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At least 199 records · Page 11Linked to original sources
PubMed1999

The "floppy" Nissen fundoplication is a completely competent antireflux valve.

BACKGROUND: The antireflux capacity of various gastric fundoplications combines the creation of a valve (flapper or nipple) with recreation of a sharp cardioesophageal angle. Experimental comparison of valve competency and appropriate valve geometry is incomplete despite wide application of these techniques. Our primary aim was to compare the competency of several antireflux valves in explanted cadaver stomachs. Our secondary aim was to understand better the geometry of the gastric fundus in empty and full stomachs. METHODS: Stomachs with 6-8 cm of distal esophagus were harvested from 18 fresh cadavers. With the stomach empty, the greater and lesser curvature length and the transverse dimensions of the anterior and posterior surface of the stomach in the fundus, body, and antrum were measured. The pylorus was tied off over a catheter; the stomachs were inflated with water; and reflux occurred. Intragastric pressure was measured during inflation with a needle inserted in the side of the stomach. A clamp was then placed on the esophagus, and the stomach was inflated to a pressure of 10 mmHg. Gastric measurements were recalculated in the distended stomach. The stomachs were deflated, the clamp removed, and a 2-cm Nissen fundoplication as well as 270 degrees and 180 degrees posterior fundoplications were performed over a 60 Fr dilator. The stomachs were reinflated while the pressure was transduced. The inflation was stopped when reflux occurred or when the fundoplication disrupted. RESULTS: The stomachs expanded symmetrically when filled with water except for the fundus in which the anterior gastric wall lengthened by more than 100% and the posterior gastric wall lengthened by about 50%. In the untreated stomachs, reflux occurred at a pressure of 3.0 +/- 1.0 mmHg. After fundoplication, reflux never occurred, but the sutures pulled out of the stomach or esophagus at 28.6 +/- 16.8 mmHg. Posterior fundoplications refluxed water in several stomachs. CONCLUSIONS: When filled, the anterior fundus expands to a greater degree than the posterior fundus, offering more tissue for creation of floppy fundoplication. The "floppy" Nissen fundoplication is completely competent, suffering a degradation before allowing reflux. The posterior partial fundoplication is unpredictable in its competency.

Cadaver↗
PubMed1963

ENTEROMEGALY AND CARDIOMEGALY IN CHAGAS DISEASE.

Chagas disease due to a trypanosome infection may lead to extensive destruction of ganglion cells in the peripheral autonomic system and may result in gross enlargement of the oesophagus, colon, and heart. From studies on nerve cell counts it is concluded that the number of ganglion cells in the oesophagus must be reduced to less than half to produce functional disturbances in the oesophagus and to one tenth to produce a megaoesophagus. Problems of terminology are discussed.

Autonomic Nervous System↗
PubMed1987

[Gastric fundus necrosis following acute gastric dilatation].

Total gastrectomy with immediate re-establishment of digestive continuity successfully treated a patient with gastric fundus necrosis due to acute dilatation of stomach. The very particular circumstances of onset of this major complication are outlined, diagnosis being dependent on radiological and endoscopic findings. In cases with necrosis of the fundus the extensive nature of the ischemic lesions as shown by results of histopathology strongly suggests the need for total gastrectomy in these patients.

Bulimia↗
PubMed1995

Trophic effects in the acid-producing part of the rat stomach after pyloric stenosis.

BACKGROUND: Pyloric stenosis produces gastric hypersecretion and is thought to stimulate the growth of the gastric mucosa in the rat, the dog, and man. However, the mechanisms behind the hypersecretion and the trophic effect of pyloric stenosis are little known. The purpose of the present study was to examine whether the postulated trophic effects described include growth of the histamine-producing enterochromaffin-like (ECL) cells and whether circulating gastrin can be held responsible. METHODS: Pyloric stenosis was produced in rats by tying a ligature around the pylorus, thereby narrowing the passage through the sphincter. The animals were left for 4 to 12 weeks. RESULTS: The operation dilated the stomach, increased the serum gastrin concentration approximately twofold, and increased the oxyntic mucosal weight, volume, and surface area but not the mucosal thickness and total DNA content. The interglandular space was increased, and the DNA concentration was reduced. The density of the ECL cells (that is, the number of ECL cells per visual field) was reduced at 4 weeks and back to control values at 8 and 12 weeks. The calculated total volume of the ECL cell population was unchanged at first but showed a less than twofold increase 12 weeks after the operation. The volume density of the ECL cells (that is, the proportion of the mucosa made up of ECL cells) was reduced at 4 and 8 weeks and was back to normal at 12 weeks. The ECL cells are rich in histidine decarboxylase (HDC); whenever the cells are stimulated, the enzyme activity increases. The HDC activity in the oxyntic mucosa was reduced at first and returned to control values 12 weeks later. CONCLUSIONS: Pyloric stenosis per se does not affect the total number of oxyntic mucosal cells, but causes the ECL cell population to grow somewhat, probably because of the moderate hypergastrinemia. Interestingly, however, there was no increase in the HDC activity, suggesting that the ECL cells are not much activated by the operation.

Animals↗
PubMed1991

Involvement of nitric oxide in the reflex relaxation of the stomach to accommodate food or fluid.

The fundus of the guinea-pig stomach actively dilates in response to low increases in intragastric pressure. This physiological response, now called adaptive relaxation, accommodates the intake of liquid or food. It is independent of external innervation, resistant to ganglion blockade, but reflex in origin. The nerves involved are neither adrenergic nor cholinergic in nature. Non-adrenergic, non-cholinergic (NANC) nerves have now been recognized in many parts of the gastrointestinal tract and have recently been linked with release of nitric oxide (NO) on electrical stimulation. Here we show that adaptive relaxation in isolated stomach of the guinea pig is mediated by a NANC neurotransmitter substance indistinguishable from NO derived from L-arginine. This is substantiated by inhibition of adaptive relaxation by NG-monomethyl-L-arginine or N omega-nitro-L-arginine methyl ester, both inhibitors of NO synthesis, and by methylene blue, an inhibitor of soluble guanylate cyclase. There are two distinct neuronal pathways signalling NO-dependent adaptive relaxation, as evidenced by tetrodotoxin sensitivity. The first is a local reflex arc, the afferent fibres of which sense changes in intragastric pressure. The second is stimulated by an agonist for ganglionic nicotinic receptors. Thus, the functional significance of NO release from NANC nerves in the stomach is to bring about adaptive relaxation through a reflex response to increases in intragastric pressure.

Animals↗