Lipopolysaccharide temporarily impairs sphincter of Oddi motility.

The aim of our study was to determine the effect of lipopolysaccharide (LPS) on sphincter of Oddi (SO) motility. Opossums received saline, Escherichia coli LPS (1.0 mg/kg), or E. coli LPS (1.0 mg/kg) and aminoguanidine (50 mg/kg), and the SO was removed 6-24 h later. At 12 h LPS decreased electrical field stimulation (EFS)-induced relaxation and increased baseline tone. These changes were reversed when the animals were pretreated with aminoguanidine. The dose-dependent decrease in EFS-induced relaxation by N(omega)-nitro-l-arginine was impaired after LPS, but not in animals that received LPS and aminoguanidine. The impaired EFS-induced relaxation after LPS was reversed when l-arginine was added to the tissue bath. Serum levels of NO(-)(2)/NO(-)(3) were increased with LPS as compared to saline or both LPS and aminoguanidine. Inducible nitric oxide synthase mRNA was readily seen in SO segments after LPS. LPS impairs EFS-induced relaxation and increases baseline tone of the SO. The effects of LPS on SO motility appear to be mediated by nitric oxide.

Effect of endotoxin on opossum gallbladder motility: a model of acalculous cholecystitis.

OBJECTIVE: To determine whether endotoxin causes histologic changes in the gallbladder consistent with acalculous cholecystitis, and to determine the effects of endotoxin on gallbladder motility. SUMMARY BACKGROUND DATA: Acute acalculous cholecystitis is frequently seen in critically ill, septic patients, after prolonged fasting and gallbladder stasis. The pathogenesis of acalculous cholecystitis is unknown; however, previous studies have suggested that ischemia may play a role. METHODS: Adult opossums received Escherichia coli lipopolysaccharide. The gallbladder was removed for histologic examination or for physiologic studies 4 hours to 2 weeks later. For histologic examination, gallbladder strips underwent standard hematoxylin-and-eosin processing. For physiologic studies, they were mounted in a tissue bath to determine responses to cholecystokinin octapeptide or electrical field stimulation. RESULTS: Intravenous endotoxin at a dose of 0.005 mg/kg resulted in disrupted mucosal surfaces and areas of hemorrhage; higher doses of endotoxin resulted in coagulation necrosis, hemorrhage, areas of fibrin deposition, and extensive mucosal loss, consistent with an acute ischemic insult. Endotoxin abolished the contractile response to cholecystokinin octapeptide in gallbladder strips 4 hours after endotoxin administration. The 0.005-mg/kg dose of endotoxin decreased the contractile response to cholecystokinin octapeptide for up to 96 hours after endotoxin administration and decreased the contractile response to electrical field stimulation for 48 hours after administration. Inhibition of nitric oxide synthase reversed the decreased contractile response to cholecystokinin octapeptide. CONCLUSIONS: Endotoxin causes an ischemic insult to the gallbladder similar to that seen in acalculous cholecystitis. Also, endotoxin may lead to gallbladder stasis by decreasing gallbladder contractile responses to hormonal and neural stimuli.

Are gastric, jejunal, or both forms of enteral feeding gastroprotective during stress?

BACKGROUND: Clinical data suggest enteral nutrition prevents stress ulceration and intragastric nutrients prevent restraint-induced gastric injury. The purpose of these studies was to determine if jejunal nutrients can protect without gastric contact and to determine if gastric pH, motility, or mucosal perfusion is affected. METHODS: In Experiment 1, 27 rats were restrained for 2 h at room temperature followed by 2 h in cold (4 degrees C), with intragastric (IG) or intrajejunal (IJ) 2 ml/h infusions of saline or 25% glucose. Gastric lesions, pH, volumes, and glucose concentrations were measured postmortem. In Experiment 2, 23 rats had gastric strain gauges implanted >5 days prior to a 0.5 ml/h IG or IJ infusion during stress. In Experiment 3, 40 rats were anesthetized for laser Doppler measurements of gastric mucosal perfusion and arterial catheter monitoring of systemic hemodynamics. Rats received 0.5-ml boluses of concentrated glucose or saline IG or IJ, and were monitored for 60 min. RESULTS: (1) The 2 ml/h IJ and IG glucose infusions prevented gastric injury, but the elevated gastric glucose concentrations suggested equal gastric contact. (2) The 0.5 ml/h glucose IG and IJ infusions decreased gastric injury without reflux of the IJ glucose into the stomach and suppressed stress-induced hypercontractility, but not acidity. (3) Systemic perfusion pressures were unaffected by enteral glucose. IG glucose had little effect on gastric mucosal perfusion, while IJ glucose decreased gastric perfusion within 5 min. CONCLUSIONS: These studies show that large volumes of enteral glucose prevent restraint injury but IJ glucose refluxes into the stomach. The gastroprotective effects of small, nonrefluxing volumes of IJ glucose are associated with suppression of stress-induced gastric hypercontractility, but not with suppressed acidity or enhanced perfusion.

