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RAYMOND C. ROY, PHD, MD; DUKE B. WEEKS, MD
Winston-Salem, NC

Arch Otolaryngol. 1985;111(4):280-281.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

To the Editor.—In a recent commentary, Brummett¹ drew attention to a common, yet potentially life-threatening, drug interaction between nonselective β-adrenergic blockers and epinephrine. However, there were some serious typographical errors in his article and misleading recommendations as to the appropriate clinical response.

First, β₁ and β₂ have been transposed throughout the commentary. The β₁-receptors, not the β₂, are those found in the heart, which, when stimulated, increase heart rate and contractility.² Epinephrine activates both - and β₂-receptors in blood vessels to mediate the opposing effects of vasoconstriction () and vasodilation (β₂). The net effect of low doses of epinephrine in healthy patients is only an increase in heart rate because of β₁ stimulation.³ Higher doses of epinephrine produce systolic hypertension as well as tachycardia.³ If the β₁- and β₂-receptors are blocked by a . . . [Full Text PDF of this Article]

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