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Simon Gelman, MD, PhD
Birmingham, Ala

JAMA. 1985;254(13):1721.

	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.—

The observations presented in the letter by Chen et al¹ are very intriguing. It is possible that diminished intestinal blood flow during sodium nitroprusside-induced hypotension caused the ileus; however, an alterative explanation is conceivable. It has been well documented that sodium nitroprusside-induced hypotension is accompanied by an increase in catecholamine release.² Catecholamines, however, decrease intestinal motility by blocking the release of acetylcholine from intrinsic cholinergic neurons and by direct action on smooth muscles and, therefore, might cause adynamic ileus.^3,4 Any kind of sympathetic blockade during the postoperative period has been effective in the treatment of postoperative adynamic ileus.^4,5

Regardless of the mechanism involved, the clinical observations by Chen et al¹ are clinically relevant. It is conceivable that the combination of sodium nitroprusside with β-blockers, which is frequently used in clinical practice, might be accompanied by a lower incidence of adynamic ileus than . . . [Full Text PDF of this Article]

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