The cup is half full.

BACKGROUND: The clinical outcomes following feeding tube procedures are infrequently studied because most patients have other incurable conditions. METHODS: Multiple electronic databases were used to track clinical outcomes following all gastrostomies and jejunostomies performed at a single institution from October 1, 1992, through December 31, 1995. Preoperative risk factors and postoperative morbidity were available for all 104 cases; long-term status was available for all but 2 of 104. RESULTS: The in-hospital mortality was 11.4%. Mortality was lower in those receiving feeding tubes as primary procedures (7.4%) than in those who had a feeding tube placed during other major procedures (24%, P <0.05). Postoperative pneumonia was frequent (24.7%), and was associated with preoperative gastroesophageal reflux (odds ratio 4.2, P = 0.01) and history of aspiration (odds ratio 3.9, P = 0.01). Although 14.5% of the patients were newly discharged to care facilities, the majority (74%) returned to their previous residence. Median survival was just over 6 months, with 18% surviving more than 2 years. Survival was inversely related to do-not-resuscitate status (odds ratio 4.6, P <0.001), metastatic tumor (odds ratio 2.7, P <0.001), dementia (odds ratio 2.3, P = 0.005), and unresectable tumor (odds ratio 2.1, P <0.001), but was unrelated to type of feeding tube. CONCLUSIONS: Significant morbidity and mortality follow feeding enterostomies, but the majority of patients benefit and can return to their previous residence. Am J Surg. 1999;178:406-410. 1999 by Excerpta Medica, Inc.

Gastric emptying of liquids and postprandial pancreatobiliary secretion are temporarily impaired during endotoxemia.

The aims of our study were to determine mechanisms by which pancreatobiliary secretion is altered during endotoxemia. Dogs underwent placement of duodenal perfusion and aspiration catheters and antral manometry catheters. Gastric emptying of liquids, antral motility, output of bile acids and amylase, and serum levels of enteric hormones were determined after ingestion of a 360-kcal mixed-nutrient liquid meal. Each dog was then given a single dose of E. coli lipopolysaccharide (200 microg/kg, intravenously) and the studies repeated for the next three days. Endotoxin slowed gastric emptying of liquids and decreased amylase output for two days. Bile acid output was decreased on postendotoxin day 1. Pancreatic polypeptide alone was decreased on postendotoxin day 1. We conclude that the decrease in pancreatobiliary output is probably due to decreased nutrient flow into the duodenum and not due to decreased production of hormones that influence pancreatobiliary secretion. The delayed gastric emptying, decreased pancreatobiliary output, and decreased postprandial levels of pancreatic polypeptide suggest diminished vagal output as a possible explanation for the effects of endotoxin on upper gut function.

The role of antioxidant enzymes in the control of opossum gallbladder motility.

BACKGROUND: Superoxide rapidly oxidizes nitric oxide (NO) to form peroxynitrite, thus terminating the biological activity of NO. The aims of our study were to determine if superoxide alters the motor function of the gallbladder and to localize the antioxidant enzymes in the gallbladder. MATERIALS AND METHODS: Immunostaining and immunoblots were performed and enzyme activities were measured in the gallbladder. In physiologic experiments, force-displacement transducers recorded tension in gallbladder muscle strips. Superoxide was generated by the addition of xanthine with xanthine oxidase, while superoxide radicals were scavenged by the addition of superoxide dismutase (SOD) and catalase. SOD was inhibited by deithyldithiocarbamate. RESULTS: Immunostaining demonstrated superoxide dismutase and catalase immunoreactivity in ganglia situated throughout the smooth muscle. Total superoxide dismutase activity was 115 +/- 12 U/mg. Western blots detected expression of proteins of 19.4 kDa for copper/zinc SOD and 25.0 kDa for manganese SOD. Generation of superoxide increased isometric tension, while pretreatment with SOD prevented the increase in isometric tension induced by superoxide. Inhibition of SOD diminished the EFS-induced off response. CONCLUSIONS: We conclude that superoxide alters gallbladder motor function, and the presence of superoxide scavenging enzymes in enteric plexuses suggests that they may regulate gallbladder neuromuscular function by clearing endogenous superoxide.

