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Biomedical subjects

R A Hinder

Publications and source records attributed to R A Hinder.

At least 19 recordsLinked to original sources
PubMed1995

An intraluminal surgical approach to the management of gastric bezoars.

Trichobezoars are difficult to remove endoscopically, often cause nausea and vomiting, and can result in small-bowel obstruction. A patient with a trichobezoar presented to our clinic with symptoms of partial small-bowel obstruction. Multiple attempts at flexible endoscopic removal were unsuccessful. Two large-diameter percutaneous gastrostomies with an inflatable balloon and distal foam-rubber stent to assure intragastric positioning were introduced under general anesthesia. Visualization was provided by a 0 degree panavision laparoscope placed through one of the gastrostomies. The bezoar was removed through the second gastrostomy using standard laparoscopic instruments. The patient made an uneventful recovery. This is the first reported case of percutaneous removal of a trichobezoar. We conclude large-diameter gastrostomies may serve as a port of access for numerous other intraluminal procedures.

Bezoars↗
PubMed1995

In vitro free radical production in rat esophageal mucosa induced by nicotine.

Oxidative stress induced by nicotine was investigated in the esophageal mucosa of rats. The homogenized mucosa was incubated for 30 min with 50, 100, 200, 400, and 800 ng/mg protein/ml nicotine or with 200 ng/mg protein/ml nicotine for 15, 30, 45, and 60 min. Esophageal mucosa was also incubated for 30 min with 200 ng/mg protein/ml nicotine with or without the scavengers superoxide dismutase (SOD), catalase, SOD+catalase, inactivated SOD, inactivated catalase, or albumin. Incubation with 0.9% NaCl served as control. There was a strong correlation between chemiluminescence and the nicotine dose (r = 0.75) or the nicotine incubation time (r = 0.77). Thirty-minute incubation of the esophageal mucosa with 200 ng/mg protein/ml nicotine increased chemiluminescence 5.5-fold and lipid peroxidation 3.3-fold. This response was dampened by SOD or catalase and abolished by SOD+catalase. Inactivated enzymes or albumin had no scavenging effect. These results demonstrate that nicotine causes oxidative stress to the esophageal mucosa.

Animals↗
PubMed1995

Free radical scavengers prevent reflux esophagitis in rats.

Free radical damage in reflux esophagitis of rats induced by 24-hr duodenojejunal ligation was studied. Oxygen free radicals were selectively blocked. Groups were: sham operation, reflux, reflux + superoxide dismutase (SOD), catalase, dimethylthiourea, allopurinol, and inactivated SOD or inactivated catalase alone or in the combination SOD + catalase or SOD + catalase + dimethylthiourea + allopurinol. Macroscopic esophagitis was inhibited only by SOD, alone or in combination with other agents. Esophageal mucosal lipid peroxidation was 10-fold increased in the reflux group compared to the sham group (P < 0.05). This response was damped by SOD > catalase (P < 0.05) but not by the inactivated enzymes, dimethylthiourea or allopurinol. SOD + catalase showed no significant improvement on SOD alone. Total inhibition of lipid peroxidation was achieved by combining all scavengers. Total glutathione (GSH) in the esophageal mucosa was stimulated by reflux. This response was inhibited by scavengers equivalent to their efficacy in preventing lipid peroxidation. It is concluded that reflux esophagitis is associated with free radical release with O2- being the main source. Free radicals appear to stimulate GSH production in this prolonged oxidative stress.

Animals↗
PubMed1995

Esophagitis in Sprague-Dawley rats is mediated by free radicals.

Free radical-mediated esophagitis was studied during duodenogastroesophageal reflux (mixed reflux) or acid reflux in rats. The influence of reflux on esophageal glutathione levels was also examined. Mixed reflux caused more gross mucosal injury than acid reflux. Gross mucosal injury occurred in the mid-esophagus. Total glutathione (GSH) in the esophageal mucosa of control rats was highest in the distal esophagus. The time course of esophageal GSH in rats treated by mixed reflux showed a significant decrease 4 hr after initiation of reflux, followed by a significant increase from the 12th hour on. Mucosal GSH was increased in both reflux groups after 24 hr but significantly more so in the mixed than in the acid reflux group. The free radical scavenger superoxide dismutase (SOD) prevented esophagitis and was associated with decreased GSH levels. GSH depletion by buthionine sulfoximine (BSO) prevented esophagitis and stimulated SOD production in the esophageal mucosa. It is concluded that gastroesophageal reflux is associated with oxidative stress in the esophageal mucosa. The lower GSH levels in the mid-esophagus may predispose to damage in this area. Duodenogastroesophageal reflux causes more damage than pure acid reflux. Oxidative stress leads to GSH depletion of the esophageal mucosa in the first few hours following damage but then stimulates GSH production. GSH depletion by BSO does not worsen esophagitis since it increases the esophageal SOD concentration.

