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Biomedical subjects

R A Hinder

Publications and source records attributed to R A Hinder.

At least 127 records · Page 7Linked to original sources
PubMed1991

Beware of the porcelain gallbladder during laparoscopic cholecystectomy.

Technical problems of retraction and hemorrhage during laparoscopic removal of a porcelain gallbladder are described. Although laparoscopic cholecystectomy was successful, a blood transfusion was required. We believe that porcelain gallbladder is a relative contraindication to laparoscopic cholecystectomy. The merits of plain radiography, computed tomography, and ultrasound in making the diagnosis are also discussed.

Blood Loss, Surgical↗
PubMed1991

Gallstones in the peritoneal cavity. A clinical and experimental study.

Gallstones are commonly lost into the peritoneal cavity during cholecystectomy. We investigated the effect of this occurrence using a rabbit model and also by a postal questionnaire of patients in whom gallstones were lost at the time of laparoscopic cholecystectomy. No deleterious effects could be demonstrated, and it is concluded that there is no indication for a laparotomy to retrieve "escaped" gallstones during laparoscopic cholecystectomy.

Adult↗
PubMed1991

Chronic gastritis.

Explore the source record for details and available documents.

Chronic Disease↗
PubMed1990

Clinical use of 24-hour gastric pH monitoring vs o-diisopropyl iminodiacetic acid (DISIDA) scanning in the diagnosis of pathologic duodenogastric reflux.

The efficacy of o-diisopropyl iminodiacetic acid (DISIDA) scanning was compared with that of computerized analysis of 24-hour gastric pH monitoring to diagnose excessive duodenogastric reflux in 22 normal volunteers and 106 consecutive patients with foregut symptoms. DISIDA scanning had a false-positive rate of 18% in the normal volunteers. Gastric pH monitoring showed an increasing prevalence of duodenogastric reflux in patients with increasing clinical evidence of this condition, which was not seen with DISIDA scanning. Both DISIDA scanning and gastric pH monitoring identified duodenogastric reflux in most patients who had had previous pyloroplasty or antrectomy. Only gastric pH monitoring, however, showed a significantly increased prevalence of duodenogastric reflux in symptomatic patients after previous cholecystectomy compared with those who had not undergone previous surgery. These data suggest that 24-hour gastric pH monitoring is superior to DISIDA scanning in identifying duodenogastric reflux as a cause of foregut symptoms.

Adolescent↗
PubMed1990

Surgical therapy in Barrett's esophagus.

Seventy-six patients with Barrett's esophagus were cared for during a 10-year period. Fifty-six patients (74%) presented with complications of the disease. There were 20 strictures, 7 giant ulcers, 11 cases of dysplasia, and 29 patients with carcinoma. In patients with benign disease, 93% had mechanically defective sphincters and 83% had peristaltic failure of the lower esophageal body. Esophageal pH monitoring showed excessive esophageal exposure to pH less than 4 in 93% and excessive exposure to pH more than 7 in 34% of the patients tested. Ninety-three per cent of patients with excessive alkaline exposure had complications, compared to only 44% with normal alkaline exposure (p less than 0.01). Gastric pH monitoring, serum gastrin levels, and gastric acid analysis supported a duodenal source for the alkaline exposure. Antireflux surgery was performed using Nissen fundoplication in 30, Belsey partial fundoplication in 3, and Collis-Belsey gastroplasty in 2. Six required resection with colon interposition. Good symptomatic control was achieved in 77% after antireflux surgery. Four patients had symptoms and signs of duodenogastric reflux; three required a bile diversion procedure. Fifteen patients had an en bloc curative resection with colon interposition. One patient with high-grade dysplasia on biopsy was found to have intramucosal carcinoma after simple esophagectomy. Five tumors were intramucosal, seven were intramural, and four were transmural. Lymph node involvement occurred only in the latter two. Actuarial survival 5 years after curative resection was 53%. Median survival time for patients after palliative resection or no resection was 12 months. Study of en bloc specimens indicated that extent of resection should be adapted to extent of disease: esophagectomy for intramucosal disease, en bloc esophagectomy with splenic preservation for intramural and transmural disease. Serum CEA was useful in detecting recurrent disease after surgery when the primary tumor stained positively for CEA.

