Biomedical subjects
Publications and source records attributed to D Liebermann-Meffert.
Using human gastric specimens, figures are presented for gastric muscle thickness and the myoarchitecture is described. The study shows that the blood supply to the cardia, gastric fundus and body is excellent, due to the many anastomosing arteries, but is less good at the curvatures of the gastric antrum and poor at the anterior and posterior walls of this area, due to absent or minute anastomoses.
Electrodes were chronically implanted in some of 14 cats and acutely inserted in others in the muscle of the high pressure zone of the lower esophagus (LEHPZ), in the duodenum, pylorus and antrum at identical location to register the myogenic electrical activity of the LEHPZ. Simultaneously the intraluminal pressure of the LEHPZ and swallowing contractions were recorded on a 6 channel Beckman R 611 ink-pen polygraph using stationary perfusion manometry. A clear basic electrical rhythm with slow wave activity was regularly found in the LEHPZ. Strong electrical changes (action potentials) were superimposed on the slow waves which were associated with relaxation in the LEHPZ and muscle contraction in the esophagus. Electric stimulation of the duodenum and pylorus with rectangular impulses produced retrograde peristalsis in the antrum but no response in the LEHPZ. Direct stimulation of the LEHPZ and gastric fundus, however, caused a strong transient contraction of the LEHPZ.
Pyloric channel ulcers have a significantly higher recurrence rate than duodenal ulcers after proximal gastric vagotomy (PGV) without drainage. The failure of PGV cannot be explained by the pre- and postoperative secretory pattern of pyloric (PU) and prepyloric (PPU) ulcers. The morphological assessment of the pyloric and antral wall in DU, PU and PPU shows a significant thickening of the muscular layer in PU and PPU compared with DU. Histologically there is a muscular hypertrophy combined with muscular and ganglionic cell damage and fibrosis. The observed antropyloric dystrophy might be one factor for explaining the failure of PGV alone in pyloric channel ulcers. Addition of a drainage procedure for PU or even of a limited antrectomy for PPU might improve the postoperative results and must be discussed when planning surgical treatment of pyloric channel ulcers which seem to characterise as a distinct entity of peptic ulcer disease.
We examined the effect of acid and bile on the lower esophageal high pressure zone (LEHPZ) in a combined manometric, pH testing and morphologic study in 12 cats. LEHPZ pressures and swallowing waves (SW) were simultaneously recorded before, during and after perfusion of the esophagus with control fluid, acid (0.1 n HCl) natural bile and a mixture of acid and bile. Endoscopy was performed and biopsies taken before and after the experiments. Bile caused a rise of LEHPZ and SW pressure and mild esophagitis. Acid and bile acid mixture produced a marked progressive decline of LEHPZ and SW pressure (p less than 0.001), incomplete relaxation and severe discoordination of esophageal motility. Continuous pH measurements showed diminished or no clearance and reflux. All acid perfused cats developed necrotic esophagitis and strictures within 4 weeks. LEHPZ pressures returned to almost normal values after this recovering period but peristalsis was still completely discoordinated. Swallowing waves were of exaggerated magnitude and length. From our findings it is evident that bile and acid change LEHPZ competence. Bile and acid seem to have a different effect on motor function of the LEHPZ and esophageal peristalsis.
Impaired gastric emptying in gastric ulcer patients has generally been explained by gastric hypomotility. The gastric motor response to an electrical vagal stimulus was measured intraoperatively in patients with gastric ulcers (GU, n = 21), duodenal ulcers (DU, n = 25) and combined ulcers (GDU, n = 6). Amplitude and duration of the contraction and integrated motor response were found to be significantly greater in GU patients than in patients with duodenal and combined ulcers. Thus, hypermotility of the gastric muscle exists in GU patients and the delayed gastric emptying in GU disease may be the result of antropyloric motor dysfunction rather than of gastric hypotony. Abnormal motility associated with duodenogastric reflux appears to be a key feature in the pathogenesis of gastric ulcer.
