Eleven cases with acute hemorrhage and necrosis of the bowel are described. In all cases there was high dosage of digitalis and definite toxicity in seven. Digitalis was considered as the main associated factor, especially since there was no mesenteric arterial involvement and, in four cases, there was no congestive failure at autopsy. Hepatic vein or sinusoidal sphincter constriction with resulting portal splanchnic venous congestion was considered as possible mechanisms by which digitalization produced this syndrome.

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The concentration of galactose in the blood stream at determined intervals after its ingestion has been proposed as a clinical test of intestinal absorption (1). It is said not only to indicate the rate at which galactose is absorbed from the intestine, but also to be a means of measuring the ability with which and the rate at which the intestinal mucosa absorbs various substances by the mechanism of phosphorylation (1 to 4). Some workers, finding by this procedure that the thyrotoxic patient shows a higher galactose curve than does the normal subject, have attributed this result to a specific accelerating action on intestinal absorption by the thyroid hormone (2 to 5).The blood concentration of a substance following its ingestion, however, is not dependent solely on the capacity of the intestinal mucosa to absorb it. First of all, and most important, it is necessary to know whether or not, and to what extent, the material reaches the absorbing surface, and so is available for absorption. The hexoses are absorbed chiefly from the duodenum and jejunum (6 to 9), and from the stomach only when in hypertonic solution (10, 9). Consequently, alterations in gastric and intestinal motility, whether due to organic or functional disturbances, may profoundly affect the availability of the ingested galactose in the absorbing area (6, 29b, 29c). In spite of the experimental evidence that glucose and galactose orally administered are absorbed at a constant rate and independent of their concentration (11,12,8), this holds true only within certain limits (13, 6). When widely varying concentrations of a sugar are introduced directly into the intestine the absorption rate is proportional to the concentration (15, 29d, 31, 32, 36).Secondly, it has been demonstrated in animals that irrespective of the actual rate of hexose absorption, the concentration in the blood is chiefly dependent on metabolic factors (11,12). In this respect the liver is the principal, though not the sole, organ involved (14, 15, 19b, 24, 35). Hepatic dysfunction especially has been held responsible by some authors for the hypergalactemia found after the ingestion of that sugar in the thyrotoxic patient (29a). Furthermore, in such a condition, as well as in cases with various nutritional, endocrine, and urinary tract disturbances, the renal output of the sugar is often altered (16 to 24, 14, 15). Thus the rate of its excretion constitutes a third' factor that influences the concentration of galactose in the blood (24, 29e).Finally, it has been claimed, as we shall show, that the blood concentration of galactose is in some way affected by the coincident concentration of glucose (15,16,20,21,25).In an attempt to obviate some of these disturbing factors, we have employed the absorption technique devised by Nicholson and Chornock (26), which makes possible over a fixed period of time the presence of a known quantity of the galactose in a predetermined area of the intestinal tract. Thus it measures accurately the availability of the galactose for absorption and t...