Effects of endotoxin on regulation of intestinal smooth muscle nitric oxide synthase and intestinal transit.

BACKGROUND: The disrupted intestinal transit during endotoxemia may be mediated by nitric oxide (NO). We hypothesized that the isoforms of nitric oxide synthase (NOS) are up-regulated in intestinal smooth muscle during endotoxemia and that the scavenging of NO will normalize transit. METHODS: Rats were given Escherichia coli lipopolysaccharide (LPS) 10 mg/kg intravenously and were killed 4 hours later. To determine the activity of NOS isoforms in the jejunum and ileum, the conversion of tritiated L-arginine to tritiated L-citrulline was measured. Western immunoblots were performed by incubating the extracted protein with specific polyclonal antibodies. To determine intestinal transit, rats were divided into 4 groups: 0.9% sodium chloride 1 mL/h intravenously for 5 hours, LPS 10 mg/kg intravenous bolus plus 1 mL/h 0.9% sodium chloride intravenously, LPS plus oxyhemoglobin 0.5 g/kg/h intravenously, and oxyhemoglobin 0.5 g/kg/h intravenously. RESULTS: LPS increased the constitutive and inducible NOS enzyme activities in the jejunum and ileum. Western blots demonstrated that LPS up-regulates both the NOS1 and NOS2 isoforms in jejunal and ileal smooth muscle. Oxyhemoglobin alone increased intestinal transit compared with controls, whereas endotoxemia increased intestinal transit, which was ameliorated with infusions of oxyhemoglobin. CONCLUSIONS: NO may play a major role in mediating the rapid intestinal transit induced by endotoxemia.

Changes in intestinal transit and absorption during endotoxemia are dose dependent.

BACKGROUND: Septic patients are often intolerant of enteral feedings due to a combination of motility disturbances and impaired absorptive function. Our laboratory has previously demonstrated that endotoxemia results in rapid intestinal transit and decreased jejunal absorption of water, electrolytes, and glucose. We hypothesized that the changes in jejunal transit and absorption during endotoxemia may be dependent on the dose of endotoxin. MATERIALS AND METHODS: Under general anesthesia, rats underwent placement of an internal jugular line, a femoral arterial line, and a 20-cm jejunal Thiry-Vella loop. The jejunal segment was perfused with an isotonic solution containing polyethylene glycol. For 90 min, baseline measurements of blood pressure, heart rate, jejunal absorption of water, electrolytes, and glucose, and jejunal transit were made. Following this baseline period I, rats were given 0.9% NaCl (1 ml/kg) or one of three doses of Escherichia coli lipopolysaccharide (0.5, 1.0, or 5.0 mg/kg). Studies were then repeated for an additional 90 min. RESULTS: Changes in blood pressure and heart rate were similar among the four groups of animals. Endotoxin decreased water and glucose flux, increased potassium flux, and quickened intestinal transit in a dose-dependent fashion. CONCLUSIONS: We conclude that endotoxemia causes dose-dependent changes in jejunal transit and absorption. The effects of increasing doses of endotoxin on jejunal absorptive and motor function do not appear to be mediated by changes in blood pressure or heart rate.

Effect of endotoxin on canine colonic motility and transit.

