The disadvantaged student.
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Biomedical subjects
Publications and source records attributed to H Schapiro.
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We have reviewed the broad spectrum of disease caused by chemodectomas. This spectrum extends from the benign to the aggressively malignant with many graduations in-between. Our analyses included cases from the literature and nine new cases seen over the past twenty-five years. Surgery as the primary and most definitive form of therapy, is recommended if feasible, with total excision as the goal, in both benign and malignant histologies. An excellent outcome is to be expected in benign cases. At present, no predictor exists to foretell the behavior of malignant lesions, which can range from the aggressive to the slowly progressive. Both radiotherapy and chemotherapy have been tried in malignant cases. No consistent good result has occurred from the use of either. The future will hopefully bring us more effective therapy.
Studies in animals demonstrate a gastric hormonal phase of pancreatic exocrine secretion. Endogenous or exogenous gastrin causes a marked elevation in the pancreatic enzymes and a lesser increase in the pancreatic volume and bicarbonate. It is possible that these "gastrin" effects may be the basis of a "cephalic" phase of pancreatic secretion. These observations have been only partially confirmed in human subjects with and without the Zollinger-Ellison syndrome. The physiologic importance of these ecbolic actions as well as a possible trophic effect remains to be elucidated.
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Chemoneurolysis of the canine antral submucosa with 25% ethyl alcohol solutions reduced ulcer formation and increased the survival times in animals subjected to the Exalto-Mann-Williamson ulcer-producing procedure.
Infiltration of the gastric fundic submucosa with 25 per cent ethyl alcohol markedly reduces the mean acetylcholinesterase rate of activity in the fundic mucosa and submucosa. This can be considered as evidence for a reduction in the acetylcholine concentration caused by a destruction of the submucosal plexus.
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Glucagon can depress normal animal and human pancreatic exocrine secretions and modify experimentally-induced pancreatitis in animals. It has yet to be demonstrated that glucagon has any efficacy in the treatment of the diseased pancreas in man. Glucagon might act on the exocrine pancreas by 1. reducing pancreatic blood flow, 2. decreasing gastric secretion, 3. lowering serum calcium levels by the release of calcitonin, 4. acting to inhibit the secretin mechanism, 5. causing a hyperglycemia and 6. degranulating pancreatic acinar cells. While a reduction in pancreatic blood flow, an inhibition of the secretin mechanism and a hyperglycemia seemed to have been ruled out as possible mechanisms of action, there is too little available data to effectively speculate on the mechanism(s) of action of glucagon on the exocrine pancreas.
Double denervated gastric pouches were constructed in dogs. One gastric pouch served as a control, and the other gastric pouch had its submucosa infiltrated with 25% ethyl alcohol (submucosal chemoneurolysis). Neurolysis of these gastric pouches did not alter their histological appearance but did eliminate their gastric secretory responses to histamine, meat and pentagastrin. The dogs exhibited elevated serum gastrin levels after feeding.
Double denervated gastric pouches were constructed in dogs. One gastric pouch served as a control, and the other gastric pouch had its submucosa infiltrated with 25% ethyl alcohol, (submucosal chemoneurolysis). Neurolysis of these gastric pouches eliminated their gastric secretory responses to histamine, meat and pentagastrin without altering their histological appearance. Transplantation of 75% of the gastric antrum into the colon caused a hypergastrinemia and increased the sensitivity of the control gastric pouches to the various stimuli but had no such effect on those gastric pouches infiltrated with ethyl alcohol.
Acute hemorrhagic pancreatitis was created in dogs using the closed duodenal loop technique. After 18 hours, a a constant rate of pancreatic exocrine secretion was stimulated with secretin. A direct relationship was observed between the percentage inhibition of secretin-stimulated pancreatic exocrine flow and the dose of antidiuretic hormone administered to dogs with acute hemorrhagic pancreatitis. The acute hemorrhagic pancreatitis reduced the sensitivity of the exocrine pancreas to secretin and antidiuretic hormone.
Ethyl alcohol infiltration of the submucosa of canine denervated gastric pouches markedly reduced the gastric secretory responses to histamine and food without changing the histologic appearance. It is postulated that the ethyl alcohol destroyed the submucosal nerve plexus which regulates the parietal cells.
Acute hemorrhagic pancreatitis was experimentally induced in the dog by the closed-duodenal-loop technique. The disease process was modified and partially reversed by intravenous infusions of vasopressin, as indicated by some of our tests for pancreatitis as well as histologic examination of the pancreas.
Vasopressin (ADH) is known to reduce secretin-stimulated pancreatic exocrine secretion. The present study attempts to relate this inhibitory effect to the vasoconstrictive potency of ADH. Regional blood flow in most of the vascular areas. The greatest reduction in blood flow was seen in the gastrointestinal area especially in the left gastric artery, cranial and caudal pancreaticoduodenal arteries, as well as the cranial and caudal mesenteric arteries. Renal blood flow was not altered by those concentrations of ADH that reduced gastrointestinal blood flow. ADH reduced pancreaticoduodenal blood flow in concentrations comparable to those concentrations that reduced pancreatic secretory flow. The reduction of gastrointestinal blood flow was due to increased impedance and not to diminished cardiac inotropy.
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A direct relationship was observed between the percentage inhibition of secretin-stimulated pancreatic exocrine flow and the dose of antidiuretic hormone administered with the minimal effective concentration being 0.75 m units/kg or 0.012 m units/ml. An alteration in the molecular configuration of the antidiuretic hormone modified its ability to inhibit secretin-stimulated pancreatic exocrine secretion.