Biomedical subjects
R G Sherding
Publications and source records attributed to R G Sherding.
Cellular localization and hormonal regulation of pancreatic intrinsic factor secretion in dogs.
Gastric mucosal cells are considered to be the principal site of intrinsic factor (IF) production in most mammals. Recent observations in dogs suggest that the pancreas is the major site of IF production in this species. The present study was undertaken to determine the cellular origins of canine pancreatic IF by combining in situ hybridization with immunocytochemistry and to examine the potential role of physiological pancreatic secretagogues, cholecystokinin octapeptide (CCK-8) and secretin, as mediators of canine pancreatic IF secretion. A human IF cDNA probe (J. Hewitt et al., Genomics 10: 432-440, 1991), validated for use in the dog, identified IF mRNA in parietal cells in the gastric fundus, gastric gland cells in the pyloric antrum, and in secretory duct cells of the pancreas. Immunocytochemistry using antibody against rat IF confirmed that these cells, as well as secretory ducts of salivary glands, synthesized an immunoreactive protein. In stimulated secretions of anesthetized dogs, mean 45-min outputs of IF, haptocorrin, and trypsinogen were 13-, 8-, and 16-fold greater during stimulation with CCK-8 than with secretin. No synergistic effects of combined stimulation were observed for IF or haptocorrin, although a synergistic effect was observed for trypsinogen. These findings demonstrate that IF is synthesized in the canine stomach, pancreas, and probably salivary glands and that CCK-8 mediates IF secretion from pancreatic duct cells.
Chylous ascites in three dogs.
Chylous ascites was diagnosed in 3 dogs. Mesenteric lymphangiography was performed in 2 dogs and helped delineate abnormalities of the lymphatic system. The cause of chylous ascites in each dog appeared to be different. In 1 dog, a ruptured mesenteric lymphatic was identified at surgery. Evidence of abdominal lymphatic obstruction was found in another dog. Chylous ascites in the third dog appeared to be a complication of mesenteric lymphangiography for chylothorax.
Serum lipoprotein concentrations and hepatic lesions in obese cats undergoing weight loss.
Serum lipoprotein concentrations, routine serum biochemical values, and morphologic changes of the liver were evaluated in cats undergoing weight loss. Food was withheld from 6 obese and 6 control cats for 3 days (days 0 to 2), followed by feeding 50% of previous food intake for 26 days (days 3 to 28). Percutaneous liver biopsy specimens were obtained from all cats on days 0, 7, 14, and 28. Blood samples for serum biochemical analysis and lipoprotein profiles were obtained on days 0, 3, 7, 14, and 28. All cats lost weight throughout the study, and none developed signs of clinical illness, including those of idiopathic hepatic lipidosis syndrome. Serum total cholesterol concentrations decreased initially in all cats, but rapidly returned to normal after day 3 in obese cats, suggesting altered cholesterol metabolism during dietary restriction. Low-density lipoprotein concentrations decreased throughout the study in control cats, but were unchanged in obese cats. Examination of liver biopsy specimens from each cat revealed minimal lipid accumulation in all specimens, although some specimens contained hydropic degeneration.
Effect of lenperone hydrochloride on gastroesophageal sphincter pressure in healthy dogs.
Treatment of healthy dogs with the butyrophenone derivative, lenperone hydrochloride, at two different doses significantly decreased gastroesophageal sphincter pressure (GESP). No dose-related effect was identified. Individual variation in the response to lenperone hydrochloride was noted which was consistent on a day-to-day basis. Lenperone hydrochloride is unsuitable for chemical restraint of dogs undergoing esophageal manometry because it decreases GESP and because the magnitude of the decrease varies considerably between dogs.
Esophageal acid clearance test in healthy dogs.
Esophageal acid clearance in healthy dogs was evaluated by placing a pH probe in the distal esophagus and determining the number of swallows and time required for esophageal pH to reach 4.0 after injection of a 10 mL bolus of 0.1 N hydrochloric acid. The increase in pH occurred in a stepwise fashion and was associated with esophageal peristalsis as determined by esophageal manometry. The number of swallows required for acid clearance varied from four to 12 with a mean of 8 +/- 1.8. The time required for acid clearance varied from 150 to 480 s with a mean of 285 +/- 75. No significant difference was noted after 0.16 mg/kg of lenperone hydrochloride was given intramuscularly. The esophageal acid clearance test in dogs appears similar to that reported in humans.
Acute hypocalcemia associated with infarction of parathyroid gland adenomas in two dogs.
