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Biomedical subjects

M E Bonsack

Publications and source records attributed to M E Bonsack.

13 recordsLinked to original sources
PubMed2000

Abdominal adhesions to prosthetic mesh evaluated by laparoscopy and electron microscopy.

BACKGROUND: Most adhesion experiments involve observations at a single time point. We developed a method to evaluate abdominal adhesions to surgical mesh by sequential laparoscopy. STUDY DESIGN: An abdominal wall defect was created in rats and repaired with polypropylene mesh. Sequential laparoscopic evaluation of adhesion formation was performed in each animal. The percentage of mesh area involved was scored (0% to 100%). At various time intervals animals were sacrificed and samples were obtained for light and scanning electron microscopy. RESULTS: Adhesions were already present on day 1, increased by day 7, and did not progress thereafter. Mesh surfaces free of adhesions were covered with a confluent mesothelial cell layer, first seen by scanning electron microscopy on day 5 and complete by day 7. CONCLUSIONS: Intraabdominal adhesions are best studied by sequential laparoscopy. Adhesions develop within 1 day of prosthesis placement. Adhesion-free surfaces are carpeted with mesothelial cells by day 7 and remain free thereafter, for duration of study.

Abdomen↗
PubMed2000

Seprafilm reduces adhesions to polypropylene mesh.

BACKGROUND: Adhesions to polypropylene mesh used for abdominal wall hernia repair may eventuate in intestinal obstruction or enterocutaneous fistula. A Seprafilm Bioresorbable Membrane translucent adhesion barrier has been shown to inhibit adhesions. This investigation was designed to determine if Seprafilm alters abdominal visceral adhesions to polypropylene mesh. METHODS: A 2.5-cm square abdominal muscle peritoneal defect was created and corrected with polypropylene mesh. Mesh alone was used in 17 rats. In another 17, the Seprafilm membrane was applied between the viscera and the mesh. Five animals had the bioresorbable membrane placed in the subcutaneous space and between the mesh and the viscera. Laparoscopy was performed 7, 14, and 28 days later to evaluate adhesions as a percentage of mesh surface involved. RESULTS: Polypropylene mesh alone was associated with adhesions in every rat. The average area involved was 90%, the minimum was 75%. Adhesions were present within 24 hours and progressed up to 7 days with no change thereafter. When the Seprafilm barrier was used, the mean area involved was 50%. In 16 such rats, the area involved was smaller than any control animal. No adhesions formed in 5 animals. Scanning electron microscopy demonstrated a mesothelial cell layer covering the mesh after 4 weeks. CONCLUSIONS: The use of the Seprafilm adhesion barrier resulted in a significant reduction of adhesion formation to polypropylene mesh (P <.001).

Abdomen↗
PubMed1999

Radioprotection of the intestinal mucosa of rats by probucol.

Probucol is a lipid-regulating drug that also has antioxidant properties. This study was designed to test the possibility that probucol could provide radioprotection of the intestine when administered either intralumenally or systemically. Tissue damage was evaluated histologically by quantifying the number of crypts per circumference and the mucosal height. Animals were sacrificed 5 days after 11 Gy of X irradiation. In one series of experiments, a loop of mid small bowel was exteriorized operatively and compartmentalized into segments, each filled with probucol or saline. Intralumenal administration of probucol prior to irradiation led to a significantly greater number of crypts per circumference and mucosal height compared to saline-filled irradiated controls. In another series of experiments, five groups of rats were irradiated: (1) probucol in the small bowel lumen, (2) intravenous probucol, (3) probucol by gavage, (4) probucol added to standard rat chow and (5) saline control. In the rats given probucol intravenously prior to X irradiation, crypt numbers and mucosal height were significantly enhanced. Probucol given by gavage also resulted in protection. Rats fed a diet containing probucol showed no significant protection. Topical administration was more effective than systemic. Probucol protects the intestinal mucosa from acute radiation damage when given topically, intravenously or by gavage, but does not do so when given as a dietary supplement.