Animals↗
PubMed1995

Free radical production in nicotine treated pancreatic tissue.

The ability of nicotine to induce oxidative stress in the pancreatic tissue of rats was investigated. Homogenized pancreatic tissue of Sprague-Dawley rats was incubated with nicotine in a dose of 200 ng/mg protein/ml for 15, 30, 45, and 60 min or was incubated for 30 min with nicotine in a dose of 50, 100, 200, 400, and 800 ng/mg protein/ml. Pancreatic tissue was also incubated with 200 ng/mg protein/ml nicotine with or without the scavengers superoxide dismutase (SOD), catalase, SOD+catalase, inactivated SOD, inactivated catalase, or albumin. Incubation with 0.9% NaCl served as control. There was a positive correlation between the duration of nicotine incubation and chemiluminescence (r = 0.6) or lipid peroxidation (r = 0.71) and also between the nicotine dose and chemiluminescence (r = 0.54) or lipid peroxidation (r = 0.66). Thirty minutes incubation of pancreatic tissue with nicotine in a dose of 200 ng/mg protein/ml increased chemiluminescence 5 fold and lipid peroxidation 2.5 fold. This response was dampened by SOD or catalase and abolished by SOD+catalase. Inactivated enzymes or albumin had no scavenging effect. These results demonstrate that nicotine causes oxidative stress to the pancreatic tissue of rats.

Animals↗
PubMed1995

Reflux esophagitis in humans is mediated by oxygen-derived free radicals.

BACKGROUND: Oxidative stress in reflux esophagitis was investigated before and after antireflux surgery. PATIENTS AND METHODS: Oxidative stress was studied in the distal and proximal esophagus of control patients (without esophagitis, but with other gastrointestinal disorders), of patients with various grades of esophagitis (including Barrett's esophagus), and in patients who had a Nissen fundoplication. Oxidative stress was assessed by chemiluminescence, lipid peroxidation (LP), and by measuring superoxide dismutase (SOD). RESULTS: Chemiluminescence and LP increased with the degree of esophagitis and was highest in patients with Barrett's esophagus; SOD decreased with damage, except in cases of Barrett's esophagus associated with mild esophagitis. Chemiluminescence and LP in reflux patients were higher in the distal than in the proximal esophagus, and SOD was lower, whereas no such difference was found in controls. Findings after Nissen fundoplication were similar to those of controls. CONCLUSIONS: Reflux esophagitis is mediated by free radicals depleting SOD. Barrett's esophagus is a severe form of oxidative damage; in some patients, high SOD levels may prevent severe esophagitis. Antireflux surgery prevents oxidative damage.

Barrett Esophagus↗
PubMed1995

Pathologic duodenogastric reflux associated with persistence of symptoms after cholecystectomy.

BACKGROUND: The aim of this study was to determine whether increased duodenogastric reflux contributes to postcholecystectomy symptoms. METHODS: Gastric pH monitoring, hepatobiliary scintigraphy, gastric emptying scans, and gastric acid analysis were performed in asymptomatic (n = 10) and in symptomatic (n = 27) patients after cholecystectomy. Normal subjects (n = 20), patients with dyspepsia related to gastric acid hypersecretion (n = 20), patients with reflux gastritis after gastric surgery (n = 10), and patients with confirmed primary pathologic duodenogastric reflux (n = 10) were studied as controls. Symptomatic patients also underwent upper gastrointestinal endoscopy. RESULTS: Symptomatic patients had significantly increased interprandial gastric exposure to pH < 3 compared with asymptomatic subjects, which correlated well with a high incidence of hepatobiliary scans positive for abnormal duodenogastric reflux and chronic gastritis on endoscopy. Gastric alkaline exposure in symptomatic patients was similar to that seen in patients with primary pathologic duodenogastric reflux and patients with duodenogastric reflux related to gastric surgery. Gastric acid secretion and gastric emptying were not altered. Five patients tested before and after laparoscopic cholecystectomy showed that nocturnal gastric alkalization was enhanced after operation. CONCLUSIONS: This study suggests that excessive duodenogastric reflux may be responsible for persistence of symptoms after cholecystectomy.

Adult↗
PubMed1995

Profound duodenogastric reflux causes pancreatic growth in rats.

