Gastric Fundus Carcinoma

2020 ◽  
Author(s):  
Keyword(s):  
Gastric Fundus

The Impact of Nissen-Rossetti Fundoplication on the Perfusion in Microcirculation of the Gastric Fundus

2007 ◽  
Vol 79 (9) ◽  
Author(s):  
Stanisław Przywara ◽  
Grzegorz Wallner ◽  
Andrzej Dąbrowski ◽  
Tomasz Skoczylas ◽  
Jacek Wroński ◽  
...  
Keyword(s):  
Gastric Fundus ◽  
The Impact

scholarly journals An extremely rare case of a gastric accessory spleen: case report and review of the literature

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Guiqin Chen ◽  
Lei Nie ◽  
Tijiang Zhang
Keyword(s):  
Rare Case ◽  
Accessory Spleen ◽  
Gastric Fundus ◽  
Pathological Examination ◽  
Review Of The Literature ◽  
Gastric Bleeding ◽  
Computed Tomographic ◽  
Normal Spleen ◽  
Elevated Lesion ◽  
Lesser Curvature

Abstract Background The accessory spleen has no anatomical or vascular relationship with the normal spleen, The tissue structure and physiological function of the accessory spleen are the same as those of the normal spleen, which usually locate in the splenic hilum and the tail of the pancreas. The aims of this manuscript are to present a rare case of the gastric accessory spleen and a review of the literature. Case presentation A 19-year-old male patient was sent to the emergency department with stomach bleeding after drinking alcohol. The computed tomographic scan showed a 1.2 cm × 1.7 cm mass at the lesser curvature of the gastric fundus. Gastrointestinal endoscopy displayed a submucosal elevated lesion on the gastric fundus, and gastrectomy was performed. Postoperative pathological examination proved an accessory spleen in the stomach. The postoperative course was uneventful, and the patient was discharged on the 6th day after the surgery. Conclusions The accessory spleen at the fundus of stomach is extremely rare, especially in this case, which is accompanied by acute gastric bleeding, and it is difficult to diagnosis before operation. Many literatures reported that it was misdiagnosis as tumor, so it is necessary to diagnose accessory spleen correctly.

Linkage of [Ca2+]i in single isolated D cells to somatostatin secretion induced by cholecystokinin

1996 ◽  
Vol 270 (6) ◽  
pp. G897-G901 ◽  
Author(s):  
J. DelValle ◽  
J. Wakasugi ◽  
H. Takeda ◽  
T. Yamada
Keyword(s):  
Channel Blocker ◽  
Gastric Fundus ◽  
Initial Transient ◽  
Somatostatin Secretion ◽  
Phospholipid Signaling ◽  
Dose Dependent Fashion ◽  
Direct Linkage ◽  
D Cells ◽  
Transient Elevation ◽  
Dose Dependent

The Ca2+/inositol phospholipid signaling cascade has been implicated in the mechanism by which cholecystokinin (CCK) stimulates gastric somatostatin release, but a direct linkage between intracellular events in gastric D cells and somatostatin secretion has not been established. To address this problem we developed a method for correlating somatostatin release with the measurement of intracellular Ca2+ concentration ([Ca2+]i) in isolated D cells. Resting [Ca2+]i in single D cells was 100 +/- 5.7 nM (means +/- SE, n = 41), and CCK induced a rise in [Ca2+]i in a dose-dependent fashion, producing a maximal stimulatory effect (243 +/- 15% of control, n = 12) at a peptide concentration of 2 x 10(-8) M. The CCK-mediated increase in [Ca2+]i was biphasic, with a rapid, initial transient elevation followed by a sustained plateau. The rise in [Ca2+]i was accompanied by a concomitant increase in release of somatostatin-like immunoreactivity (SLI). Removal of extracellular Ca2+ had no effect on the initial transient elevation in [Ca2+]i induced by CCK but abolished both the sustained plateau in [Ca2+]i and the release of SLI. The selective CCK antagonist L-364, 718 (10(-7) M) inhibited the effects of CCK on both [Ca2+]i and SLI release. The nonspecific Ca2+ channel blocker NiCl2 (10(-3) M) and the L-type Ca2+ channel blocker nifedipine inhibited the sustained rise in [Ca2+]i and the release of SLI but left the initial transient increase in [Ca2+]i unaltered. These results indicate that CCK-stimulated release of SLI from D cells in the gastric fundus is linked to influx of extracellular Ca2+ via L-type Ca2+ channels.

scholarly journals Characterization of prostanoid receptors mediating contraction of the gastric fundus and ileum: studies using mice deficient in prostanoid receptors

2000 ◽  
Vol 131 (4) ◽  
pp. 745-755 ◽  
Author(s):  
Yuji Okada ◽  
Akiyoshi Hara ◽  
Hong Ma ◽  
Chun-Yang Xiao ◽  
Osamu Takahata ◽  
...  
Keyword(s):  
Gastric Fundus ◽  
Prostanoid Receptors

Muscarinic modulation of nitrergic neurotransmission in guinea-pig gastric fundus

2004 ◽  
Vol 16 (2) ◽  
pp. 155-165 ◽  
Author(s):  
N. I. Kortezova ◽  
L. I. Shikova ◽  
E. A. Milusheva ◽  
D. E. Itzev ◽  
V. A. Bagaev ◽  
...  
Keyword(s):  
Guinea Pig ◽  
Gastric Fundus ◽  
Muscarinic Modulation

Small intestinal motility in fasted and postprandial states: effect of transient vagosympathetic blockade

1987 ◽  
Vol 252 (3) ◽  
pp. G301-G308 ◽  
Author(s):  
S. A. Chung ◽  
N. E. Diamant
Keyword(s):  
Small Bowel ◽  
Intestinal Motility ◽  
Gastric Fundus ◽  
Phase Iii ◽  
Entire Small Bowel ◽  
Vagal Blockade ◽  
Small Intestinal Motility ◽  
Proximal Small Bowel ◽  
Small Intestinal ◽  
Gastric Contractions

We investigated vagal control of the migrating myoelectric complex (MMC) and postprandial pattern of the canine small intestine. Gastric and small intestinal motility were monitored in six conscious dogs. The vagosympathetic nerves, previously isolated in bilateral skin loops, were blocked by cooling. To feed, a meat-based liquid food was infused by tube into the gastric fundus. MMC phases I, II, III, and IV were observed in the fasted state. On feeding, the fed pattern appeared quickly in the proximal small bowel but was delayed distally. Vagal blockade abolished all gastric contractions and spiking activity as well as the small bowel fed pattern. During vagal blockade, the small bowel exhibited MMC-like migrating bursts of spikes in both the fasted and fed states. The migration and cycling of these bursts were not significantly different from the MMC, but the duodenal and jejunal phase II was absent or shortened. On termination of vagal blockade, normal fasting or fed activity reappeared but with a delay in the fed pattern distally. We conclude: the ileum is the least sensitive to vagal blockade; the fasting vagal influence is exerted primarily on phases I and II of the duodenal and jejunal MMC; the fed pattern throughout the entire small bowel is normally dependent upon vagal integrity; the phase III-like bursts of activity seen during vagal blockade likely represents the intrinsic small bowel MMC, which is vagally independent.

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