Diarrhea is a common problem in patients who have episodes of sepsis and are being fed enterally. Endotoxemia results in gastrointestinal motor dysfunction characterized by slowed gastric emptying and rapid intestinal transit; however, the effect of endotoxin on colonic motility is unknown. The aim of our study was to determine the effects of a single sublethal dose of endotoxin on colonic motility and transit. Seven dogs underwent construction of a 50 cm colonic Thiry-Vella fistula. Five manometry catheters were sewn into the colonic lumen at 8 cm intervals along the fistula. Following recovery, the fistula was perfused with an isotonic solution at 2.9 ml/min, and fasting and postprandial colonic motility was determined. Liquid transit was assessed by bolus of a nonabsorbable marker instilled into the proximal end of the Thiry-Vella fistula. Recordings of gastrointestinal contractile activity were made digitally to determine contractile frequencies and motility indexes. Following completion of the baseline studies, each dog was given a single dose of E. coli lipopolysaccharide, 200 microgram/kg intravenously, and studies were repeated daily for the next 3 days. Endotoxin doubled the fasting colonic contractile frequency on postendotoxin day 1 and also increased motility indexes on that same day. Fasting motility indexes and contractile activity were decreased on postendotoxin days 2 and 3. The postprandial frequency of contractions and motility indexes were decreased on postendotoxin day 3. Fasting colonic liquid transit was rapid on postendotoxin day 1, whereas postprandial liquid transit was rapid on both postendotoxin days 1 and 2. Endotoxin temporarily speeds liquid transit and increases both the frequency and strength of colonic contractions. These effects may contribute to the diarrhea that occurs during episodes of sepsis.

Endotoxin temporarily impairs canine colonic absorption of water and sodium.

Diarrhea is a common manifestation of sepsis. We hypothesized that endotoxin may impair colonic absorption of water and electrolytes, an effect which may be related to altered liquid transit in the colon. Five dogs underwent construction of 50-cm colonic Thiry-Vella fistulas (TVF). Following recovery, absorption studies were performed by perfusing the TVF with an isotonic solution at 2.9 ml/min containing polyethylene glycol (5 g/L). Fasting and postprandial colonic absorption of water, electrolytes, and glucose were determined. Liquid transit was assessed by bolus of a nonabsorbable marker (PSP) instilled into the proximal end of the TVF. Following completion of the baseline studies, each dog was given a single dose of Escherichia coli lipopolysaccharide 200 micrograms/kg i.v. and the studies were repeated daily for the next 3 days. Following endotoxin bolus, colonic absorption of water and sodium were decreased during fasting, while postprandial colonic absorption of water was also decreased. Colonic absorption of water and sodium returned to baseline values on postendotoxin day 2. Colonic secretion of potassium was decreased on postendotoxin days 1 and 3 in both the fasting and the fed periods. Fasting and postprandial liquid transit was also rapid on postendotoxin day 1, which correlated with the decreased absorption seen on that day. Liquid transit returned to baseline values on postendotoxin day 2. We conclude that endotoxin temporarily impairs postprandial colonic absorption, which may be due to the rapid liquid transit that occurs. These effects may contribute to the diarrhea seen during and after septic episodes.

Gastric mucosal protection from enteral nutrients: role of motility.

BACKGROUND: Cold restraint stress increases the force of gastric contractions and produces gastric mucosal injury in rats. The aim of our study was to determine whether enteral glucose or hyperglycemia alone would alter the stress-induced gastric motility pattern and ameliorate the associated gastric mucosal injury. METHODS: Adult male rats underwent surgical placement of gastric catheters, jugular venous catheters, and gastric strain gauge transducers 5 days before cold restraint. Three groups of rats received different substances during the same cold restraint stress protocol. Group 1 received 0.9% NaCl, 2 mL/h infused both intravenously (i.v.) and intragastrically (i.g.); group 2 received 0.9% NaCl, 2 mL/h i.g. plus 25% glucose, 2 mL/h i.v.; and group 3 received 0.9% NaCl, 2 mL/h i.v. plus 25% glucose i.g. Following baseline gastric motility measurements, all rats were restrained for 2 hours at 20 degrees C followed by 2 hours at 4 degrees C. RESULTS: Restraint even at room temperature increased the force of gastric contractions; the cold environment gradually prolonged gastric contractions. Enteral glucose blunted the effects of stress on gastric motility, increased gastric residual volume, decreased gastric acidity, and prevented gastric mucosal injury. Parenteral glucose had little effect on any gastric parameters. CONCLUSIONS: Enteral glucose prevents the abnormal gastric motility pattern that is necessary to produce the gastric mucosal injury associated with cold restraint stress, but hyperglycemia alone has little effect on the pathophysiology of cold restraint.

Effects of sucralfate vs antacids on gastric pathogens: results of a double-blind clinical trial.

