John P. Delaney

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.

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.

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.

The Role of Luminal Contents in Radiation Enteritis

A guinea pig model was used to evaluate luminal content as a factor in the development of acute radiation enteritis. Surgical bypass of one half of the small bowel created an isolated segment free of luminal contents. Radiation effects on this empty intestine were compared with effects on bowel in continuity, on intestine containing bile only, and on intestine containing pancreatic enzymes plus food. The animals were subjected to a single dose of 1600 rad via an abdominal port and killed 4 days later. Surviving crypts per circumference provided one index of the severity of the injury. Intestinal damage was further evaluated by histologic grading. Surviving crypts were significantly fewer for irradiated segments of bowel containing any of the components of the intestinal stream compared to either nonirradiated controls or irradiated but empty bowel. Histologic scoring revealed a gradation of injury, with progressively more severe damage in empty irradiated bowel, and in intestine containing only pancreatic secretion, bile, and all components of the luminal stream. We conclude that both bile and pancreatic secretions in the lumen enhance acute radiation‐induced small‐bowel injury.

Gastrointestinal Blood Flow in the Dog

That the radiorubidium distribution method provides good estimates of blood flow to the gastrointestinal organs was demonstrated by comparing the arterial concentration course of the isotope with the simultaneous venous concentration for the individual organs. Blood flow to stomach, intestine and colon are accurately assessed by this method. Estimates for pancreas, gall bladder, esophagus and duodenum are probably correct. Average perfusion rates in the pentobarbital anesthetized dog are, in cc/min.g of tissue: —esophagus, 0.21; stomach, 0.51; duodenum, 0.70; small intestine, 0.72; colon, 0.82; pancreas, 0.60; and gall bladder, 0.39.

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.

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.

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.

Reflux gastritis: The consequences of intestinal juice in the stomach

The consequences of exposure of the intact stomach to intestinal contents were examined in six dogs. Diversion of duodenal contents through the stomach lead to the following changes: histologic gastritis in both antrum and corpus, increase in resting and postprandial serum gastrin levels, increased parietal cell density in four of six animals, and enhanced maximal acid secretory capacity in three of six animals. No significant changes were seen in insulin-stimulated acid secretion, insulin-stimulated pepsin secretion, antral gastrin levels, or G cell numbers. We conclude that chronic exposure of the intact stomach to duodenal contents results in gastritis and an amplified gastrin response to food. Parietal cell numbers and maximal acid secretory capacity are increased in some animals.

Susceptibility of Experimental Atrophic Gastritis to Ulceration

The hypothesis that gastric ulcer develops in pre-existing areas of atrophic gastritis was subjected to experimental scrutiny. A full thickness wedge of vascularized canine gastric corpus was explanted onto the anterior abdominal wall. Thus exposed, the mucosa developed inflammatory cell infiltration, necrosis, and sloughing. Later, new gland formation by undifferentiated mucus-containing cells occurred. After 6 to 8 weeks the mucosa was reconstituted but contained no parietal or chief cells, secreted no acid in response to histamine stimulation, and histologically resembled human atrophic gastritis. Eight explants returned to the corpus of the stomach at this time retained an atrophic appearance at the time of killing 19 to 21 days later. In 10 dogs, return of the wedge to the stomach was followed by 14 daily injections of histamine suspended in beeswax. Eight of these 10 animals developed penetrating ulcers in the atrophic reimplanted mucosa. No ulcers occurred in eight full thickness wedges which were histologically normal, having been reimplanted into the stomach immediately following construction and subjected to gastric hypersecretion induced by histamine. Blood flow to the atrophic reimplanted mucosa was not significantly different from flow to histologically normal re-implanted mucosa or from intact corpus mucosa. These results suggest that the presence of atrophic gastritis renders stomach mucosa susceptible to acid peptic digestion and ulcer formation.