[Anti-inflammatory drugs and gastrointestinal lesions, or vice versa].
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Biomedical subjects
Publications and source records attributed to F Mearin.
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Chronic (obesity) and acute intraabdominal pressure increases appear to favor gastroesophageal reflux, but the mechanism is not completely understood. We hypothesized that it could be due to an alteration in the resistance gradient between the stomach and the gastroesophageal junction, even increasing intragastric resistance above resistance at the gastroesophageal junction. Hence, we used a pneumatic resistometer to measure gastric and gastroesophageal resistance to flow in 11 lean healthy controls and eight morbidly obese individuals without gastroesophageal reflux disease. Resistance was quantified at rest and during acute intraabdominal pressure increases, both in the recumbent and sitting positions. We found that gastroesophageal junction resistance was higher than gastric resistance in lean as well as in obese subjects (P less than 0.001). In obese individuals both gastric and gastroesophageal junction resistance were increased (P less than 0.001), thus a normal gastric-gastroesophageal junction resistance gradient was maintained. Body position did not modify resistance. Acute increases in intraabdominal pressure decreased the gastric-gastroesophageal junction resistance gradient similarly in obese and lean subjects. We conclude that obesity by itself does not appear to predispose to gastroesophageal reflux, but it creates intraabdominal conditions that may favor reflux whenever the gastroesophageal barrier becomes weakened.
It was hypothesized that symptoms in functional dyspepsia are originated by an altered mechanism at the brain-gut axis (one or several) in the process of gastric accommodation to a meal. To test the key mechanisms potentially involved in symptomatic gastric accommodation, the sensorial responses (on a 0-10 perception score) and the gastric tone responses (by electronic barostat) to either gastric accommodation (n = 10) or to cold stress (n = 10) were measured in 20 patients with functional dyspepsia and 20 healthy controls. The mechanical accommodation of the stomach to gastric distention (compliance) was similar in patients (52 +/- 8 mL/mm Hg) and controls (57 +/- 6 mL/mm Hg). However, isobaric gastric distention elicited more upper abdominal discomfort in dyspeptics than in controls (perception scores, 4.7 +/- 0.9 vs. 1.1 +/- 0.5, respectively; mean +/- SE; P less than 0.005). Cold stress induced a similar gastric relaxatory response in dyspeptics and controls (delta vol, 145 mL +/- 40 mL vs. 141 mL +/- 42 mL, respectively); hand perception (scores, 8.3 +/- 0.4 vs. 7.9 +/- 0.4, respectively) and autonomic responses were also similar. It is concluded that an abnormal afferent sensorial pathway (altered gastric perception) may be a major mechanism of symptom production in functional dyspepsia.
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It has been suggested that low-frequency transcutaneous electric nerve stimulation (TENS) alleviates the dysphagia produced by achalasia and scleroderma of the esophagus. The present study was conducted to elucidate whether TENS treatment improves dysphagia because of changes it induces on esophageal motility. We studied nine achalasia patients before forceful dilatation of the cardias, nine achalasia patients after dilatation, and nine patients with scleroderma. High-frequency TENS was applied to the hand for 30 min while esophageal motility was monitored by manometry. In none of the groups did TENS produce any change in the basal tone of the lower esophageal sphincter, lower esophageal sphincter relaxation, or esophageal body wave amplitude. Low-frequency TENS, used in another seven untreated achalasia patients, also did not improve esophageal motility. Our data indicate that high- or low-frequency TENS does not induce detectable changes in esophageal motility in patients with achalasia or scleroderma.
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Little information is available regarding acute upper gastrointestinal bleeding as a presenting sign of gastric carcinoma. Of 427 patients with gastric cancer, 36 (8.4%) underwent early endoscopy due to hematemesis. The hemorrhage was self-limited in 16 patients (44.4%), most of whom underwent elective surgery. Twenty patients (55.6%) had persistent or massive bleeding, and 13 of these underwent early surgery with a surgical mortality of 3 cases (23.1%); the remaining 7 patients were not operated on, and died secondary to the hemorrhage. The total mortality rose to 10 patients (27.7%). The mean age was higher in patients with persistent or massive bleeding, mainly in those who did not undergo surgery and died. We conclude that the immediate outcome is related to age and previous general condition, rather than to the definite diagnosis of gastric cancer. Moreover, emergency endoscopy may be useful in determining the exact source of hemorrhage and in identifying potential candidates for emergency surgery.
