Pressor responses to norepinephrine in humans before and after corticosteroids.
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Biomedical subjects
Publications and source records attributed to M H WEIL.
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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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Clinical observations have indicated that patients who are in shock and who have coexisting acidosis respond relatively poorly to sympathomimetic amines. In experiments with dogs, it was found that, in the presence of acidosis, the pressor action of epinephrine, norepinephrine and metaraminol was considerably reduced. The effect on cardiac rhythm was also considerably lessened after the pH value of the blood had been lowered. In view of these observations in animals, six human patients with profound shock and acidosis were studied. All had a considerably lessened pressor response to vasopressor agents; then, after elevation of the blood pH by intravenous infusion of a 1-molar solution of sodium lactate, responsiveness was restored. These observations emphasize the desirability of close observation of the acid-base status, and early treatment of acidosis, as an important aspect in the management of patients with shock.
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