BACKGROUND: Unblinded studies suggested that sucralfate prophylaxis for stress ulcers is associated with a lower rate of nosocomial pneumonia than acid-reducing approaches. We performed a randomized, double-blind, double-sham clinical trial comparing the exact microbial effects of each treatment. METHODS: One hundred forty patients entered this study before major elective surgery, allowing baseline cultures of gastric and pulmonary secretions to be obtained intraoperatively. Postoperatively, the patients were treated with standard doses of either sucralfate or antacids, plus a sham of the other drug. Cultures were repeated twice daily for 3 days. Molecular epidemiological typing was used to track the appearance of specific microbes and their transmission from site to site, and clinical end points were compared. The number of patients chosen was for sufficient statistical power to detect differences in the microbial measures, as detecting differences in clinical measures would have required increasing the sample size by an order of magnitude. RESULTS: Gastric pH was affected by the form of stress ulcer prophylaxis throughout the study, and this pH effect affected the number of new gastric organisms appearing in the 2 different groups. Colonization of the airway with new gastric organisms occurred more frequently in the antacid than in the sucralfate group, and colonization of the airway with organisms of gastric origin was associated with occurrence of postoperative pneumonia. CONCLUSIONS: Both sucralfate and antacids offered safe and effective stress ulcer prophylaxis in this double-blind clinical trial of postoperative patients in an intensive care unit. In association with the drug's effects on gastric pH, more new pathogens appeared in the gastric contents of antacid-treated than sucralfate-treated patients.

Gastric contractions, secretions and injury in cold restraint.

The clinical syndrome of stress ulceration has been studied for years using rodent cold restraint stress models, although the pathogenesis of the characteristic focal gastric mucosal lesions produced in these models has been controversial. We used gastric strain gauges to characterize fully the gastric motility effects of a 4-h cold restraint protocol, and we determined the relationship of variations in gastric contents and in gastric contractions to the amount of gastric mucosal injury. Additionally, we examined rat stomachs histologically, and determined the location of focal haemorrhagic mucosal lesions on the mucosal rugae. We found a consistent relationship between force of gastric contractions and gastric mucosal injury, and also a relationship between the initial duration of contractions during restraint and ultimate mucosal injury. Volume, acidity and mucus in the gastric contents were unrelated to mucosal injury. The majority (91%) of the mucosal lesions had some relationship to a rugal fold, with 59% of all lesions at the base of a rugal fold. Thus, the mechanical forces of gastric hypercontractility may contribute to the gastric mucosal injury of rodent cold restraint models.

Endotoxin temporarily impairs canine jejunal absorption of water, electrolytes, and glucose.

Enteral feeding during and after episodes of sepsis may be beneficial. The aim of our study was to determine the effects of a single sublethal dose of endotoxin on canine jejunal absorption. Following a 240 kcal liquid meal, absorption studies were performed in eight dogs with 75 cm jejunal Thiry-Vella fistulas. These fistulas were perfused with an isotonic solution containing polyethylene glycol to calculate absorption. Each dog was then given a single dose of Escherichia coli lipopolysaccharide, 200 microg/kg intravenously, and the studies were repeated for the next 3 days. Following endotoxin bolus infusion, net absorption of water, electrolytes, and glucose was decreased for 2 days and returned to baseline values on postendotoxin day 3. A single sublethal dose of endotoxin temporarily impairs canine jejunal absorption. Although enteral feeding may be advantageous, jejunal absorption may be temporarily impaired following an episode of endotoxemia.

Pathophysiology of adynamic ileus.

We hypothesized that the inhibitory neurotransmitters nitric oxide (NO) and vasoactive intestinal peptide (VIP) may play a role in the disrupted gastrointestinal motility of endotoxemia. Strain gauge transducers on the stomach and small intestine of dogs determined interdigestive gastrointestinal motility. Tissue levels of NO synthase and VIP and serum levels of nitrite/nitrate (NO(2)-/NO(3)-) and VIP were measured. Following completion of the baseline studies, dogs were given a single dose of E. coli lipopolysaccharide, 200 microg/kg intravenously, and the studies were repeated for the next three days. Following endotoxin bolus, the migrating motor complex (MMC) was delayed for two days while serum VIP was increased on postendotoxin day 1 and serum NO(2)-/NO(3)- was increased on postendotoxin day 2. There were no changes in gut smooth muscle levels of NO synthase or VIP. We conclude that a single, sublethal dose of endotoxin results in prolongation of the MMC with distinct but independent increases in serum levels of VIP and NO(2)-/NO(3)-.

Team-based versus preceptor-based assignment of junior surgery students.