Our objectives in this study were (a) to determine the role of antroduodenal resistance in the control of fasting duodenogastric bile reflux in the dog and (b) to elucidate the contribution of the pylorus both to resistance and to reflux. Thus, we measured simultaneously throughout the interdigestive motor cycle (a) antroduodenal pressure activity by manometry, (b) antroduodenal resistance by a pneumatic resistometer, and (c) bile acid concentrations in duodenal and gastric juices. Experiments were performed in 15 conscious dogs (9 with pylorus intact and 6 with extramucosal pyloric myotomy). We found that antroduodenal resistance was lowest during phase I, increased gradually during phase II, and peaked during phase III (linear trend, p less than 0.001). Duodenogastric bile reflux was low during phase I, peaked during late phase II, and decreased again during phase III (quadratic trend, p less than 0.05). Therefore, variations in net resistance and reflux were differently related to the phases of the interdigestive motor complex. Pyloric myotomy significantly decreased antroduodenal resistance (linear trend different from control, p less than 0.001), but had no significant effect on duodenogastric bile reflux. We conclude (a) that changes in net antroduodenal resistance do not regulate duodenogastric bile reflux and (b) that the pylorus is an important determinant of antroduodenal resistance, but has no major role in the control of fasting duodenogastric bile reflux.
We have developed a pneumatic resistometer to monitor antroduodenal resistance to flow for prolonged periods of time in conscious dogs. To investigate the specific contribution of the pylorus to antroduodenal resistance we compared resistance during fasting in four control dogs and in four dogs with extramucosal pyloric myotomy (1.5 cm long). After pyloric myotomy, as in controls, resistance to flow changed cyclically, being lowest during phase I and highest during phase III of the interdigestive motor cycle. Pyloric myotomy decreased resistance during phase III. Atropine (0.1 mg X kg-1 X h-1) administered during motor quiescence (phase I) reduced resistance in the control group (P less than 0.05) but not in myotomized animals. Bethanechol (0.2 mg X kg-1 X h-1) significantly increased resistance in both groups (P less than 0.05). We conclude that antroduodenal resistance to flow is related to cyclic interdigestive motility. The pylorus is the predominant determinant of antroduodenal resistance during motor quiescence, but its contribution diminishes markedly during motor activity.
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Diabetes mellitus has been associated with a variety of gastrointestinal motor disturbances. Pyloric activity, however, has not been specifically investigated. We have quantified the pyloric manometric profile in 24 diabetics with recurrent nausea or vomiting, or both, without evidence of mechanical obstruction. Twelve healthy volunteers served as controls. A multilumen pneumohydraulic perfusion assembly with five side openings, each 1 cm apart, was positioned fluoroscopically across the antroduodenal junction and used to monitor pressure activity for 5 h (3 h fasting and 2 h fed). Three patterns of pyloric activity were defined and quantified: (a) baseline elevation of greater than or equal to 3 mmHg for greater than or equal to 1 min (tonic pattern); (b) antral-type phasic pressure activity mixed with duodenal phasic activity (phasic pattern); and (c) phasic pattern superimposed on tonic activity (combined tonic-phasic pattern). The duration of the total pyloric activity before and after the meal was greater in diabetics than in controls (p less than 0.005). Furthermore, episodes of unusually prolonged (greater than or equal to 3 min) and intense (greater than or equal to 10 mmHg) tonic contraction, "pylorospasm," were observed in 14 of 24 diabetics but in only 1 control (p = 0.025). In diabetics, episodes of pylorospasm had a peak amplitude of tonic activity of 13 +/- 1 mmHg and a duration of 7 +/- 0.7 min (mean +/- SE). We conclude that pyloric dysmotility forms part of the widespread disruption of gut motility that affects some patients with diabetes.
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Changes in antroduodenal resistance to flow may participate in the regulation of gastric emptying and duodenogastric reflux. Little is known, however, about the relationship between antroduodenal resistance and the physiological patterns of contractile activity in this area. We have developed an instrument that maintains an electronically regulated constant-pressure gradient of 2 mmHg across both ends of a flaccid cylinder positioned fluoroscopically across the pylorus. Because resistance bears a constant inverse relationship to flow at a fixed pressure gradient, changes in the recorded rate of airflow through the cylinder are a measure of antroduodenal resistance. In vitro studies showed that, under these conditions, airflow was a function of the diameter and length of the air path and the frequency and duration of external pressure waves greater than 2 mmHg. In vivo studies in four dogs examined the relationship between interdigestive phases of motor activity and variations in resistance exerted by the antroduodenal area. We found that flow rates varied markedly with each phase. Antroduodenal resistance was lowest during motor quiescence (phase I), rose gradually during irregular activity (phase II), and reached its peak during maximal contractile activity (phase III) (P less than 0.05). Resistance was similar for antegrade and retrograde flow. Additional studies suggested that the pyloric area contributes mostly to resistance during phase I, whereas duodenal resistance at least matches that of the pylorus during phase III.