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J. Douglas Hudson, MD; Robert J. Joynt, MD

Arch Neurol. 1967;16(6):624-627.

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

It is well known that after stress of various types, there may be a diminished output of urine which, in most instances, has no deleterious effect. Pringle et al¹ first noted this in 1905 on patients after surgical procedures. It has also been observed following trauma and general anesthesia.^2,3 This response has been extensively investigated and various hypotheses have been offered, such as depression of renal blood flow or conservation of sodium secondary to hormonal influences. Objections to these hypotheses were that the change in renal blood flow is usually transient, and the decrease in urinary output occurs prior to sodium conservation.⁴ The absence of this response in patients with diabetes insipidus, the characteristics of the urine (low volume and high specific gravity), and the similarity in blood and urine values to those of patients given vasopressin injection (Pitressin) and a water load suggested that there . . . [Full Text PDF of this Article]

Author Affiliations
From the departments of neurology and radiology (neuroradiology) and the Neurosensory Center, College of Medicine, University of Iowa, Iowa City.

Footnotes
Submitted for publication June 13, 1966; accepted Jan 21, 1967.

Read by title before the American Neurological Association, Washington, DC, June 13-15, 1966, and read before the fourth annual meeting of the American Society of Neuroradiology, Washington, DC, June 15-16, 1966.

Reprint requests to University of Rochester School of Medicine, 260 Crittenden Blvd, Rochester, New York 14620 (Dr. Joynt).

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