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dc.contributor.authorSwiss, Edward D.en_US
dc.date.accessioned2014-09-09T14:51:07Z
dc.date.available2014-09-09T14:51:07Z
dc.date.issued1954
dc.date.submitted1954
dc.identifier.otherb14658264
dc.identifier.urihttps://hdl.handle.net/2144/8926
dc.descriptionThesis (Ph.D.)--Boston University.en_US
dc.description.abstractVeratrum 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. [Truncated]en_US
dc.language.isoen_US
dc.publisherBoston Universityen_US
dc.rightsBased on investigation of the BU Libraries' staff, this work is free of known copyright restrictions.en_US
dc.subjectCardiovascular systemen_US
dc.subjectVeratrine.en_US
dc.titleThe action of veratrum derivatives on the mammalian cardiovascular system.en_US
dc.typeThesis/Dissertationen_US
etd.degree.nameDoctor of Philosophyen_US
etd.degree.leveldoctoralen_US
etd.degree.disciplinePharmacologyen_US
etd.degree.grantorBoston Universityen_US


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