Adenocarcinoma↗
PubMed1990

Gastric mucosal injury caused by hemorrhagic shock and reperfusion: protective role of the antioxidant glutathione.

Oxygen free radicals have been implicated as mediators of gastric mucosal injury caused by ischemia/reperfusion. We investigated the role of exogenous and endogenous glutathione (reduced glutathione, GSH) in gastric mucosal injury associated with hemorrhagic shock and reperfusion. Mucosal GSH content was found to be consistently higher in the antrum than in the corpus. Ischemia (hemorrhage to 25 to 30 mm Hg) followed by retransfusion of shed blood, but not ischemia alone, caused a marked drop in gastric mucosal GSH and gross mucosal injury, which was confined to the corpus and spared the antrum. Chemical depletion of gastric mucosal GSH with diethylmaleate or inhibition of GSH synthesis with buthionine sulfoximine increased mucosal injury in the corpus and also rendered the antral mucosa susceptible to ischemia/reperfusion injury. Pretreatment with exogenous GSH provided marked protection against gross mucosal ischemia/reperfusion injury and prevented the ischemia/reperfusion-induced drop in mucosal GSH. These data suggest that the mucosal availability of the antioxidant GSH is an important protective factor against the development of gastric mucosal ischemia/reperfusion injury and supports a major role of oxygen radical release in the pathogenesis of gastric ischemia/reperfusion injury.

Animals↗
PubMed1989

Analysis of thirty-two patients with Schatzki's ring.

Schatzki's ring is a distinct anatomical entity associated with hiatal hernia; however, its significance is unclear. Thirty-two patients with a radiologically demonstrated Schatzki's ring were compared with 32 patients with hiatal hernia and no Schatzki's ring. Schatzki's ring was confirmed on endoscopy in 59 percent of patients. Seventy-five percent of patients with Schatzki's ring presented with dysphagia compared with 41 percent of control patients (p less than 0.01). Heartburn and regurgitation were less frequent than in control subjects (38 percent versus 91 percent, p less than 0.0001). Schatzki's ring patients were found to have a lower incidence of proven gastroesophageal reflux on 24-hour pH monitoring. Those with proven reflux were found to have a more efficient lower esophageal sphincter than control patients. Sixty-two percent of Schatzki's ring patients without proven reflux had a history of chronic ingestion of drugs known to be damaging to the esophageal mucosa, whereas only 26 percent of patients with reflux had this history. This was found in 16 percent of controls. Sixty-two percent of Schatzki's ring patients without reflux responded to a single dilatation compared with 37 percent of those with reflux. These findings suggest an etiologic relationship between pill lodgement and Schatzki's ring in patients without reflux and indicate that different therapy should be employed in these patients.

Adult↗
PubMed1989

Does delayed gastric emptying contribute to gastroesophageal reflux disease?

We studied 76 patients with symptoms of heartburn, regurgitation, or both and 38 asymptomatic control subjects by measuring the gastric emptying of technetium-99m-labeled oatmeal. In addition, we performed 24-hour esophageal pH monitoring and manometric studies of the esophagus on all study participants. Endoscopy was performed on all patients. Patients with proved reflux on 24-hour pH monitoring, in comparison to those without reflux and the control subjects, had a shorter lower esophageal segment with a lower pressure and more esophagitis. Delayed gastric emptying occurred with equal frequency in patients with and without reflux. Esophageal reflux was not associated with delayed gastric emptying. Delayed emptying was associated with less esophagitis than found in those with normal gastric emptying, suggesting that the prolonged presence of food in the stomach may have a buffering effect on gastric acidity. We concluded that delayed emptying is not a major factor in the pathophysiology of gastro-esophageal reflux disease and that therapy aimed at speeding gastric emptying cannot be supported by our results.

Adult↗
PubMed1989

Luminal acid reduces gastric mucosal blood flow in the ischemic stomach.

