Colonic carcinoma after duodenocolic anastomosis.
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Adult↗
Biomedical subjects
K S Ephgrave
Publications and source records attributed to K S Ephgrave.
Effect of endotoxin on canine gastrointestinal motility and transit.
Ileus is common during sepsis; however, the etiology of this gastrointestinal dysmotility is unclear. The aim of our study was to determine the effects of a single, sublethal dose of endotoxin on canine gastrointestinal motility, gastric emptying, gastric acid secretion, and colonic transit. Six dogs underwent placement of manometric catheters in the stomach and small bowel and insertion of a gastric and a cecal cannula. After the animals recovered, fasting and fed gastrointestinal motility was recorded, and gastric emptying and colonic transit were studied with nonabsorbable liquid and solid markers, respectively. Following completion of baseline studies, each dog was given a single dose of Escherichia coli lipopolysaccharide (200 micrograms/kg intravenously) and the studies were repeated on Postendotoxin Days 1-3. The single bolus of endotoxin abolished the migrating motor complexes, decreased the fasting motility index, decreased hydrogen ion output, slowed liquid gastric emptying, and prolonged colonic transit for 2 days. Gastrointestinal motility and transit returned to baseline on Postendotoxin Day 3. In conclusion, a single, sublethal dose of endotoxin temporarily disrupts fasting and postprandial canine gastrointestinal motility and transit.
Animals↗
Effects of resuscitation on acute gastric mucosal injury: reperfusion injury versus rapid mucosal restitution.
Gastric mucosal injury after hemorrhagic shock may be a consequence of both ischemia and reperfusion, as toxic oxygen-derived compounds are generated when ischemic tissues are reperfused. The present study was designed to estimate the magnitude of the reperfusion component of gastric mucosal injury, in comparison with the known capacity of the gastric mucosal surface to rapidly restore or restitute its surface after removal of various insults. Twelve dogs were subjected to 2 hr of hemorrhagic shock, with intragastric acid infused to produce gastric mucosal injury. Half were sacrificed 15 min after return of shed blood, while half were fully resuscitated with additional crystalloids and sacrificed 2 hr later. Gross and microscopic injury to the gastric mucosal surface were not increased by resuscitation. Particularly in the antrum, the resuscitated animals had significantly less gastric mucosal injury than unresuscitated animals. The amount of gastric mucosal injury was strongly inversely related to the success of resuscitation after 2 hr, specifically correlating with left ventricular pressure, cardiac index, mean arterial pressure, and systemic pH. Our data suggest that gastric mucosal restitution rather than reperfusion injury may predominant within a few hours of hemorrhagic shock and show that the degree of shock-induced gastric mucosal injury is inversely related to hemodynamic performance after resuscitation.
Animals↗
Molecular epidemiology of gastric colonization by Enterococcus faecalis in a surgical intensive care unit.
We applied restriction endonuclease analysis of genomic DNA using pulsed field gel electrophoresis (PFGE) to study gastric colonization with Enterococcus faecalis among patients hospitalized in the surgical intensive care unit (SICU). Isolates were obtained by culturing prospectively the gastric contents of 140 patients in the SICU. In addition, cultures of respiratory specimens were obtained daily and cultures of blood, normally sterile body fluids, wounds, and urine were obtained when indicated clinically. A total of 177 isolates were obtained from 45 patients. Concentrations of E. faecalis in gastric fluid ranged from 1 x 10(2) colony forming units (CFU)/ml to greater than 5 x 10(7) CFU/ml (mean 8.0 x 10(6) CFU/ml). Overall, 33 different DNA types were identified by PEGE. In examining strain variation among isolates obtained from multiple anatomic sites over time, we found that the same DNA type was recovered from gastric aspirates, sputum, and wounds in a given patient and that these strains were carried over time. In general, given individuals were colonized with their own unique DNA type; however, one DNA type (type C) was shared by 11 different patients, and seven DNA types were shared by two individuals each. These results demonstrate the potential importance of gastric colonization as a reservoir for nosocomial strains of E. faecalis in an SICU setting.
Colony Count, Microbial↗
Captopril decreases stress ulceration without affecting gastric perfusion during canine hemorrhagic shock.
The renin-angiotensin axis has recently been called the source of disproportionate splanchnic vasoconstriction during shock, and blocking this axis decreased gastric stress ulceration during swine cardiogenic shock. The present study tested whether the angiotensin converting enzyme inhibitor captopril would prevent stress ulceration when given after the onset of canine hemorrhagic shock, and whether any detrimental effects would result from enhancing splanchnic perfusion with captopril during hemorrhagic shock. We found that captopril treatment was associated with a decrease in gastric mucosal injury and with a marked decrease in systemic acidosis. Captopril enhanced blood flow to the small intestine, pancreas, liver, and spleen, but not flow to the stomach, during shock. Following the reinfusion of shed blood, the captopril-treated animals had decreased mean blood pressures and increased heart rates compared with untreated animals. We found captopril alleviated the stress ulceration produced by canine hemorrhagic shock, but concluded that the likely mechanism was alleviating systemic acidosis through enhanced perfusion of other viscera rather than a specific enhancement of gastric perfusion.