Although duodenogastric reflux is a physiological event, excessive reflux may be a pathogenetic factor in several diseases of the foregut, including cancer. Long term profound duodenogastric reflux produces pancreatic and gastric tumours in rats. The trophic effect of surgically induced duodenogastric reflux on the pancreas was investigated and the mechanisms involved were examined. Rats with profound reflux from a split gastroenterostomy were compared with sham operated and unoperated controls after two and six weeks. In the six week experiment, one reflux and one sham group were given the cholecystokinin (CCK) receptor antagonist devazepide (25 nmol/kg/h). Duodenogastric reflux caused a significant increase in pancreatic weight, DNA, and plasma CCK and gastrin concentrations at both two and six weeks. Devazepide substantially reduced the pancreatic weight increase after six weeks but did not abolish it completely. CCK and gastrin were not affected by devazepide. These results suggest that CCK is largely responsible for the pancreatic growth induced by reflux but another factor may also be involved. The trophic effect of duodenogastric reflux may contribute to the increased incidence of pancreatic cancer reported after gastric surgery.

Animals↗
PubMed1995

The technique of laparoscopic Nissen fundoplication.

Patients with severe GERD resistant to medical therapy are benefited greatly by laparoscopic fundoplication provided that there is careful preoperative patient selection and evaluation. Preoperative evaluation should include contrast esophagography, EGD with biopsies, stationary manometry, and 24-hour pH analysis. Significant esophageal shortening or severe dysplasia are contraindications to laparoscopic fundoplication. A short, loose Nissen fundoplication should be performed in patients with adequate esophageal body function, whereas patients with esophageal dysmotility should be offered a partial fundoplication such as the Toupet procedure. If these guidelines are followed, long-term good results can be expected, with minimal complications, and all of the advantages of the minimally invasive approach.

Follow-Up Studies↗
PubMed1995

Laparoscopic Nissen fundoplication.

Most patients with gastroesophageal reflux disease (GERD) can be treated effectively with medical therapy; however, in patients with severe GERD who are unresponsive to medical therapy, the lower esophageal sphincter (LES) is often found to be mechanically incompetent. Surgical therapy, which improves the LES antireflux barrier, may then be a good option. A very effective and popular antireflux procedure is the Nissen fundoplication, which can be safely done via the laparoscopic route. Preoperative evaluation should include contrast radiography, esophagoduodenoscopy (EGD) with biopsies, esophageal manometry, and 24-hour pH monitoring. Indications for surgery include failure or inability to continue on medical therapy, GERD-related respiratory symptoms, and severe complications of GERD, such as ulceration, stricture, and Barrett's esophagus. A short, loose Nissen fundoplication is ideal for patients with normal esophageal body motility. Operative complications are infrequent, and they include gastric perforation, bleeding, and pneumothorax. Following the laparoscopic approach, nearly all patients can leave the hospital on the first or second postoperative day. Follow-up esophageal manometry and 24-hour pH monitoring show the same good long-term results as seen after open Nissen fundoplication. Laparoscopic Nissen fundoplication can be performed safely and effectively with all of the advantages of a minimally invasive approach.

Esophagus↗
PubMed1994

Is Barrett's metaplasia the source of adenocarcinomas of the cardia?

OBJECTIVE: To investigate the prevalence of Barrett's esophagus in patients with adenocarcinomas located at the gastroesophageal junction. DESIGN: A case series of patients who underwent esophagogastrectomy for adenocarcinoma was retrospectively reviewed. Tumors were grouped by location as esophageal, cardiac, and subcardiac, and the prevalence of specialized intestinal metaplasia in the histological specimens was determined. SETTING: A university department of surgery that specializes in esophageal diseases. PATIENTS: One hundred patients with adenocarcinoma of the esophagus, cardia, or proximal stomach. MAIN OUTCOME: Cardiac adenocarcinomas were associated with Barrett's esophagus in 42% of the patients. RESULTS: Specialized intestinal metaplasia was identified in the histological sections from the resected specimen in 42% (13/31) of cardiac adenocarcinomas and in 79% (38/48) of esophageal adenocarcinomas but in only 5% (1/21) of subcardiac adenocarcinomas. The preoperative endoscopic biopsy results concurred with the final diagnosis of Barrett's esophagus in 33 of the 38 esophageal tumors, six of the 13 cardiac tumors, and the one subcardiac tumor but failed to detect specialized intestinal metaplasia in 54% (7/13) of cardiac tumors. Cardiac tumors were associated with shorter lengths of Barrett's mucosa than esophageal tumors (2.7 +/- 1.8 cm vs 7.4 +/- 3.4 cm, P < .01). The Barrett's metaplasia was dysplastic in 36 of the 38 esophageal tumors, 10 of the 13 cardiac tumors, but not in the subcardiac tumor. CONCLUSIONS: Adenocarcinomas located at the gastroesophageal junction were associated with Barrett's metaplasia in nearly one half of the patients. The length of the Barrett segment tends to be short and may be missed during endoscopy. The presence of high-grade dysplasia within Barrett's mucosa supports a barrett's origin for half of the adenocarcinomas arising at this location.