Luminal gastric acid is essential for the formation of acute gastric mucosal lesions during ischemia. The mechanism by which luminal acid promotes gastric injury is, however, unclear. We investigated the effect of exogenous luminal acid on gastric mucosal blood flow using the radiolabeled microsphere technique. In rats with intact gastric blood supply application of exogenous luminal acid increased blood flow to the mucosa of the corpus and antrum. However, after ligation of the left gastric artery, which compromised mucosal blood flow to the corpus, application of luminal exogenous acid further decreased blood flow to the corpus. This indicates that the ability of the normal stomach to respond to luminal acidification with an increase in blood flow, which is thought to support clearance of back diffusing H+, is reversed in the ischemic stomach. The exposure to high luminal H+ concentrations may therefore promote gross injury in the ischemic stomach by further compromising nutritional mucosal blood flow.

Animals↗
PubMed1989

Relationship of a satisfactory outcome to normalization of delayed gastric emptying after Nissen fundoplication.

Delayed gastric emptying in patients with gastroesophageal reflux disease may be due to an incompetent distal esophageal sphincter and/or a gastric abnormality. To determine the influence of the Nissen fundoplication on gastric emptying we studied the rate of gastric emptying before and after operation in 25 patients with proved gastroesophageal reflux disease. Nine patients had no gastric pathology, 9 had gastric acid hypersecretion, 5 had gastritis, and 2 had evidence of significant duodenogastric reflux. All were treated by Nissen fundoplication. Those with gastric acid hypersecretion also had a proximal gastric vagotomy (PGV) and the two patients with pathologic duodenogastric reflux were treated by a bile diversion procedure. We found that in gastroesophageal reflux disease with associated gastric pathology there was a higher prevalence of delayed gastric emptying before operation than in patients without gastric pathology. Nissen fundoplication was associated with speeding of gastric emptying in patients with or without gastric pathology. Proximal gastric vagotomy performed in association with Nissen fundoplication augmented the speeding of gastric emptying, which was advantagenous in most cases but detrimental in two. Every patient in whom gastric emptying was not normalized had postoperative symptoms. Only two of 20 patients with normal postoperative gastric emptying had postoperative symptoms. Both patients had preexisting gastric pathology. Based on these findings, the side effects associated with Nissen fundoplication are due to the failure to normalize gastric emptying rather than the operation.

Follow-Up Studies↗
PubMed1989

Direct cytotoxic effect of oxygen radicals on the gastric mucosa.

Oxygen radical release has been proposed as a pathogenetic factor in the formation of acute gastric mucosal injury. We assessed the ability of the naturally occurring oxygen radical generating system hypoxanthine/xanthine oxidase (HX/XO) to cause gross gastric mucosal injury and measured the effect on regional mucosal blood flow. Local intra-arterial infusion of HX/XO into the vascular network of the stomach caused marked gross mucosal injury in the antrum and corpus. This injury occurred even in the absence of exogenous luminal acid and was aggravated by luminal acidification with 1 ml of 0.1N HCl. The selective oxygen radical scavenger superoxide dismutase (SOD) prevented mucosal injury caused by HX/XO. The effects of HX/XO and SOD were not mediated by alterations in regional gastric mucosal blood flow, as measured by the radiolabeled microspheres and reference sample method. These findings suggest that oxygen radicals are capable of causing substantial gastric mucosal injury by a direct cytotoxic effect independent of luminal acid or mucosal blood supply and give support to the concept that oxygen radical release may be a major primary pathogenetic factor in the development of acute gastric mucosal injury.

Animals↗
PubMed1989

Verapamil improves survival of rat hyperemic island skin flaps.