Pathomorphology of antropyloric wall in peptic ulcer disease includes: 1. Asymmetrical hypertrophy of the muscle, 2. Reversible changes and irreversible damage of a part of muscle cells and ganglia, 3. Tissue infiltration: Eosinophils and mast cells, 4. Scar formation (fibrosis) in the muscle and submucosa, 5. Edema formation of the submucosa. This is not found in controls but constant in peptic ulcer disease. Changes do not depend upon the ulcer site, size and number and are common in the antropyloric wall of all patients with peptic ulcer but most pronounced in gastric ulcer.
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Impaired gastric emptying in gastric ulcer patients has been explained by gastric hypomotility. Amplitude and duration of the contraction and integrated motor response to an electrical vagal stimulus, however, have been found to be significantly greater in 21 GU patients than in 25 DU and 6 combined ulcer patients. This shows hypermotility of the gastric muscle in GU patients. Delayed gastric emptying in GU disease, therefore, seems to result rather from antropyloric motor dysfunction than from gastric hypotony. Abnormal motility associated with duodeno-gastric reflux appears to be a key feature in the pathogenesis of gastric ulcer.
Macroanatomic structures in the lower esophagus and at the GE-junction are shown and definitions are given. Muscle structures and thickening in the GE-junction region and fundus are shown and their relationship to the intraluminal high pressure zone is discussed. Anchorage of the esophagus to the diaphragm through the phreno-esophageal membrane in relation to aging, disposition and hiatal hernia is discussed. Vascularization of the esophageal wall by numerous submucosal arteries is shown.
The greater omentum is an organ of excellent absorption ability and or infect defence. Transposition at vascular pedicle is a simple and very useful procedure. According to our experience with 8 patients it is most suitable to fill hollow spaces for example in the liver (echinococcus cysts); it is also very useful for covering huge contaminated irradiation defects frequently occurring with pelvic exenteration.
In order to measure muscle thickness and to define the muscular architecture at the gastroesophageal function, both en bloc fixation and a new method of preparing dried fiber specimens were used. Specimens were obtained from 32 kidney donors and human cadavers. Wall thickness was measured at 32 identical locations in the esophagus and stomach. The oblique gastroesophageal ring (GER) was the site of greatest muscular thickness and served as a reference point. From the GER the muscle thickness tapered (P less than 0.05 to P less than 0.001) in both a cephalic (esophageal) and caudal (gastric) direction for a length of 31 mm +/- 2.5 SD. The increase in thickness was due to an increase in the muscle mass (fiber aggregation) of the inner muscle coat. The muscle bundles of this coat split up 10.2 mm +/- 3.0 SD above the GER (fixed specimen) and for a length of 25 mm +/- 8 SD formed short transverse muscle clasps on the lesser curve side. Those muscle bundles on the greater curve side formed long oblique gastric fiber loops. The angle of His was inconstant in location and distal to the uppermost gastric oblique fibers (18 mm +/- 7 SD) and to the GER (9 mm +/- 6 SD).
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Relationship between gastric ulcer (n = 100) site and antropyloric wall hypertrophy was examined in a prospective study. Irrespective of ulcer multiplicity most ulcers were found to be located at the lesser curvature and at the posterior wall (p less than 0,001); men had significantly more ulcers at the posterior wall than females (p less than 0, 001). Single ulcers and those connected with pyloric stenosis were more distant to the pylorus than multiple ulcers (p less than 0,001). Ulcer location did not relate to hypertrophy of the pyloric channel wall. Observed differences between single and multiple ulcers were limited to wall parts only: the musculature of high located single ulcers was significantly less hypertrophied 2,5 cm orally of the pylorus (p less than 0,02) and that of high multiple ulcers was more hypertrophied at the pylorus (p less than 0,02) than in the other parts. These findings suggest that ulcer variations do not influence the diffuse antropyloric disease in gastric ulcer patients and suggest that the generalized antral changes are prior to gastric ulcer occurance.
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