Adenocarcinoma↗
PubMed1994

Gastric remnant cancer has a better prognosis than primary gastric cancer.

OBJECTIVE: To study the prognosis of gastric remnant cancer following radical resection (group 1) compared with that of primary gastric cancer of the upper third of the stomach following radical resection (group 2). DESIGN: Cohort study with a 5-year follow-up. SETTING: A university hospital in Austria. PATIENTS: Group 1 consisted of 43 patients, and group 2, of 61. Postoperative deaths and deaths during the follow-up period that were not related to gastric cancer were excluded. Fifteen patients in group 1 (34.9%) presented with stage I cancer; 10 (23.3%), stage II; 13 (30.2%), stage III; and five (11.6%), stage IV. Twenty patients in group 2 (32.8%) presented with stage I cancer; 12 (19.7%), stage II; 15 (24.6%), stage III; and 14 (22.9%), stage IV (Union Internationale Contre le Cancer staging classification, 1987). MAIN OUTCOME MEASURES: Overall and stage-related 5-year survival rates. RESULTS: The overall 5-year survival rate was 53.5% in group 1 and 32.8% in group 2 (P < .05). The stage-related 5-year survival rate in group 1 was 100% for stage I and 80% for stage II. In group 2, the stage-related 5-year survival rate was 65% for stage I and 25% for stage II (both, P < .01). No significant difference was noted for stages III and IV. CONCLUSIONS: The prognosis of cancer of the gastric remnant presenting as stage I or II is good and is significantly better than that of the equivalent stages of primary cancer of the upper third of the stomach.

Adolescent↗
PubMed1994

Thoracoscopic esophageal myotomy--a surgical technique for achalasia diffuse esophageal spasm and "nutcracker esophagus".

Thoracoscopic myotomy has been performed for diffuse esophageal spasm "nutcracker esophagus" and achalasia. Technical considerations for thoracoscopic long myotomy such as trocar placement, length of myotomy, extent of myotomy distal to the gastroesophageal junction, hiatal closure, fundoplication and degree of esophageal mobilization are discussed.

Esophageal Achalasia↗
PubMed1994

Effect of gastroduodenal juice and dietary fat on the development of Barrett's esophagus and esophageal neoplasia: an experimental rat model.

BACKGROUND: Reflux of duodenal content into the lower esophagus of rats enhances the formation of nitrosamine-induced esophageal cancer and results in the induction of adenocarcinoma. We investigated the extent of the mucosal injury that was produced when the lower esophagus of rats was exposed to the reflux of gastroduodenal juice in the presence or absence of a carcinogen and tested the hypothesis that induction of esophageal cancer in this model would be influenced by the intake of dietary fat. METHODS: Esophagoduodenostomy with gastric preservation was performed in 165 Sprague-Dawley rats in order to expose the lower esophagus to the reflux of gastroduodenal juice. Postoperatively selected groups of rats were treated with the carcinogen methyl-n-amylnitrosamine (MNAN). Subsequently, rats were fed diets of differing fat and calorie content for 20 weeks until they were put to death. RESULTS: Refluxed gastroduodenal juice, in the absence of MNAN, induced esophageal inflammatory changes (diffuse papillomatosis and hyperkeratosis) in 38 of 39 rats (97%), specialized columnar metaplasia (Barrett's esophagus) in four of 39 (10%), dysplasia in three of 39 (8%), and squamous cell carcinoma in one of 39 (3%). Diet did not influence the incidence of neoplasia in the absence of MNAN treatment. In rats treated with MNAN, refluxed gastroduodenal juice induced inflammation in 110 of 111 rats (99%), columnar metaplasia in 14 of 111 (13%), and cancer in 63 of 111 (57%). Fifty-eight percent of esophageal tumors were squamous cell carcinoma and 42% were adenocarcinoma. The highest incidence of tumors was observed in rats fed the semipurified high-fat diet (24 of 29; 83%) compared with rats fed the semipurified control diet (13 of 29; 45%), semipurified, calorie-restricted diet (15 of 27; 55%), and chow diet (11 of 26; 42%), p < 0.05. CONCLUSIONS: Reflux of gastroduodenal content into the lower esophagus of rats can induce both Barrett's metaplasia and neoplasia. Addition of a carcinogen increases the tumor yield and results in a proportion of the lesions being adenocarcinoma. This carcinogenic process is promoted by a diet with a high fat content.

