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Previous studies in rats showed that the administration of recombinant human growth hormone markedly increased intestinal absorption of electrolytes and water and suggested that growth hormone would be a useful antidiarrheal agent. We therefore examined the effect of recombinant human growth hormone on the human jejunum in vivo, using a triple lumen nonabsorbable marker technique. Healthy subjects were studied on two different test days, one as a control and a second where recombinant human growth hormone was injected subcutaneously in a dose of 100 microg/kg. With this dose we achieved equal or higher growth hormone serum levels than in previous rat studies. However the administration of recombinant human growth hormone did not stimulate absorption or inhibit secretion of water and electrolytes in the human jejunum in vivo. We believe that the discrepancy between humans and rats is most likely due to the species difference rather than to differences in methods that were used. Therefore recombinant human growth hormone cannot be considered a useful proabsorptive antidiarrheal agent in humans.

In people with constipation, it is not known if decreased frequency of defecation is associated with abnormalities in the weight or in the consistency of stools or if the weight or the consistency of stools correlates with the severity of various discomforts associated with bowel movements. In neither normal nor constipated subjects has the consistency of stools been carefully correlated with their relative contents of water and solids. Our aim was to gain insight into these questions. Twenty subjects with idiopathic chronic constipation and 20 age- and sex-matched control subjects were recruited by advertisement. Stools were collected for one week. After each bowel movement, the subject's perception of various discomforts associated with the bowel movement were recorded. The stools were then analyzed. The results and conclusions were as follows: (1) Stool weight per bowel movement was similar in the two groups but stool weight per week was markedly reduced in constipated subjects. (2) Reduced stool weight per week in constipated subjects was due to a nearly proportional reduction in stool water and stool solids output. (3) Using data from both groups, there was a curvilinear correlation between percent insoluble stool solids and stool hardness, as measured by a texture analyzer; hardness increased only slightly as percent insoluble solids increased between 7 and 20%, but hardness increased dramatically when percent insoluble solids exceeded 25%. (4) Only 6% of stools from constipated subjects (2 of 34) had abnormally high values for percent stool solids and physical hardness. (5) In subjects with constipation, the severity of various discomforts associated with bowel movements (such as straining) correlated poorly with the weight or the hardness of stool that was produced by the bowel movement.

The response of the colon to aldosterone is believed to be an important adaptive mechanism to excessive sodium losses in diarrhea. However, the degree to which mineralocorticoid activity actually influences fecal output of sodium in people with diarrhea is unknown. To gain insight into this question, 10 normal people were treated with placebo, fludrocortisone (an aldosterone agonist), and spironolactone (an aldosterone antagonist) during three experimental periods lasting nine days. On days 5-8, diarrhea was induced by ingestion of phenolphthalein. Diet was controlled. Fecal sodium was 40 meq/day on placebo and 29 meq/day on fludrocortisone, consistent with mineralocorticoid stimulation of intestinal sodium absorption. However, contrary to our expectations, spironolactone therapy was also associated with a fall in fecal sodium output, to 28 meq/day. To explain this paradoxical effect of spironolactone, we suggest that sodium depletion caused by spironolactone's natriuretic action on the kidney caused the release of an unknown stimulant of intestinal sodium absorption, whose action more than overcame the reduced colonic absorption resulting from inhibition of aldosterone activity by spironolactone. This interpretation implies that the intestinal adaptation to sodium depletion in diarrhea involves both aldosterone and an aldosterone independent factor, working in concert to reduce fecal sodium output.