Inability to maintain cellular calcium homeostasis is a critical factor in the pathogenesis of cellular ischemic injury and may mediate oxygen radical release in the reperfusion period. We assessed the effect of the selective calcium channel blocker verapamil on the performance of rat hyperemic island skin flaps. Pretreatment with verapamil markedly improved survival of skin flaps after 6 hours of venous cross-clamping compared with animals receiving placebo only (99% vs 53.3%; p less than 0.01). Verapamil also prevented the formation of lipid peroxidation products and the depletion of the endogenous antioxidant glutathione, suggesting that the beneficial effect of verapamil is the result of protection against oxygen radical injury. After 12 hours of venous cross-clamping, verapamil did not improve survival of skin flaps despite protection against lipid peroxidation. Oxygen radical release is therefore a crucial event in the pathogenesis of skin flap necrosis after short-term ischemia but is of less significance in long-term ischemia.

Animals↗
PubMed1989

Alkaline gastroesophageal reflux: implications in the development of complications in Barrett's columnar-lined lower esophagus.

Barrett's esophagus is a common finding in patients with gastroesophageal reflux and is associated with a high incidence of serious complications (stricture, ulceration, and carcinoma). The reason that only a portion of patients with reflux develop Barrett's esophagus and why some are prone to develop complications is unknown. Twenty-three patients with Barrett's esophagus underwent endoscopy, 24-hour esophageal pH monitoring, and manometry. Nine of these patients with gastritis underwent 24-hour gastric pH monitoring, and three with symptoms of duodenogastric reflux underwent 99mTc-labeled hepato-iminodiacetic acid scanning. Patients with complicated (n = 12) and uncomplicated (n = 11) Barrett's esophagus were compared with each other and with patients with reflux esophagitis (n = 53) and normal volunteers (n = 50). Patients with Barrett's esophagus showed an increased exposure to acid and alkaline gastric juice compared with patients with esophagitis and normal volunteers. In the patients with Barrett's esophagus with and without complications, there was no significant difference in age, incidence of defective lower esophageal sphincter, incidence of defective peristalsis, extent of the Barrett's epithelium, or percent time the esophageal pH was less than 4. In contrast, the percent time the esophageal pH was greater than 7 was significantly greater in patients with complications. This alkaline exposure is likely to be related to duodenogastric reflux. This was supported by positive gastric pH scores for duodenogastric reflux and 99mTc-labeled hepato-iminodiacetic acid scans in patients with Barrett's complications. These findings suggest that the development of complications in Barrett's esophagus is the result of the damaging effect of refluxed duodenal juice.

Alkalies↗
PubMed1988

Gastric mucosal lesions induced by hemorrhagic shock in baboons. Role of oxygen-derived free radicals.

In this study we sought to define the role of oxygen-derived free radicals during ischemia and reperfusion in the production of acute damage to the gastric mucosa of baboons. The protective effect of the xanthine oxidase inhibitor, allopurinol, the superoxide scavenger, superoxide dismutase (SOD), and a long-acting SOD-albumin was determined. Mucosal damage was evaluated using light and scanning electron microscopy. Evidence for oxidative insult to the gastric mucosa was sought by measuring tissue concentrations of reduced (GSH) and oxidized (GSSG) glutathione. Gastric mucosal blood flow was estimated using the microsphere technique. A similar pattern of tissue damage was found at the end of ischemia in all three groups. Thirty minutes after reperfusion, severe mucosal damage (grade 3) increased only in the untreated control. In the two treated groups, grade 3 damage remained unchanged during reperfusion and a decrease in the percentage of moderate damage (grade 2) was seen. Both GSH and GSSG tissue concentrations were lower in the untreated controls as compared to the scavenger-treated groups, making it questionable whether GSH/GSSG tissue levels adequately reflect oxidative stress. We conclude that in our ischemia-reperfusion model the generation of oxygen-derived free radicals produces mucosal damage and prevents the restitution of moderate mucosal damage during reperfusion. In ischemia, factors other than free radicals seem to be responsible for mucosal damage. The protective effect of allopurinol and SOD was not mediated by changes in gastric mucosal blood flow.

Allopurinol↗
PubMed1988

Stimulation of gastric acid secretion increases mucosal blood flow in immediate vicinity of parietal cells in baboons.