Two dogs were examined because of anorexia, lethargy, muscle tremors, weakness, and seizures that were associated with an acute onset of hypocalcemia. Both dogs had histories of chronic hypercalcemia. Examination of the parathyroid glands revealed infarction of focal parathyroid adenomas, with atrophy of the remaining parathyroid glands. It was concluded that the acute onset of hypocalcemia was caused by infarction of functional parathyroid adenomas that were previously responsible for the cause of persistent hypercalcemia. Infarction of a parathyroid adenoma should be included in a list of differential diagnoses of acute hypocalcemia in the dog, especially if hypercalcemia has been diagnosed previously.
Intestinal lymphangiectasia associated with chylothorax in two dogs.
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Effects of xylazine administration on serum amylase, pancreas-specific isoamylase and pancreatic polypeptide in normal dogs.
Changes in serum total amylase, pancreas-specific isoamylase and pancreatic polypeptide activities were measured in six dogs following multiple intramuscular injections of xylazine at 0.5 mg/kg of body weight. The activities of those analytes did not change over 24 hours of study.
Clinicopathologic findings resembling hypoadrenocorticism in dogs with primary gastrointestinal disease.
Nine dogs with primary gastrointestinal disease had clinical and laboratory findings resembling hypoadrenocorticism. The dogs had histories of anorexia, weakness or lethargy, diarrhea, vomiting, and weight loss. Hypothermia, dehydration, and emaciation also were detected on physical examination. Hyponatremia, hyperkalemia, and abnormally low Na/K ratios were found on laboratory evaluation, but results of ACTH-response tests were not compatible with hypoadrenocorticism. The primary diagnoses were trichuriasis and salmonellosis in 2 dogs, trichuriasis in 5 dogs, and perforated duodenal ulcer in 2 dogs. Most dogs responded to medical or surgical treatment of their primary gastrointestinal disease, and the original electrolyte abnormalities resolved. These findings emphasize the importance of the ACTH-response test in the diagnostic evaluation of dogs with clinicopathologic findings similar to those of hypoadrenocorticism.
Acute hepatic failure.
Acute hepatic failure is characterized by a sudden catastrophic compromise of hepatic failure that causes clinical signs such as anorexia, depression, vomiting, diarrhea, icterus, and encephalopathy. Injurious hepatotoxins, drugs, infectious agents, or metabolic disturbances can cause acute hepatic failure; however, in many cases, the inciting cause is not determined. Treatment is aimed at controlling complications such as fluid-electrolyte imbalances, hepatic encephalopathy, hypoglycemia, bleeding diathesis, gastric ulcer, sepsis, and endotoxemia, in order to provide time for liver regeneration and recovery.
Canine chronic bronchitis.
The diagnosis and management of the chronic bronchitis patient can be a challenging, but rewarding, task for the veterinarian. The normal respiratory defense mechanisms and the pathophysiologic responses to the pathologic changes are of dramatic importance in understanding the choices of therapy. The keys to successful management of the patient lie in correct assessment of the clinical features and diagnostic procedures and periodic reevaluation of the patient's response to therapy and age/environment-related progression of pathology. Lastly, the clinician must create a realistic attitude for the owner regarding chronically diseased patients.
Serum pancreatic polypeptide and amylase concentrations in dogs with experimentally induced acute pancreatitis.
Serum concentrations of immunoreactive pancreatic polypeptide (IPP) were measured serially for 7 days after experimental induction of acute hemorrhagic pancreatitis in dogs by infusion of oleic acid into the pancreatic duct. The mean serum IPP concentrations in dogs with pancreatitis were increased significantly (P = 0.013) for 96 hours after induction of pancreatitis. Providing food at 108 hours resulted in significant increases (P = 0.032) in mean serum IPP concentrations in sham-operated control dogs compared with dogs with induced pancreatitis. This was attributed to cephalic-phase release of IPP due to a conditioned response that resulted from feeding immediately after each blood sampling. Mean serum IPP concentrations returned to base line more quickly than did mean serum amylase concentrations in dogs with pancreatitis.
Postprandial release of gastric inhibitory polypeptide (GIP) and pancreatic polypeptide in dogs with pancreatic acinar atrophy. Correction of blunted GIP response by addition of pancreatic enzymes to a meal.
In order to evaluate the enteropancreatic hormone axis in dogs with pancreatic acinar atrophy, we measured the release of gastric inhibitory polypeptide and pancreatic polypeptide in response to a standard meal and a meal containing pancreatic enzymes in affected dogs and controls. Postprandial release of pancreatic polypeptide was normal in dogs with pancreatic atrophy and was not affected by addition of pancreatic enzymes to the food. Gastric inhibitory polypeptide was not released after a standard meal in affected dogs, but this blunted response was corrected by the addition of pancreatic enzymes to the food. Feeding the enzyme alone did not stimulate a gastric inhibitory polypeptide response. These results, in part, support similar observations previously reported in children with exocrine pancreatic insufficiency associated with cystic fibrosis. We conclude that dogs with idiopathic pancreatic acinar atrophy can be used as an animal model for future study of enteropancreatic hormonal abnormalities that occur in human beings with exocrine pancreatic insufficiency.