Animals↗
PubMed1998

Radioprotection of the rat intestinal mucosa by tirilazad.

PURPOSE: To assess intestinal radioprotection by systemic or lumenal tirilazad mesylate and to test potential tumour radioprotection. MATERIALS AND METHODS: Segments of the mid small bowel were surgically exteriorized. Tirilazad was given either intravenously or intralumenally 30 min prior to 11 Gy of X-irradiation to the exteriorized intestine. Tissues were harvested 5 days later to measure crypts per circumference and mucosal height. Potential tumour protection was assessed in a mouse sarcoma model. Tumours implanted in the hind limb were allowed to grow until a standard volume was attained, then irradiated (10 Gy) 30 min after intravenous (i.v.) administration of saline or tirilazad. Tumour growth was recorded for the next 22 days to determine if pretreatment with tirilazad interfered with radiation effects. RESULTS: Systemic tirilazad provided no protection against intestinal damage and did not alter tumour growth after irradiation. Topical tirilazad yielded highly significant protection of intestinal mucosa. CONCLUSIONS: These preliminary observations showed that topical tirilazad diminished radiation enteritis. Systemic drug had no effect on the severity of damage to the intestine nor did it inhibit radiation effects on a tumour.

Animals↗
PubMed1995

Intestinal radioprotection by vitamin E (alpha-tocopherol).

OBJECTIVES: The major objective of this study was to test vitamin E as a potential radioprotectant for the small bowel of the rat. SUMMARY BACKGROUND DATA: Vitamin E has previously been shown to provide radioprotection in animal models: increased survival after whole-body irradiation, diminished absorptive malfunction, and modest diminution in postirradiation hemolysis. The lumenal route for intestinal radioprotection has not been tested. METHODS: Rat mid-small bowel was surgically exteriorized and segmented by ties into compartments, each of which was filled with a test solution 30 minutes before 1100 cGy of x-irradiation was administered. After the rats were killed 5 days later, the various segments were evaluated for surviving crypts, mucosal height, and goblet cell preservation. Lumenal agents included alpha-tocopherol phosphate and alpha-tocopherol acetate. In a separate study, dietary supplements of alpha-tocopherol were given for 10 days before irradiation, and the same irradiation sequence was carried out. RESULTS: Small bowel crypt cell numbers, mucosal height, and goblet cell numbers were significantly protected from radiation effects by dietary alpha tocopherol pretreatment and by lumenal application of the vitamin. CONCLUSIONS: These studies indicate that vitamin E can serve as a partial protectant against acute irradiation enteritis, whether given as chronic oral systemic pretreatment or as a brief topical application.

Animals↗
PubMed1994

Radioprotection of the rat small intestine with topical WR-2721.

BACKGROUND: The classic radioprotectant WR-2721 has been shown to reduce the severity of small bowel injury when administered systemically shortly before irradiation is delivered. This study tested the possibility that WR-2721 could provide protection when applied topically to intestinal mucosa. The second question addressed was the influence of pH on the effectiveness of this agent. METHODS: The model used involved irradiation of exteriorized rat small bowel. A length of intestine was compartmentalized. The various individual segments were filled with a lumenal Tris buffer (pH 9), WR-2721, or a combination of these two, then irradiated with 1100 cGy. The animals were sacrificed 5 days later. Surviving crypt cells and mucosal height were the criteria used to quantitate mucosal injury. RESULTS: The pH 9 buffer alone provided a small (16%) but significant preservation of crypt cell numbers. WR-2721 improved crypt survival by 54% at neutral pH, 83% at pH 9. CONCLUSIONS: These data indicate that WR-2721, when applied topically to the small bowel mucosa of the rat before irradiation, provides substantial protection against radiation damage. The degree of benefit is amplified greatly when the drug is in an alkaline medium.

Administration, Topical↗
PubMed1994

Misoprostol in the intestinal lumen protects against radiation injury of the mucosa of the small bowel.