In acute experiments carried out in 27 baboons under general anesthesia, the regional gastric mucosal and muscle layer blood flow and gastric acid secretion were measured during 4 hr. Baboons were allocated to each of the following six groups: control, gastric acid stimulation with histamine 40 micrograms/kg/hr intravenous, inhibition of basal or stimulated acid secretion with either ranitidine 50 mg intravenous or omeprazole 1 microgram/kg/hr. There were no significant cardiovascular alterations during the experiments. Histamine stimulation produced a concomitant rise in acid secretion and increase in blood flow only to the mucosal layer of the parietal-cell-bearing area of the stomach. Neither the underlying muscle layer nor the non-parietal-cell-bearing fundic or antral mucosa took part in this response, suggesting that a mechanism controlling blood flow is present in close proximity to the parietal cells. It was also established that the increase in blood flow occurs in response to parietal cell activity and not as a result of the action of histamine on the vascular system. Suppression of both basal and stimulated acid secretion did not cause a fall of mucosal blood flow below basal levels in any part of the stomach, indicating that drugs that inhibit parietal cell activity can be used in conditions where gastric mucosal ischemia should be avoided.

Animals↗
PubMed1988

Microsphere estimates of blood flow: methodological considerations.

The microsphere technique is a standard method for measuring blood flow in experimental animals. Sporadic reports have appeared outlining the limitations of this method. In this study we have systematically assessed the effect of blood withdrawals for reference sampling, microsphere numbers, and anesthesia on blood flow estimates using radioactive microspheres in dogs. Experiments were performed on 18 conscious and 12 anesthetized dogs. Four blood flow estimates were performed over 120 min using 1 X 10(6) microspheres (15 microns) each time. The effects of excessive numbers of microspheres (13 million), pentobarbital sodium anesthesia (30 mg/kg), and replacement of volume loss for reference samples with dextran 70 were assessed. In both conscious and anesthetized dogs a progressive decrease in gastric mucosal blood flow and cardiac output was observed over 120 min. This was also observed in the pancreas in conscious dogs. The major factor responsible for these changes was the volume loss due to reference sample withdrawals. Replacement of the withdrawn blood with dextran 70 led to stable blood flows to all organs. The injection of excessive numbers of microspheres did not modify hemodynamics to a greater extent than did the injection of 4 million microspheres. Anesthesia exerted no influence on blood flow other than raising coronary flow. We conclude that although blood flow to the gastric mucosa and the pancreas is sensitive to the minor hemodynamic changes associated with the microsphere technique, replacement of volume loss for reference samples ensures stable blood flow to all organs over a 120-min period.

Animals↗
PubMed1988

Induction of anacidity restores gastric aminopyrine clearance in canine hemorrhagic shock.

The determinants of gastric aminopyrine clearance were studied in a canine hemorrhagic shock model. Adult mongrel dogs were anesthetized, and their stomachs perfused with 0.1 N HCl through an esophageal and a duodenal cannula. Blood flow to the serosal layer of the anterior gastric wall was measured by a laser flowmeter. Hemorrhagic shock was induced by controlled arterial bleeding to a mean systolic blood pressure of 40 +/- 5 mm Hg (n = 8), resulting in a 36 +/- 8% drop of gastric wall blood flow. In contrast, the aminopyrine clearance did not reveal the expected drop and remained unchanged during shock. When acid secretion was abolished by intravenous omeprazole (1.3 mg/kg bolus plus 0.75 mg/kg/h infusion), aminopyrine concentrations dropped in the gastric perfusate and rose in the serum during shock, resulting in a similar decrease in the clearance (53 +/- 25%) as compared to the flowmeter readings. In control experiments without hemorrhagic shock, omeprazole did not affect the concentrations of aminopyrine in serum and in the perfusate, or the recovery of 14C-labeled aminopyrine in the mucosa at the end of the experiment. These studies indicate that the aminopyrine clearance is impaired in hemorrhagic shock, and that complete inhibition of acid secretion by omeprazole restores the apparent aminopyrine clearance by divergent effects on blood and gastric juice concentrations of aminopyrine.

Aminopyrine↗