Analysis of Variance↗
Postoperative pneumonia: a prospective study of risk factors and morbidity.
BACKGROUND: Postoperative pneumonia (PP) is a major complication that has been linked to microaspiration of pathogens originating in the gastrointestinal tract. This prospective study was performed to define the role of gastric bacterial aspiration in the development of PP. METHODS: Informed consent was obtained before operations from 140 veterans scheduled for major elective procedures requiring nasogastric tubes, and cultures were obtained of the gastric contents and sputum twice daily after operation. RESULTS: PP developed in 26 (18.6%) of 140 patients. The patients who had PP did not differ from those with no pneumonia after operation except for a history of chronic obstructive pulmonary disease, which was found in 38.5% of those with PP compared with 20% of patients with no pneumonia (p < 0.05). Morbidity was increased in association with PP, because length of stay in the surgical intensive care unit (6.2 vs 2.6 days), days intubated (2.7 vs 0.6), total postoperative days (15.3 vs 8.4), and mortality rates (19.2% vs 1.7%) were greater than in patients with no pneumonia. Gastric pathogens were present on entry in 38% of patients, and 32% of these had PP compared with 13% whose initial gastric cultures were sterile (p = 0.01). Colonization of sputum for greater than 24 hours with gastric pathogens occurred in 28% of patients. These patients had a 40% incidence of PP compared with 12% in patients without such evidence of microaspiration (p < 0.01). CONCLUSIONS: PP is a morbid postoperative complication associated with not only chronic obstructive pulmonary disease but also the presence of gastric bacteria during operation and transmission of gastric bacteria to the pulmonary tree after operation.
Adult↗
Effects of intragastric and intravenous glucose on restraint model of stress ulceration.
Intragastric glucose prevents acute stress-induced gastric mucosal injury in the restrained rat. Because increased gastric contractions contribute to mucosal injury in this model and because parenteral glucose infusions have been shown to suppress gastric contractility, we hypothesized that centrally mediated responses to hyperglycemia might contribute to the cytoprotective effect of intragastric glucose. We compared intragastric and intravenous 25% glucose with saline infusions during cold restraint and measured their impact on gastric lesions, serum glucose levels, gastric residual volume (an indirect indicator of net gastric contractility), acidity, and mucin concentration. We found that both intravenous and intragastric glucose infusions increased serum glucose to over 500 mg/dl after 4 hr of stress. Intragastric glucose increased residual volume and gastric pH, as well as decreased gastric mucosal injury, but intravenous glucose had no effects on gastric function. We found that none of the potentially protective effects of intragastric glucose are mediated by central responses to hyperglycemia, and likewise that intravenous glucose has no effect on gastric mucosal injury.
Animals↗
Cholecystokinin does not mediate glucose's cytoprotective effects.
Cold restraint stress produces acute gastric mucosal injury in association with altered gastric motility. Enteral nutrients prevent this injury in conjunction with inhibition of gastric emptying. Because cholecystokinin (CCK) is released by nutrients known to be cytoprotective and is thought to inhibit gastric emptying, we performed three experiments to see if CCK contributes to the gastric mucosal protection afforded by enteral nutrients. Our data show that enteral glucose protects the gastric mucosa and increases gastric volume, gastric luminal pH, and gastric mucin. Neither physiologic nor pharmacologic doses of CCK protected the mucosa. None of the other significant effects of glucose on gastric function during cold restraint were affected by exogenous CCK. Furthermore, antagonism of CCK receptors with L-364,718 did not have any independent effects, nor did it diminish the protection associated with enteral glucose. We conclude that enteral glucose protects the gastric mucosa from cold restraint injury in association with a number of potentially beneficial effects on gastric physiology, but none of the effects of glucose in this model appear to be mediated by CCK.
Animals↗
Preoperative screening with ultrasonography for laparoscopic cholecystectomy: an alternative to routine intraoperative cholangiography.
