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Biomedical subjects

G C Gerritsen

Publications and source records attributed to G C Gerritsen.

At least 37 records · Page 2Linked to original sources
PubMed1981

Capillary basement membrane thickening associated with the small intestine of the ketonuric diabetic Chinese hamster.

Morphometric evaluation of intestinal capillary basement membranes demonstrated a significant thickening in those of ketonuric diabetic Chinese hamsters compared to age-matched nondiabetic controls. A highly significant correlation was found between increased capillary basement membrane thickness and progression of ketonuria. Age was also positively related to elevation in capillary basement membrane thickness of control and diabetic hamsters. Capillary basement membrane thickness of diabetic animals was not significantly related to a combination of progredient ketonuria and advance in age.

Aging↗
PubMed1979

Radiologic abnormalities and autonomic neuropathology in the digestive tract of the ketonuric diabetic Chinese hamster.

Barium x-ray patterns of ketonuric diabetic Chinese hamsters displayed marked dilatation of the stomach, small and large intestine. Hypomotility was manifested by flocculation of barium in the small and large bowel. Impaired transit time was further characterized by prolonged emptying of the stomach (mean 570 min diabetics; 200 min controls) and delayed stool formation (mean 230 min diabetics; and 100 min controls) and passage (mean 457 min diabetics; 210 min controls). Ultrastructural analysis of Auerbach's myenteric plexuses of the small intestine indicated acute degeneration in certain distal, unmyelinated axons. Swelling, deposition of glycogen, aggregation of neurofilaments and dense accumulation of lamellar bodies were observed. The severity and frequency of barium flocculation, glycogen deposition, aggregation of neurofilaments and lamellar inclusion bodies in axons were directly related to duration of ketonuria. The data strongly suggest that autonomic neuropathology in the plexuses of Auerbach may be a critical factor underlying gastrointestinal dysfunction in the ketonuric diabetic Chinese hamster.

Animals↗
PubMed1977

Abnormalities in pelvic visceral nerves. A basis for neurogenic bladder in the diabetic Chinese hamster.

In order to determine whether bladder dysfunction and hydronephrosis in diabetic Chinese hamsters are associated with nerve pathology, the pelvic visceral nerves of diabetic and normal hamsters were examined with histochemical and electron microscopic techniques. Acetylcholinesterase activity was reduced in the nerves and on smooth muscle fibers in the urinary bladder of diabetic hamsters when compared to controls. Depression of enzyme staining was most marked in those hamsters with the most severe hydronephrosis. Frequent examples of aberrant myelination were found in the pelvic plexus and urinary bladder of diabetics. Many of these myelinated fibers exhibited wide periaxonal spaces lined by unusual processes of Schwann cells. An increase in the number of microtubules in axons and circular profiles of Schwann cells, which failed to enclose axons, gave evidence of axonal degeneration or Schwann cell injury in diabetic nerves. These findings suggest that pathologic changes in pelvic visceral nerves may underlie urinary bladder dysfunction in the diabetic Chinese hamster.

Acetylcholinesterase↗
PubMed1976

A study of the morphological changes in the small intestine of the spontaneously diabetic Chinese hamster.

Several morphological changes were observed microscopically in the small intestine of some diabetic Chinese hamsters. Although some alterations lacked statistical significance due to variation, most diabetics displayed a greater incidence and severity compared with nondiabetic controls. The following structural deviations were seen in the small intestines of some diabetics: increased surface area, elevated number of goblet cells per villus, decreased muscle thickness with connective tissue infiltration, reduced number of Auerbach's plexuses, lymphocyte aggregations accompanied by blunted villi, blood vascular lesions and deformed villi due to excessive loss of epithelial cells.

Animals↗
PubMed1975

Responses to arginine of the perfused pancreas of the genetically diabetic Chinese hamster.

Nonketotic, genetically diabetic Cinese hamsters show subnormal pancreatic insulin release and impaired suppression of glucagon in response to glucose. To study the pancreatic effects of other agents, dynamic insulin and glucagon release was measured from the in vitro perfused pancreases of normal and diabetic Chinese hamsters in response to various combinations of arginine (20mM), glucose (100 or 150 mg. per 100 ml.), and theophylline (10 mM). Theophylline alone caused identical insulin and glucagon release in diabetics and normals. Glucose, alone and in the presence of theophylline, caused subnormal insulin release and less suppression of glucagon release in the diabectics than in the normals. Arginine, in the presence of glucose and theophylline, caused excessive glucagon release but nearly normal insulin release in the diabetics. Arginine, in the absence of glucose or theophylline, caused excessive glucagon release in the diabetics and undetectable insulin release in either diabetics or normals. Pancreatic content after perfusion did not correlate with release during perfusion. Infusion of arginine alone markedly decreased the amount of extractable pancreatic insulin and glucagon. These results indicate that the pancreatic alpha cell of the diabetic Chinese hamster responds excessively to arginine, as is seen in the human diabetic. This defect is not related to acute insulin release or the presence of glucose. Further, these results confirm that the diabetic Chinese hamster's alpha and beta cells respond normally to theophylline, but are relatively insensitive to glucose.

Animals↗