Search PubMed⌕ Search

Biomedical subjects

J T McCall

Publications and source records attributed to J T McCall.

At least 55 records · Page 3Linked to original sources

Pancreatic, gallbladder, and gastric responses to intraduodenal calcium perfusion in man.

To determine the effect of intraduodenal calcium on pancreatic, gallbladder, and gastric functions in healthy man, a validated perfusion method was employed to quantify total pancreatic, biliary, and gastric outputs during duodenal perfusion of either 6 mM, 12 mM,or 25 mM of elemental calcium (as isotonic calcium chloride solutions). Intraluminal calcium stimulated pancreatic enzyme secretion and gallbladder contraction in a dose-related fashion, achieving comparable responses to those produced by intravenous cholecystokinin-pancreozymin (CCK-z). Responses to calcium were reproducible when repeated in the same individual. Gastric acid outputs and serum gastrin levels increased significantly only with higher calcium perfusions (25 mM). Although duodenal calcium perfusion (25 mM) slightly increased serum calcium concentrations, induced hypercalcemia (by intravenous calcium infusion) of similar magnitude had no effect on pancreatic or gallbladder function. It is suggested that intraduodenal calcium may induce release of CCK-PZ (and/or other neurohormonal factors) from the gut, causing stimulation of these digestive organs.

Adult↗

Time course and zonal variations of ischemia-induced myocardial cationic electrolyte derangements.

Myocardial cationic electrolytes were determined at regular time intervals up to 24 hours after coronary artery ligation in the dog. Replicate electrolyte ratios were computed for different areas of the heart at each time interval. For purposes of statistical analysis, ratios from two border areas and four areas remote from the infarct were pooled as values for ZONE B and ZONE N, respectively, and compared with those from the infarct proper, ZONE I. Ischemia-induced tissue Mg++/Ca++ changes paralleled those of K+/Na+ with respect to time course and zonal variations. In ZONE I, both K+/Na+ and Mg++/Ca++ fell precipitously during the first hour, and the falls became more gradual thereafter, approac hing those of extracellular fluid at 24 hours. Changes in ZONE B, which appeared normal histologically, followed a similar downward trend but differed in magnitude from those in ZONE I (P smaller than 0.01). Changes in ZONE N were small but did not always overlap values in sham-operated dogs. It was concluded that lowered tissue K+/Na+ and Mg++/Ca++ were sensitive, but not specific, indices of myocardial ishemia, and multiple samplings of ionic ratios were essential for proper interpretation of ischemia-induced myocardial electrolyte derangements.

Animals↗

Pigmented corneal rings in a patient with primary biliary cirrhosis.

A patient with primary biliary cirrhosis who had high hepatic, serum, and urine copper levels was found by slit-lamp biomicroscopy to have pigmented corneal rings similar to Kayser-Fleischer rings. Wilson's disease was excluded on the basis of the elevated serum ceruloplasmin and copper levels, the lack of neurological disease despite advanced liver disease, a negative family history, and the typical clinical features of primary biliary cirrhosis. Although the exact chemical nature of the corneal rings is unknown, the cornea may be another tissue associated with elevated tissue copper levels in primary biliary cirrhosis.

Cornea↗

Wilson's disease (hepatolenticular degeneration) of late adult onset: report of case.

Wilson's disease usually has its onset in childhood, adolescence, or early adulthood. The clinical picture of hepatic dysfunction without dysfunction of the central nervous system is more typical of the disease in the child or the adolescent than in the adult. We are presenting the case of a man whose age at onset of the disease was 55 years and who had the hepatic complications of Wilson's disease without clinical evidence of disease of the central nervous system. All patients with chronic hepatitis (chronic active liver disease) or cirrhosis of unknown etiology should be screened for the possibility of Wilson's disease. This screening should include slit-lamp biomicroscopy for Kayser-Fleischer rings, determination of serum ceruloplasmin concentration, and measurement of 24-hour urinary excretion of copper. If doubt exists concerning the diagnosis, either a radiocopper kinetic study, using 64Cu or 67Cu, or, if the patient's condition permits, a liver biopsy with measurement of hepatic copper concentration should be done. The rubeanic stain of hepatic tissue for copper is unreliable in making or excluding the diagnosis of Wilson's disease.

Ceruloplasmin↗