Abstract
Hemodynamic studies have demonstrated that the fall of blood pressure in shock caused by endotoxin in dogs does not result primarily from dilatation or “vasomotor collapse.” Indeed, vasoconstriction is increased and may be excessive. Progression of shock has recently been blamed on such excessive vasoconstriction. For this reason the use of sympathomimetic drugs as vasopressor agents has been challenged and sympatholytic or adrenolytic agents have been recommended.
In the present study, vasopressor and vasodilator drugs were used for the treatment of shock in dogs caused by endotoxin. Vasodilator drugs, when used after the onset of shock, hastened a fatal outcome but vasopressor agents were not detrimental when used in moderate doses.
The effectiveness of the vasopressor agent is not necessarily due to a primary vasoconstrictor action on arteries and arterioles, as previously assumed.
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Selected References
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