270
FINDLAY E. RUSSELL
I n those cases where spontaneous contractures are abolished, Murtha
found that the muscle still responded to electrical stimulation, although
contractile force had been reduced approximately 50 yo.
In the vagotomized dog, cardiac contractile force decreases 50%
within the first minute following injection of the poison. There is
a concomitant, precipitous fall in systemic arterial pressure. A fall in
blood pressure was also observed by Murtha in both intact and partially
eviscerated mammals, indicating that the mechanism proposed by
Kellaway (changes in the splenic circulation) is not responsible for the
cardiovascular crisis. The toxin does not produce vasodilatation in
the vessels of the mammalian leg or kidney, nor does it affect the rate
of blood flow in the isolated rabbit ear. In cervical cord-sectioned,
bilaterally vagotomized mammals the immediate precipitous fall in
arterial blood pressure was not observed by Murtha, although there
was some subsequent decrease in blood pressure.
These findings, along with those observed with isolated heart
preparations, indicate that the toxin has a direct effect on the heart,
an effect which is in part responsible for the cardiovascular crisis ; and
while the poison may produce changes in the peripheral vascular system
these changes are not of sufficient magnitude to precipitate deleterious
changes in the systemic arterial blood pressure. It will be interesting to
learn what alterations the toxin produces in pulmonary artery pressure
and flow, since changes in the pulmonary vascular bed appear to be
responsible for the precipitous fall in systemic arterial pressure
sometimes provoked by certain animal venoms (Russell et al., 1962;
Halmagyi et al., 1965), as well as by a number of other toxic substances.
The work by Murtha also indicates that a significant part of the
cardiovascular crisis is in some manner concerned with the direct
action of the toxin on the central nervous system, although the experiments do not exclude the perhaps improbable conjecture that cerebral
anoxia secondary to cardiac centered vascular failure may be a, factor.
Murtha suggests that the central nervous system effects may be
mediated through the spinal cord.
Murtha’s work on the phrenic nerve-diaphragm preparation also
confirms earlier findings. The toxin depresses mammalian phrenic
nerve potentials, suppresses the indirectly elicited contractions of
the diaphragm and often reduces the directly stimulated contractions.
In the anesthetized, artificially respired mammal the toxin suppresses
contraction of the quadriceps muscle following reflex stimulation at
a time when stimulation of the motor nerve produces muscular contraction. Recovery from the effects on nerve and reflex transmission
usually occurred simultaneously. These and other studies indicate
FINDLAY E. RUSSELL
I n those cases where spontaneous contractures are abolished, Murtha
found that the muscle still responded to electrical stimulation, although
contractile force had been reduced approximately 50 yo.
In the vagotomized dog, cardiac contractile force decreases 50%
within the first minute following injection of the poison. There is
a concomitant, precipitous fall in systemic arterial pressure. A fall in
blood pressure was also observed by Murtha in both intact and partially
eviscerated mammals, indicating that the mechanism proposed by
Kellaway (changes in the splenic circulation) is not responsible for the
cardiovascular crisis. The toxin does not produce vasodilatation in
the vessels of the mammalian leg or kidney, nor does it affect the rate
of blood flow in the isolated rabbit ear. In cervical cord-sectioned,
bilaterally vagotomized mammals the immediate precipitous fall in
arterial blood pressure was not observed by Murtha, although there
was some subsequent decrease in blood pressure.
These findings, along with those observed with isolated heart
preparations, indicate that the toxin has a direct effect on the heart,
an effect which is in part responsible for the cardiovascular crisis ; and
while the poison may produce changes in the peripheral vascular system
these changes are not of sufficient magnitude to precipitate deleterious
changes in the systemic arterial blood pressure. It will be interesting to
learn what alterations the toxin produces in pulmonary artery pressure
and flow, since changes in the pulmonary vascular bed appear to be
responsible for the precipitous fall in systemic arterial pressure
sometimes provoked by certain animal venoms (Russell et al., 1962;
Halmagyi et al., 1965), as well as by a number of other toxic substances.
The work by Murtha also indicates that a significant part of the
cardiovascular crisis is in some manner concerned with the direct
action of the toxin on the central nervous system, although the experiments do not exclude the perhaps improbable conjecture that cerebral
anoxia secondary to cardiac centered vascular failure may be a, factor.
Murtha suggests that the central nervous system effects may be
mediated through the spinal cord.
Murtha’s work on the phrenic nerve-diaphragm preparation also
confirms earlier findings. The toxin depresses mammalian phrenic
nerve potentials, suppresses the indirectly elicited contractions of
the diaphragm and often reduces the directly stimulated contractions.
In the anesthetized, artificially respired mammal the toxin suppresses
contraction of the quadriceps muscle following reflex stimulation at
a time when stimulation of the motor nerve produces muscular contraction. Recovery from the effects on nerve and reflex transmission
usually occurred simultaneously. These and other studies indicate