Bentiromide:xylose test in healthy cats.
The N-benzoyl-L-tyrosyl-p-aminobenzoic acid (bentiromide):xylose test for simultaneous evaluation of pancreatic exocrine function and intestinal absorptive function was studied in 8 clinically healthy cats. Plasma p-aminobenzoic acid (PABA) and xylose concentrations were determined before, and at 30, 60, 90, 120, 150, and 180 minutes after, a solution of bentiromide (1 g/100 ml) and D-xylose (10 g/100 ml) was given orally at a dosage of 5 ml/kg of body weight. The peak plasma concentrations for PABA occurred between 60 and 120 minutes, with highest mean value at 90 minutes (7.5 +/- 3.2 micrograms/ml), and for xylose between 30 and 120 minutes, with the highest mean value at 60 minutes (42.6 +/- 17.8 mg/dl). Large SD in plasma PABA and xylose concentrations indicated marked individual variation between healthy cats. It was concluded that (i) large variations between clinically healthy cats may limit the diagnostic usefulness of the bentiromide:xylose test in the cat, and (ii) guidelines for interpretation of plasma PABA and xylose concentrations reported previously for clinically healthy dogs could not be applied to cats because values were lower in cats.
Bone marrow hypoplasia in eight dogs with Sertoli cell tumor.
Eight male dogs with Sertoli cell tumor had pancytopenia and bone marrow hypoplasia attributed to endogenous estrogen myelotoxicosis. Clinical signs were hemorrhage caused by thrombocytopenia, anemia caused by blood loss or diminished erythrocyte production, and infection and fever associated with granulocytopenia. Other signs attributed to hyperestrogenism were feminization and prostatic disease. Two dogs recovered after castration and supportive treatment, but 5 other similarly treated dogs died of hematopoietic failure. One dog was euthanatized.
Simultaneous evaluation of pancreatic exocrine function and intestinal absorptive function in dogs with chronic diarrhea.
The N-benzoyl-L-tyrosyl-p-aminobenzoic acid (BT-PABA):xylose test was evaluated in 5 clinically normal dogs, 5 dogs with pancreatic exocrine insufficiency (PEI), and 7 dogs with intestinal malabsorption. A solution of BT-PABA (1 g/100 ml) and d-xylose (10 g/100 ml) was given orally (5 ml/kg of body weight) to dogs in each group. Plasma p-aminobenzoic acid (PABA) curves were decreased in dogs with PEI and intestinal malabsorption (P < 0.05) but were the lowest in dogs with PEI, compared with clinically normal dogs. Xylose values in dogs with malabsorption were decreased (P < 0.05), compared with clinically normal dogs. Dogs with PEI had plasma xylose values that were intermediate to values in clinically normal dogs and dogs with intestinal malabsorption. Results of BT-PABA:xylose testing were compared with results of sodium PABA:xylose testing, to determine whether decreased PABA values obtained by the BT-PABA:xylose test were caused by free PABA malabsorption or by maldigestion of BT-PABA. The sodium PABA:xylose test was performed in dogs from each group by oral administration of a solution (5 ml/kg) of sodium PABA (0.372 g/100 ml) and d-xylose (10.0 g/100 ml). Plasma PABA values obtained by the sodium PABA:xylose test were similar in each group. Thus, different PABA values obtained by the BT-PABA:xylose test were not caused by PABA malabsorption. Xylose values were similar to values obtained by the BT-PABA:xylose test. It was concluded that: (1) the BT-PABA:xylose test is a practical test for detecting maldigestion or malabsorption in the dog; (2) dogs with intestinal malabsorption may have functional PEI; and (3) decreased PABA plasma values obtained by BT-PABA:xylose testing are not caused by malabsorption of free PABA.
Primary hypoparathyroidism in the dog.
Primary hypoparathyroidism was diagnosed in six dogs with profound hypocalcemia. Muscle tremors, tetany, generalized seizures, ataxia, and behavioral aberrations were the most common clinical signs. Lymphocytic parathyroiditis was found in four of five dogs that were biopsied. The serum concentration of immunoreactive parathyroid hormone was abnormally low in one dog in which it was measured. Treatment with vitamin D and calcium was successful in restoring and maintaining normal concentration of serum calcium in all six dogs. During treatment, large daily doses of vitamin D were required, dose response was unpredictable, serum calcium concentration fluctuated while treatment remained unchanged, and hypercalcemia occurred frequently.