BACKGROUND: Laparoscopic management of choledocholithiasis is not routinely successful. A prospective study was undertaken to determine if preoperative screening with ultrasonography and liver function tests (LFTs) could minimize the incidence of unsuspected choledocholithiasis. METHODS: One hundred twenty-one patients were studied. Patients with a common bile duct greater than 6 mm and either clinical symptoms or elevated LFT results were referred for preoperative endoscopic retrograde cholangiopancreatography (ERCP). RESULTS: Ten patients (8%) were referred for preoperative ERCP, of whom seven had choledocholithiasis, two had papillary stenosis, and one had a normal examination (90% positive ERCPs). One hundred eight patients underwent successful laparoscopic cholecystectomy. Nine patients underwent postoperative ERCP dictated by increasing common bile duct size, elevated enzyme levels, or symptoms. Four patients (3%) had choledocholithiasis that was successfully treated endoscopically. One patient had papillary stenosis, one had oriental cholangitis, and three had normal results on examination. CONCLUSIONS: In this study ultrasonography and LFTs identified patients at high risk for choledocholithiasis, allowing preoperative referral for endoscopic stone extraction.
Adult↗
Naloxone and restraint stress: effects on gastric mucosal injury and gastric function.
Contradictory findings have been reported from previous investigations of the effects of opiate receptor blockade on stress-related gastric injury. We performed two studies of the effects of naloxone on gastric mucosal injury and gastric function in cold restraint stress. In the first, naloxone had a linear, dose-dependent effect, reducing mucosal injury both parenterally and enterally. Gastric acidity was not related to the dose of naloxone, or to the amount or extent of mucosal injury. Gastric residual volume, by contrast, was related to both naloxone dose and gastric mucosal injury. In the second study we investigated the effect of gastric distention by enteral vehicle in the restraint model, and the interaction of the vehicle with the effects of naloxone. Periodic distention of the stomach with enteral vehicle did not alter the drug's effects on mucosal injury or on gastric residual volume. Because cold restraint stress produces harmful gastric contractions, naloxone is likely to be protective by altering gastric motility.
Animals↗
Laparotomy and multiple system organ failure.
A retrospective review of laparotomies was undertaken to define the indications for abdominal procedures in patients with multiple system organ failure. This study suggests patients with (MSOF) must be thoroughly evaluated with non-invasive technology to determine the presence of an intra-abdominal septic focus prior to consideration of exploratory laparotomy.
Abdomen, Acute↗
Enteral nutrients prevent stress ulceration and increase intragastric volume.
Tube feedings and intragastric glucose prevent stress ulceration by unknown mechanisms. We tested the hypothesis that glucose protects the gastric mucosa by direct repletion of glycogen stores. We compared the effects of enteral glucose with enteral lipids in the rat restraint model. The rats were given equal volumes of 0.9% saline, 20% lipids, or 25% glucose during a 4-h period of restraint stress. The effects of each treatment on gastric residual volume and luminal pH, as well as on stress lesion formation were measured. Both enteral nutrients significantly reduced the number of mucosal lesions compared to saline. In conjunction with their protective effect, both nutrients significantly increased both gastric residual volume and luminal pH. As stress-induced prolonged gastric contractions are related to mucosal injury in this model, the nutrient solutions may have been protective in part because they increased gastric volume and prevented mechanical trauma to the mucosa. We conclude that tube feedings do not prevent stress ulceration by glucose's repletion of local glycogen stores, as lipids and glucose were equally effective. Both increased intragastric volume and increased intraluminal pH associated with administration of enteral nutrients may contribute to their protection of the gastric mucosa from stress ulceration.
Animals↗
Dimethyl-prostaglandin E2 prevents stress ulceration with minimal complications.
Gastric mucosal damage produced by topical application of necrotizing agents is diminished by topical or systemic pretreatment with a variety of E and F prostaglandins. The rat restraint model of gastric mucosal injury is more analogous to clinical stress ulceration than are models using intragastric application of toxic solutions; however, previous use of prostaglandin E1 in the restraint model resulted in a prohibitive incidence of GI morbidity. The current study used the restraint model of stress ulceration to compare the effects of a more potent prostaglandin analogue, 16,16-dimethyl prostaglandin E2, with hyperosmolar glucose and antacids. All three agents afforded significant protection from grossly apparent mucosal lesions, alone and in combination. Although other physiologic effects of each agent differed, the only effect which correlated with prevention of mucosal lesions was suppression of gastric acidity. Since effective doses of cytoprotective prostaglandins did not produce notable morbidity in comparison with other agents, they may prove to be a useful adjunct to stress ulcer prophylaxis in clinical settings.
16,16-Dimethylprostaglandin E2↗
Naloxone exerts a dose-dependent gastric cytoprotective effect.
Previous work has shown that naloxone inhibits the ulcerogenic effects of indomethacin and stress, although the site, mechanism or dose are unknown. We investigated whether naloxone possessed gastric cytoprotective properties, generating a dose-response curve existed for both intragastric (IG) and intravenous (IV) administration. One hundred and two rats were subjected to a four hour period of restraint, with the last two hours at 4 degrees C. Naloxone was given hourly during restraint at doses of 0 (Control), 1, 5, 10, 20 mg/kg. After sacrifice, the residual gastric volume, and pH were measured and the number of mucosal lesions scored. The cytoprotection offered by naloxone was different from control (p = 0.0001), with the intravenous route having a greater effect (p = 0.038). While this protective effect did not correlate with changes in gastric acidity, it correlated with the dose of naloxone.
