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AN EXPERIMENTAL ETIOLOGIC STUDY

RAYMOND GREGORY, M.D.; PAUL L. EWING, Ph.D.; HARRY LEVINE, M.D.

Arch Intern Med. 1945;75(6):381-394.

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

Many workers¹ have confirmed the original observations of Sanguinetti² that an elevation of the nitrogen content of the blood may be associated with gastroenteric bleeding. Opinions concerning the pathogenesis of this condition are not in agreement. Sanguinetti² attributed the azotemia to absorption of protein from the intestine, augmentation of general metabolism and chloropenia. Alsted^1c studied the condition in patients and suggested blood pressure effects and intestinal absorption as possible causes. Bookless^1s expressed the belief thatthe elevated blood urea levels were mainly due to rapid breakdown of tissue protein. Black^1r suggested and Johnson¹⁰ stated that azotemia does not occur in patients in the absence of reduction in renal function. The former believed the evidence inadequate to establish renal impairment as the causal mechanism. Stevens, Schiff, Lublin and Garber^1g reported that elevation of blood urea associated with gastrointestinal bleeding was not due to impairment of renal function in the . . . [Full Text PDF of this Article]

Author Affiliations
GALVESTON, TEXAS

From the Departments of Medicine and Pharmacology, The University of Texas School of Medicine.

Footnotes
Hoffman-LaRoche, Inc., supplied the heparin used in these studies.

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