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Diuretics and Nonocclusive Infarcts

Sarko M. Tilkian, MD; Frank K. Daugherty, MD; Robert P. Rood, MD
JAMA. 1975;231(1):25. doi:10.1001/jama.1975.03240130019013.
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To the Editor.—  The article, "Diuretic Agents: Inciting Factor in Nonocclusive Mesenteric Infarction?" (229: 1451, 1974), by John B. Sharefkin, MD, and William Silen, MD, describes three cases of nonocclusive mesenteric infarctions following diuretic and digitalis therapy and suggests hypovolemia, diuretic-induced, together with vasospasm, possibly digitalis-induced, as the mechanism for the infarction. Although some hypovolemia seems to have occurred, the slight elevation in blood urea nitrogen level of two of the patients renders the hypovolemia theory not too impressive.Another more likely explanation may be the hypothesis forwarded by Alexander Leaf, MD,1,2 suggesting cell swelling as the possible cause of nonocclusive infarcts. The cell swelling is caused by potassium efflux coupled with sodium chloride and water influx across the cellular semipermeable membrane, and thus interference with cell metabolism and possibly impingement on micro-circulation. The current knowledge of the mechanisms of adenosine triphosphate (ATP)-dependent active sodium-potassium transport involving the specific


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