Systemically administered misoprostol, a PGE1 analog, has been shown to be an intestinal radioprotector. The purpose of this study was to determine if administration of misoprostol into the intestinal lumen can also reduce the severity of acute radiation enteritis. The rat small bowel was operatively exteriorized and segmented by means of suture ties. The remainder of the intestine and the rat were shielded in a lead box. Misoprostol was introduced into the lumen in various doses. After 30 min exposure to misoprostol, the isolated, exteriorized, segmented bowel was subjected to 11 Gy X irradiation. Five days later the animals were sacrificed and the intestines harvested for evaluation. Surviving crypt numbers per circumference and mucosal height were the criteria used for quantification of damage. Mucosa exposed to misoprostol at the time of radiation delivery showed significantly increased crypt numbers and mucosal height compared to adjacent saline-filled intestine.

Animals↗
PubMed1993

Lumenal route for intestinal radioprotection.

The intestine, being highly sensitive to radiation injury, is the limiting factor in the delivery of abdominal and pelvic radiation. Attempts at intestinal radioprotection have generally involved systemic administration of agents that are moderately toxic and that may protect the target malignancy. The lumenal route for intestinal radioprotection provides a high concentration at the mucosa without significant systemic effects. This paper reviews studies of intestinal radiation radioprotection by intralumenal agents. Our model involved irradiation of exteriorized rat small bowel containing drugs in isolated segments. Surviving crypts were quantitated as a measure of injury 5 days later, and the individual segments were compared. Modest protection was found with lumenal alkalinization and with neutralization of bile salts or pancreatic enzymes. Similar protection was identified with some nonsteroidal anti-inflammatory agents, methylprednisolone, and selected antioxidants. Marked protection was observed with lumenal Lazaroid.

Animals↗
PubMed1992

The influence of lumenal pH on the severity of acute radiation enteritis.

The severity of acute radiation injury to small bowel mucosa was studied as a function of lumenal pH at the time of irradiation. Rats were anaesthetized and 15 cm of mid small bowel was exteriorized with the rest of the animal and intestine shielded in a lead box. The target intestine was segmented into three portions, each of which was filled with Tris buffer, adjusted to pH 5, 7 and 9 respectively. Twenty minutes later the exteriorized bowel was given 1100 cGy X-irradiation. Rats were sacrificed 4, 5 and 6 days later and the intestine histologically assessed for injury. The indices of injury were surviving crypt numbers, mucosal height and mucus-containing goblet cells. To verify that pH was the critical variable an identical study was done employing three buffers chemically different from Tris: MES (pH 5.5), ADA (pH 7), and CAPSO (pH 9). These animals were sacrificed 5 days postirradiation. For all three parameters, and on each day postirradiation, the pH 9 segment showed less damage than did the segments with lumenal pH 7 or 5. We conclude that lumenal pH at the time of irradiation plays a significant role in the severity of acute mucosal injury. Alkaline pH is relatively protective.

Animals↗
PubMed1979

Gastrin cell populations after highly selective vagotomy in the dog.

Highly selective vagotomy was performed on five dogs. Postoperatively, gastrin cell (G cell) hyperplasia occurred in all dogs. Mean preoperative G cell numbers increased from 350 to 530/cm mucosal length (p less than 0.02). Antral tissue gastrin also increased by 100 per cent (6.7 x 10(6) to 13.7 x 10(6) pg/gm tissue, p less than 0.05). Basal and stimulated serum gastrin were unchanged following highly selective vagotomy. The cause for G cell hyperplasia is not clear, but is probably multifactorial.

Animals↗
PubMed1979

Adrenal corticosteroids cause gastrin cell hyperplasia.

Chronic exogenous high dose adrenal cortical steroid administration to dogs resulted in a 137% increase in G-cell mass with an associated enhancement of peak serum gastrin levels. Adrenalectomy caused a halving of G-cell numbers without significant changes in serum gastrin levels. Adrenal cortical steroids appear to have an important trophic role for the G-cell.

Adrenal Cortex Hormones↗