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
Hudson JD, Joynt RJ. Water Retention Following. Arch Neurol. 1967;16(6):624–627. doi:10.1001/archneur.1967.00470240062008
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