Adenocarcinoma↗
PubMed1994

Gastroesophageal reflux disease is associated with enteric hormone abnormalities.

Basal and postprandial levels of the foregut hormones gastrin, cholecystokinin (CCK), motilin, and pancreatic polypeptide, and the distal gut hormones neurotensin and peptide YY were measured in 20 patients with gastroesophageal reflux disease (GERD). GERD was defined by abnormal esophageal exposure to pH less than 4. Ten GERD patients had decreased lower esophageal sphincter (LES) pressure (mean: 4.5 mm Hg, range: 0.8 to 6.8 mm Hg), and 10 patients had normal LES pressures (mean: 14.1 mm Hg, range: 9.7 to 22.4 mm Hg). Eight age-matched healthy subjects were also studied. Basal levels of peptide YY were moderately decreased in GERD patients compared with controls irrespective of LES pressure. In patients with abnormal LES pressure, basal levels of motilin and the postprandial response of CCK were significantly decreased compared with controls; and basal levels of neurotensin and the postprandial response of gastrin were significantly increased compared with controls. Pancreatic polypeptide levels were similar in all groups. These gut hormone changes, which are more marked in patients with poor LES pressure, may reflect primary or secondary abnormalities in GERD.

Esophagogastric Junction↗
PubMed1994

Laparoscopic Nissen fundoplication is an effective treatment for gastroesophageal reflux disease.

OBJECTIVE: The open Nissen fundoplication is effective therapy for gastroesophageal reflux disease. In this study, the outcomes in 198 patients treated with the laparoscopic Nissen fundoplication was evaluated for up to 32 months after surgery to ascertain whether similar positive results could be obtained. SUMMARY BACKGROUND DATA: To ensure surgical success, patients were required to have mechanically defective sphincters on manometry and increased esophageal acid exposure on 24-hour pH monitoring. The patients either had severe complications of gastroesophageal reflux disease or had failed medical therapy. These requirements have been found to be necessary to ensure a successful surgical outcome. METHODS: The disease was complicated by ulceration (46), stricture (25) and Barrett's esophagus (33). Patients underwent standard Nissen fundoplications identical in every detail to open procedures except that the procedures were carried out by the laparoscopic route. RESULTS: Perioperative complications included gastric or esophageal perforation (3), pneumothorax (2), bleeding (2), breakdown of crural repair (2) and periesophageal abscess (1). The only mortality occurred from a duodenal perforation. Six patients required conversion to the open procedure. The median hospital stay was 3 days. One hundred patients were observed for follow-up for 6 to 32 months (median 12 months), with outcomes similar to the open Nissen fundoplication. Further surgery was required for two patients who had recurrent gastroesophageal reflux and one who developed an esophageal stricture. Ninety-seven percent are satisfied with their decision to have the operation. CONCLUSIONS: The laparoscopic Nissen fundoplication can be carried out safely and effectively with similar positive results to the open procedure and with all of the advantages of the minimally invasive approach.

Anesthesia, General↗
PubMed1994

Interposition of 'narrow' cycloperistaltic segments into isolated segments of jejunum--influence on fluid perfusion.

Two isolated segments of jejunum with the ends exteriorised as jejunostomies were created in each of 8 dogs. Towards the end of one of the two, a cycloperistaltic (C-P) segment, with a diameter 70% of that of the jejunum, was interposed. Fluid containing C-labelled polyethylene glycole [corrected] was infused at 4 ml/min through each of the 16 preparations and the results were compared. The presence of a C-P segment significantly reduced the volume of output (with C-P segment--mean (+/- standard deviation) 155.27 +/- 14.81 ml/h v. without C-P segment--210.09 +/- 19.41 ml/h) (P < 0.001) and increased absorption (with C-P--45.44 +/- 20.86 ml/h v. without C-P--20.48 +/- 8.42 ml/h) (P < 0.001) and pooling (with C-P--39.29 +/- 16.99 ml/h v. without C-P--9.42 +/- 17.16 ml/h) (P < 0.001). The C-P segment therefore delayed the passage of the perfused fluid.

Anastomosis, Surgical↗