PubMed Health⌕ Search

Biomedical subjects

M Bonsack

Publications and source records attributed to M Bonsack.

11 recordsLinked to original sources
PubMed1992

Intestinal radioprotection by two new agents applied topically.

The purpose of this study was to test two novel antioxidant drugs, each capable of inhibiting membrane peroxidation and of free radical scavenging, as topical radioprotectants for the intestine. A loop of rat midintestine was exteriorized and radiated while the remainder of the animal was protected in a lead box. The intestine was first compartmentalized and each segment filled with a test solution. Radiated segments of intestine were compared, drug filled with vehicle filled, and both with normal unradiated intestine. The animals were killed 5 days after 1100 cGy radiation to the exteriorized loop. Crypt numbers and mucosal height were used as the measures of injury protection. On the basis of crypt numbers, the 21-amino steroid (U-74500A) gave approximately 40% and the vitamin E-like compound (U-78518F) gave 60% reduction in crypt loss. The authors conclude that lumenal antioxidant drugs can provide partial protection of the intestinal mucosa from acute radiation damage and that these two specific agents are effective and potentially useful.

Animals↗
PubMed1992

Acute radiation enteritis in rats: bile salts and trypsin.

Surgically exteriorized rat intestine divided into segments containing saline solution, a bile salt binder, or a trypsin inhibitor were radiated (1100 cGy) and subsequently evaluated for histologic damage. Five days after radiation, crypt cell numbers, mucosal height, and mucous cell numbers were significantly greater in segments protected by the binding of bile salts or the absence of trypsin activity compared with saline-bathed mucosa. Thus both proteolytic enzymes and bile salts in the lumen contribute to the acute enteritis that follows a single dose of x-radiation.

Acute Disease↗
PubMed1989

Abdominal radiation causes bacterial translocation.

The purpose of this study was to determine if a single dose of radiation to the rat abdomen leads to bacterial translocation into the mesenteric lymph nodes (MLN). A second issue addressed was whether translocation correlates with anatomic damage to the mucosa. The radiated group (1100 cGy) which received anesthesia also was compared with a control group and a third group which received anesthesia alone but no abdominal radiation. Abdominal radiation lead to 100% positive cultures of MLN between 12 hr and 4 days postradiation. Bacterial translocation was almost nonexistent in the control and anesthesia group. Signs of inflammation and ulceration of the intestinal mucosa were not seen until Day 3 postradiation. Mucosal damage was maximal by Day 4. Bacterial translocation onto the MLN after a single dose of abdominal radiation was not apparently dependent on anatomical, histologic damage of the mucosa.

Abdomen↗
PubMed1985

Proliferation of gastric endocrine cells after vagotomy in the rat.

The effects of truncal vagotomy on gastrin cell and somatostatin cell populations and circulating hormone levels were studied in rats. Truncal vagotomy produced significant gastrin cell hyperplasia, with the largest increase in gastrin cell density observed 2 weeks postvagotomy. Gastrin cell hyperplasia was sustained up to 6 months. Both antral somatostatin cell and corpus somatostatin cell numbers demonstrated significant and sustained increases after vagotomy; the largest increases were observed 2 weeks after operation. Early elevation of circulating gastrin to 3 times the baseline level was followed by sustained, lower level hypergastrinemia. Plasma somatostatin levels were decreased 2 days after vagotomy, with a return to control values 2 weeks after operation. Gastrin cells and somatostatin cells are dynamic populations, capable of changes in both number and secretory function after truncal vagotomy.

Animals↗
PubMed1985

The role of luminal pH in production of gastrin cell hyperplasia in the rat.

Truncal vagotomy is associated with diminished gastric acid production, gastrin cell hyperplasia, and elevated serum gastrin levels. To study the role of reduced antral luminal acidity in the production of gastrin cell proliferation, gastrin cell densities were quantitated in preparations involving exposure of the antral mucosa to a non-acid lumen at different levels of the gastrointestinal tract. Female Sprague-Dawley rats were divided into the following experimental groups: intact controls, shams, antral diverticulum on the jejunum, antral diverticulum on the ileum, and antral diverticulum on the colon. At death, 2 weeks, 2 months, and 6 months after operation, luminal pH was at least 5.8 for each group of rats with antral diverticula. No significant changes in gastrin cell numbers were observed in rats with jejunal or ileal diverticula. For those animals with colonic diverticula, gastrin cell counts were increased 55% at 2 weeks (503 +/- 23 cells per cm versus 320 +/- 13 cells per cm for shams). At 2 months gastrin cell numbers had increased further (639 +/- 54 cells per cm) in rats with antral diverticula on the colon. Gastrin cell proliferation was sustained at 6 months in this group. A factor other than reduced luminal acidity induces gastrin cell proliferation in antral mucosa exposed to colonic content. The responsible agent is not present in the small-bowel lumen. A non-acid luminal environment is not, by itself, a sufficient stimulus for gastrin cell hyperplasia.

Animals↗
PubMed1984

Relationship of antral gastrin cells and serum gastrin to thyroid function in the rat.

Using a quantitative immunocytochemical technique, antral gastrin cell populations in the rat were studied in various states of thyroid function. Simultaneous determinations of circulating serum gastrin were made by RIA. Rats made hypothyroid by ingestion of methimazole (0.01% solution in drinking water for 30 days) demonstrated a significant 32% decrease in gastrin cell density (306 +/- 9/cm vs. 207 +/- 11/cm for controls) associated with a significant 50% decrease in serum gastrin (143 +/- 12 vs. 307 +/- 20 pg/ml for controls). Induction of hypothyroidism and hypoparathyroidism by surgical thyroparathyroidectomy resulted in similarly significant decreases in gastrin cell numbers (229 +/- 12/cm) and serum gastrin (169 +/- 14 pg/ml). Animals that underwent thyroparathyroidectomy followed by T4 replacement (2.5 micrograms/100 g X day, ip) for 30 days had a mean gastrin cell density that was not significantly different from that of controls; serum gastrin was decreased to 207 +/- 11 pg/ml. The administration of excess T4 (200 micrograms/100 g X day, ip) for either 15 or 30 days was associated with a significant increase in gastrin cell numbers (413 +/- 23/cm at 15 days; 352 +/- 21/cm at 30 days). Mean serum gastrin was increased by 82% after 15 days of T4 administration (558 +/- 51 pg/ml) and by 65% at 30 days (506 +/- 36 pg/ml). We conclude that T4 is trophic for gastrin cells in the rat.

Animals↗
PubMed1978

Quantitation of antral gastrin cell populations in the dog.

A method for enumerating G cells in dog antral mucosa by a fluorescent antibody technique was shown to be valid with respect to specificity and reproducibility. The state of intracellular gastrin storage does not influence G cell identification by this technique. To obtain values representative of the entire antrum, all G cells in long strips of antral mucosa must be counted. Results are best expressed as G cells per centimeter length of mucosa. Even with large mucosal samples there are considerable variations in G cell density within a single antrum. The "average" dog antrum contains about 35 million G cells. We observed as much as 2-fold range in G cell density from one dog to another. Each animal should, therefore, serve as its own control when influences on G cell populations are to be studied experimentally.

Animals↗