BACKGROUND: Clinical evaluations of junior surgery students frequently lack sufficient detail for effective formative or summative feedback. We hypothesized that this was in part due to a lack of personal accountability associated with large general surgery teams, and that altering the format to assign students to specific surgical faculty preceptors rather than to teams would affect the clinical evaluation products. METHODS: Over a 1-year period, 154 junior medical students grouped into 8 successive clerkships were assigned alternately in the usual Team (3-5 junior students, with 2-4 general surgery faculty, 2-4 residents, and 0-2 senior students) or a new Preceptor format (1-2 students to each faculty preceptor). In order to keep the ratio of students to faculty low, approximately one-third of the Preceptor format students were assigned to subspecialists. RESULTS: The preceptor format resulted in the use of more adjectives to describe students in the open-ended portions of the faculties' clinical evaluations (mean of 3.2 as compared with 2.5, P = 0.003), and a greater proportion of students recommended for overall clinical Honors (47% as compared with 25%, P = 0.004). The clerkship format had no impact on exam performance, students' perceptions of the faculty, or the amount of students' self-reported clinical activity. Nevertheless, twice as many Team format students felt they had too few patients, whereas twice as many Preceptor students felt their informal instruction had been less than "good." CONCLUSIONS: Preceptor assignment increased the number of students recommended for Honors, but this did not correlate with students' exam performance. From the students' standpoint, each format had advantages and disadvantages. Limiting the number of students on the general surgery teams and adding structured formative feedback from faculty before the end of the clerkship might give students the instructional advantages of the Preceptor format without sacrificing those of the Team format.

The effect of endotoxin on canine jejunal motility and transit.

Intestinal transit is rapid during endotoxemia; however, little is known regarding the small intestinal motility changes which produce this rapid intestinal transit. The aim of our study was to determine the degree and duration of disrupted jejunal transit, and changes in jejunal motility following a sublethal dose of endotoxin. Eight dogs underwent construction of jejunal Thiry-Vella fistulas (TVF) with manometry catheters to record motility along the TVF. Following recovery, a 240-kcal liquid meal was given and the TVF was perfused with an isotonic solution. Liquid transit was assessed by bolus of a nonabsorbable marker instilled into the proximal end of the TVF. Recordings of gastrointestinal contractile activity were made digitally to determine postpandial motility. Following completion of the baseline studies, each dog was given a single dose of Escherichia coli lipopolysaccharide (200 micrograms/kg, iv) and the postprandial studies were repeated for the next 3 days. Endotoxin decreased the frequency of jejunal contractions for 2 days while the strength of jejunal contractions was diminished for 1 day. Jejunal transit of liquids was rapid on Postendotoxin Day 1. The rapid transit was associated with a greater percentage of single pressure waves propagating aborally on Postendotoxin Day 1 than the baseline percentages established prior to endotoxin. We conclude that endotoxemia temporarily disrupts postprandial jejunal motility and transit. The rapid liquid intestinal transit seen with endotoxemia may be due to changes in contractile propagation.

Gastrointestinal myoelectric activity during endotoxemia.

BACKGROUND: Gastrointestinal myoelectric activity during postoperative ileus has been well characterized. However, the common clinical scenario of ileus occurring during and after episodes of sepsis is not well understood. The aim of our study was to determine the effects of a single, sublethal dose of endotoxin on canine gastrointestinal myoelectric activity. METHODS: Eight dogs underwent placement of serosal electrodes on the stomach and small intestine and insertion of a jejunal cannula. After the animals recovered, electrical activity and jejunal mucosal blood flow were determined during fasting and with feeding. Following completion of these baseline studies dogs were given a single, sublethal dose of Escherichia coli lipopolysaccharide (200 g/kg) intravenously, and the studies were repeated daily for 3 consecutive days. RESULTS: Endotoxin resulted in an absence of the interdigestive migrating myoelectric complex for 2 days, a decrease in duodenal and jejunal action potentials during fasting and with feeding, but no decreases in jejunal mucosal blood flow. The gastrointestinal myoelectrical patterns returned to those found in health on postendotoxin day 3. CONCLUSIONS: A single, sublethal dose of endotoxin results in a temporary disruption of gastrointestinal myoelectric activity similar to that seen during postoperative ileus. The etiology of this "adynamic" ileus is unknown but does not appear to be secondary to intestinal ischemia.