MARINE TOXINS AND VENOMOUS AND POISONOUS MARINE ANIMALS
359
and extend the entire length of the sting. They appear as two deep
channels separated by the anteromedian ridge. The spine is invested
in a thin layer of gaily colored, fibrous connective tissue, the integumentary sheath. Within the anterolateral grooves are fusiform
shaped “ venom glands ” which may occupy up to three-quarters of the
total length of the spine. The glandular structures within the grooves
are composed of several types of tissues, including the venom-producing
cells, large polygonal shaped cells with pinkish-gray , finely granular
cytoplasm. According to Halstead et al. (1955a) these cells map
measure 270 p x 75 p or more, and are collected together in connective
tissue compartments within the anterolateral grooves ; they are covered
in turn by the integumentary sheath. There does not appear to be a
glandular duct through which the venom is secreted or discharged.
Envenomation probably occurs through mechanical pressure on the
spine.
( b ) Chemistry and toxicology. Saunders and Taylor (1959) found
that water extracts of the integumentary sheaths and underlying
glandular tissues from the dorsal spines of P . volitans were somewhat
turbid, reddish-orange in color, and had a pH of approximately 7.
The toxin was unstable a t room temperatures ; lyophilized and glyceroltreated extracts were found to retain 40 to 90% of their original
lethal activity following 1 year’s storage a t -20°C. The toxin was nondialyzable, and in mice had an intravenous LD,, of 1.1 mg protein/kg
body weight.
I n rabbits, small doses produced a slight decrease in arterial
blood pressure without particular effect on the electrocardiogram,
and an increase in respiratory rate. Larger doses caused a more
profound fall in blood pressure, an increase in respiratory rate, and
evidence of myocardial ischemia or injury, or conduction defects.
Lethal doses produced a precipitous fall in arterial blood pressure
and extensive electrocardiographic changes.
Respirations were
markedly depressed and finally ceased ; the blood pressure continued to
fall. On opening the chest following cessation of respirations the
auricles, and occasionally the ventricles, were usually found to be
beating ; some irregular electrical activity persisted for several more
minutes. I n several of the animals, initiation of artificial respiration
within one half minute following respiratory arrest was ineffective in
prolonging life.
Intravenous injection of the venom into mice produced ataxia,
oircling movements, and partial or complete paralysis of the legs.
This syndrome was followed by a period of inactivity, during which
359
and extend the entire length of the sting. They appear as two deep
channels separated by the anteromedian ridge. The spine is invested
in a thin layer of gaily colored, fibrous connective tissue, the integumentary sheath. Within the anterolateral grooves are fusiform
shaped “ venom glands ” which may occupy up to three-quarters of the
total length of the spine. The glandular structures within the grooves
are composed of several types of tissues, including the venom-producing
cells, large polygonal shaped cells with pinkish-gray , finely granular
cytoplasm. According to Halstead et al. (1955a) these cells map
measure 270 p x 75 p or more, and are collected together in connective
tissue compartments within the anterolateral grooves ; they are covered
in turn by the integumentary sheath. There does not appear to be a
glandular duct through which the venom is secreted or discharged.
Envenomation probably occurs through mechanical pressure on the
spine.
( b ) Chemistry and toxicology. Saunders and Taylor (1959) found
that water extracts of the integumentary sheaths and underlying
glandular tissues from the dorsal spines of P . volitans were somewhat
turbid, reddish-orange in color, and had a pH of approximately 7.
The toxin was unstable a t room temperatures ; lyophilized and glyceroltreated extracts were found to retain 40 to 90% of their original
lethal activity following 1 year’s storage a t -20°C. The toxin was nondialyzable, and in mice had an intravenous LD,, of 1.1 mg protein/kg
body weight.
I n rabbits, small doses produced a slight decrease in arterial
blood pressure without particular effect on the electrocardiogram,
and an increase in respiratory rate. Larger doses caused a more
profound fall in blood pressure, an increase in respiratory rate, and
evidence of myocardial ischemia or injury, or conduction defects.
Lethal doses produced a precipitous fall in arterial blood pressure
and extensive electrocardiographic changes.
Respirations were
markedly depressed and finally ceased ; the blood pressure continued to
fall. On opening the chest following cessation of respirations the
auricles, and occasionally the ventricles, were usually found to be
beating ; some irregular electrical activity persisted for several more
minutes. I n several of the animals, initiation of artificial respiration
within one half minute following respiratory arrest was ineffective in
prolonging life.
Intravenous injection of the venom into mice produced ataxia,
oircling movements, and partial or complete paralysis of the legs.
This syndrome was followed by a period of inactivity, during which