The action of veratrum derivatives on the mammalian cardiovascular system.
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Abstract
Veratrum derivatives are best known for their action on the cardiovascular
system, namely, a fall in blood pressure and bradycardia.
Although these agents have been known from the time of Hippocrates, the
exact site or sites of action have not been adequately elucidated. A
review of the literature indicates that the cardiovascular actions of
veratrum have been ascribed to a direct effect on the blood vessels, to
reflexes originating from the areas in the heart and lungs supplied by
the vagus nerves or the carotid sinus and to an effect on the central
nervous system. Probably all of these areas are affected to some extent
by veratrum derivatives under specific experimental conditions; however,
it is not clear which contribute most to this depressor response. The
role of the vagus nerves in the depressor action is one of the chief
sources of controversy. Most of the previous investigations have emphasized
the "von Bezold" reflex as the main mechanism of action; it has been
described as a vagal reflex with afferents originating in the left ventricle.
All agree that this reflex produces bradycardia, but the question of
whether the same afferent impulses can evoke vasodilatation by reflex
means is not clear. An adequate explanation of the role of the central
nervous system in the depressor effect has not yet been reported. It would
be desirable to know the mechanism involved in the veratrum-induced depressor
response in the intact animal, therefore an investigation of the cardiovascular
effects of veratrum derivatives was undertaken. Comparison of
past investigations is rendered difficult because of the variety of techniques
employed. In the present experiments, equidepressor doses as
determined by the dog assay method were used.
Although it has been shown that during the depressor effect of
veratrum, vasoconstrictor agents or stimuli produced a qualitatively
normal response, no quantitative data have been previously presented.
Experiments were undertaken to determine whether or not veratrum possessed
any adrenergic, sympatholytic or ganglionic blocking activity. The depressor
effect of "Veriloid" did not alter the pressor response to epinephrine,
1-norepinephrine or splanchnic nerve stimulation; therefore, it
probably does not possess adrenolytic or sympatholytic activity. "Veriloid"
did not alter the pressor response to bilateral carotid occlusion, hence
it probably does not possess ganglionic blocking activity.
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Description
Thesis (Ph.D.)--Boston University.
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