Animals↗
Pharmacokinetics of naloxone: an insight into the locus of effect on stress-ulceration.
The purpose of this study was to determine if the beneficial effect of naloxone on formation of acute gastric mucosal lesions was brought about via central or peripheral mechanisms by measuring blood concentrations of naloxone in rats during a 4-hr period of restraint stress. The study involved administration of naloxone to rats at doses of 5, 20 and 40 mg.kg-1.hr by either the intravenous or enteral routes. Blood samples were collected throughout the period of restraint and gastric stress-lesions were counted at the end of the experiments. Both routes of administration were equally effective in preventing stress-ulceration, with only rats receiving drug intravenously showing the presence of naloxone in blood samples. Inverse linear relationships existed between mean trough blood concentrations and lesions (P = .0003), as well as a linear correlation between area under the time-concentration curve and mean trough concentrations (P = .0001). Although our results show tight correlation between blood levels and effect on lesions in the group given drug intravenously, the effect must be on peripheral rather than central opiate receptors as no detectable blood levels were found when naloxone was given enterally.
Animals↗
Gastric mucosal perfusion and injury: variation in the relationship over time.
Acute erosions of the gastric mucosa occur in a variety of clinical settings characterized by a mismatch between mucosal blood supply and demand. Using a canine model incorporating the clinically important insults, we examined the relationship between the gastric mucosal injury measured by planimetry and the animal's regional gastric perfusion measured before, during, and after hemorrhagic shock. The proximal gastric mucosa developed lesions which were inversely related to the amount of gastric flow through 2 hours of shock. In later shock and after reperfusion the relationship reversed, coinciding with the appearance of visible ulcerations. This work demonstrates that early in shock gastric blood flow is inversely related to mucosal injury, but late in shock and after reperfusion increased blood flow is associated with increased mucosal damage.
Animals↗
Stress ulcers: current understanding of pathogenesis and prophylaxis.
Stress-related gastrointestinal bleeding is known to occur in approximately 25 percent of untreated seriously ill patients, but with appropriate prophylaxis is largely preventable. Since the treatment of stress bleeding is generally unsatisfactory and has a high mortality, routine prophylaxis should be instituted for susceptible patients. Multiple mechanisms contribute to stress ulcer formation, the most important of which appear to be mucosal ischemia and the inability to control back-diffused hydrogen. Antacids and histamine2-blocking agents are presently the cornerstone of effective prophylaxis, but because they have been implicated as contributors to nosocomial pneumonias due to bacterial overgrowth in the stomach, investigation is ongoing into such alternative prophylactic agents as sucralfate and prostaglandins that do not alter the normal gastric acidity. This article presents a review of the literature on the development and prevention of stress ulcer disease.
Humans↗
Comparison of approaches to stress ulcer prophylaxis in hemorrhagic shock.
Stress ulceration can be prevented clinically by prophylaxis with antacids or sucralfate, while hyperosmolar glucose and prostaglandins have prevented gastric mucosal injury in experimental models. We compared these four agents' effectiveness in gastric mucosal protection as well as their interaction with the pathophysiology of hemorrhagic shock. Gastric mucosal injury was produced in a canine model with the insults important in clinical situations: intragastric acid, intragastric bile, and gastric mucosal ischemia. Hypotension was maintained at a constant level for 3 hr, during which one of the prophylactic treatments or vehicle (H2O) was given hourly intragastrically. The stomachs were harvested for quantification of gastric mucosal injury after return of shed blood. The percentage of gastric area damaged was significantly decreased to 1.0 +/- 0.7% by antacids but was increased to 43.5 +/- 4.9% by 16,16-dimethyl prostaglandin E2 (16,16-dmPGE2), in comparison to vehicle treatment which caused 28.4 +/- 4.7% lesioned mucosa. Additionally, hemodynamic function differed between treatment groups after 1 hr of shock. Irrespective of treatment group, parameters reflecting volume status and hemodynamic function correlated significantly with the amount of gastric mucosal injury measured in individual animals. Intragastric treatments did not variably affect systemic pH or systemic glucose, and neither of these parameters was related to gastric mucosal injury. In conclusion, antacids effectively prevent stress ulceration in canine hemorrhagic shock, while the worsening of gastric mucosal injury and hemodynamic function we observed with 16,16-dmPGE2 treatment indicates that this agent could be hazardous in hypotensive patients.
16,16-Dimethylprostaglandin E2↗