Why the study?
Does chemical sympathectomy modulate the pulmonary and systemic vascular responses to vasoactive agents in anesthetized dogs?
Does chemical sympathectomy modulate the pulmonary and systemic vascular responses to vasoactive agents in anesthetized dogs?
Chemical sympathectomy induces postsynaptic supersensitivity to alpha receptor stimulation and attenuates prostaglandin F2a-induced vasoconstriction in pulmonary and systemic vascular beds.
Does not support clinical adoption; leaves open translation of sympathectomy effects on vasoconstrictor responses.
The primary aim of this study was to determine if the sympathetic nervous system modulates the cardiovascular actions of vasoactive agents. Anesthetized dogs, instrumented to determine pulmonary and systemic vascular resistances, were administered several vasoactive agents prior to and 2 days following chemical sympathectomy with 6-hydroxydopamine (6-OHDA). Classical signs of sympathectomy were used to demonstrate the effectiveness of the chemical sympathectomy regimen. Pulmonary and systemic hemodynamic responses to infusions of histamine and 5-hydroxytryptamine were unaltered by chemical sympathectomy. However, pulmonary and systemic vaso-constriction induced by prostaglandin F2a was attenuated and the pulmonary and systemic pressor responses to phenylephrine were potentiated 2 days after 6-OHDA. These results suggest the development of postsynaptic supersensitivity to α receptor stimulation in both the pulmonary and systemic vascular beds. In addition, an interaction between prostaglandin F2a and the sympathetic nervous system is also suggested.
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Adam Tucker (1980) studied this question.
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