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Biomedical subjects

M Donowitz

Publications and source records attributed to M Donowitz.

169 records · Page 10Linked to original sources
PubMed1975

Glucagon secretion in acute and chronic pancreatitis.

Plasma pancreatic glucagon concentrations were determined in the basal state and after the infusion of alanine in 10 patients with acute pancreatitis (5 in an initial episode of pancreatitis), in 10 patients with chronic pancreatic insufficiency, and in 21 healthy controls. In acute pancreatitis, basal glucagon levels were nine times normal but were higher during the initial attack than with a history of previous attacks. The glucagon response to alanine was also increased threefold to fourfold in initial attacks. In contrast, after recovery from the initial attack of acute pancreatitis, during acute episodes of pancreatitis in patients with a history of previous attacks, and in patients with pancreatic insufficiency, alanine failed to elicit a consistent rise in plasma glucagon. The data suggest that hyperglucagonemia may contribute to the hyperglycemia of acute pancreatitis, particularly during the initial episode. Loss of alpha cell responsiveness to alanine provides a sensitive index of previous pancreatitis.

Acute Disease↗
PubMed1975

Effect of dioctyl sodium sulfosuccinate on colonic fluid and electrolyte movement.

These studies evaluated the effect of dioctyl sodium sulfosuccinate (DSS), a detergent and the active ingredient of some commercially available stool softeners, on intestinal fluid and electrolyte movement. DSS produced water, sodium and chloride secretion into the in vivo rat cecum. This secretion readily reverted to net absorption following replacement of DSS by isotonic saline. In in vitro studies, DSS increased the short circuit current and diminished sodium absorption. The increase in short circuit current was not observed either when HCO3 and chloride were absent from the incubation solution or when theophylline was present. DSS also significantly increased mucosal cyclic adenosine monophosphate levels. These results which are similar to previous studies of the effect of cholera enterotoxin on ileal mucosa and bile salts on colonic mucosa are consistent with the proposal that DSS stimulates fluid and electrolyte secretion which is mediated by increased mucosal cyclic adenosine 3':5' monophosphate.

Animals↗
PubMed1975

Effect of Shigella enterotoxin on electrolyte transport in rabbit ileum.

Shigella dysenteriae I is one of several bacteria which produces an enterotoxin capable of stimulating intestinal water and electrolyte secretion. Unlike cholera and Escherichia coli enterotoxins which have been shown to increase intracellular cyclic adenosine monophosphate levels in the small intestine, the mechanism by which shigella enterotoxin causes intestinal secretion is not known. To study shigella enterotoxin-stimulated intestinal secretion, rabbit ileal mucosa exposed in vivo to Shigella dysenteriae I enterotoxin was studied in vitro in a modified Ussing chamber. Fluid and electrolyte accumulation occurred in vivo and net sodium secretion was present in vitro in the enterotoxin-exposed tissue in contrast to net sodium absorption in control mucosa. Short-circuit current (Isc) was similar in shigella enterotoxin-exposed tissue compared with control tissue. The increase adenosine monophosphate was similar to enterotoxin-exposed and control mucosa. The addition of glucose resulted in a smaller increment of Isc in shigella enterotoxin-treated tissue. Mucosal cyclic adenosine monophosphate levels in enterotoxin-exposed mucosa did not differ from those of control. These results indicate that the characteristics of rabbit ileal mucosa exposed to shigella enterotoxin and cholera enterotoxin markedly differ, although both produce electrolyte secretion both in vivo and in vitro. These studies further suggest that, in contrast to its role in cholera enterotoxin-induced intestinal secretion, cyclic adenosine monophosphate may not be in the mediator of shigella enterotoxin stimulation of intestinal fluid and electrolyte secretion.

Animals↗
PubMedDate not supplied

Drug therapy for diarrheal diseases: a look ahead.

The gastrointestinal tract is involved in both absorption and secretion of electrolytes and water, with absorption as the predominant process. In diarrheal diseases this balance is disturbed, and the result is net secretion. Most of the drugs used for the treatment of diarrhea at least partially act by stimulating absorption only, both stimulating absorption and inhibiting secretion, or inhibiting secretion only. The therapeutic usefulness of an antidiarrheal agent depends on how efficiently it alters secretion and/or absorption and on how few systemic adverse reactions it causes. When more information on the regulation of absorption and secretion has been accumulated, it may be possible to develop new drugs that can be aimed directly at these processes.

Anti-Inflammatory Agents↗