocardium. The rabbit and mouse seemed more susceptible to the toxin
than the dog ; the frog appeared quite resistant. Using the same poison,
Kellaway (1935) demonstrated further actions on the nervous and
cardiovascular systems. He suggested that the venom had a direct
effect on both the central nervous system, particularly the respiratory
and cardiovascular centers, and on the peripheral nervous system,
particularly the neuromuscular junction and the sensory nerve endings.
The poison caused a rapid fall in systemic arterial pressure and a
slowing of respiration. The latter Kellaway attributed to the central
effects of the toxin.
Fingerman and associates (1963) found that in the frog the toxin
had a marked effect on peripheral nerve and skeletal muscle. The
“ curare-like ” action was attributed to some mechanism which prevented the muscle from responding to acetylcholine. Subsequently,
Bolton et al. (1969) obtained somewhat similar results; they demonstrated a progressive diminution in the amplitude of the end plate
potential of the frog nerve-muscle preparation exposed to the toxin.
The toxin also modified the contraction of the directly stimulated
muscle, a change which was in part reversible. Attempts to detect
cytological or histochemical changes at the neuromuscular junction
were unsuccessful.
On the basis of their observations, Pepler and Loubser (1960)
concluded that the toxin had a very marked specific acetylcholinesterase inhibitory effect similar to the organo-phosphorus compounds.
This point, however, is open to considerable question. Schantz (1960)
indicated that the contraction of isolated muscle fibers in the presence
of ATP and magnesium ions is not inhibited by the poison, nor does
the toxin alter the rate of oxygen consumption in the respiring
diaphragm of the mouse.
Murtha’s work (1960) not only confirms many of the findings and
impressions of the earlier workers but it gives us considerable insight
into the various modes of action for the poison. The poison has a direct
effect on the heart and its conduction system. It produces changes
which range from a slight decrease in heart rate and contractile force
with simple P-R interval prolongation or S-T segment change, to severe
bradycardia and bundle-branch block or complete cardiac failure.
These changes are not unlike those provoked by other marine toxins
(Russell and van Harreveld, 1954 ; Russell and Emery, 1960 ; Saunders
et al. 1962), although this should not be interpreted to imply that these
toxins are indeed related. On the isolated cat papillary muscle the
toxin provokes a prompt but reversible depression in contractility.