747 THE NEUROGENIC RELAXATION OF GASTRIC FUNDUS AND ANOCOCCYGEUS MUSCLE IS INCREASED IN THE BILIARRY CIRRHOTIC RATS: A ROLE FOR NITRERGIC NEUROTRANSMISSION

2009 ◽  
Vol 50 ◽  
pp. S274
Author(s):  
M. Ghasemi ◽  
A. Karimollah ◽  
M.H. Ghahremani ◽  
A.R. Dehpour
2014 ◽  
Vol 59 (11) ◽  
pp. 2675-2681 ◽  
Author(s):  
Mehdi Ghasemi ◽  
Ali Reza Karimollah ◽  
Bardia Bakhtiari ◽  
Abbas Ghasemi ◽  
Leila Moezi ◽  
...  

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

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Guiqin Chen ◽  
Lei Nie ◽  
Tijiang Zhang

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.


1996 ◽  
Vol 270 (6) ◽  
pp. G897-G901 ◽  
Author(s):  
J. DelValle ◽  
J. Wakasugi ◽  
H. Takeda ◽  
T. Yamada

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.


1988 ◽  
Vol 255 (4) ◽  
pp. C536-C542 ◽  
Author(s):  
J. S. Walker ◽  
I. R. Wendt ◽  
C. L. Gibbs

Heat production, unloaded shortening velocity (Vus), and load-bearing capacity (LBC) were studied in the isolated rat anococcygeus muscle during isometric contractions at 27 degrees C. The relation between the total suprabasal heat produced and the stress-time integral for isometric contractions of various durations was curvilinear, demonstrating a decreasing slope as contractile duration increased. The rate of heat production at 600 s was approximately 68% of the peak value of 6.55 mW/g that occurred at 10 s. At the same time, force rose from a mean of 92 mN/mm2 at 10 s to a value of 140 mN/mm2 at 600 s. This produced a nearly threefold increase in the economy of force maintenance. The decline in the rate of heat production was accompanied by a decline in Vus from 0.56 Lo/s at 10 s to 0.28 Lo/s at 600 s, where Lo is the length for optimal force development. This suggests the fall in the rate of heat production was caused, at least in part, by a slowing of cross-bridge kinetics. The ratio of LBC to developed tension at 10 s was not significantly different from the ratio at 600 s, suggesting that the increase in tension was due to an increased number of attached cross bridges. The decline in heat production, therefore, appears contradictory, since an increased number of attached cross bridges would predict an increased rate of energy expenditure. The observations can be reconciled if either 1) the increase in force is caused by a progressive increase in the attachment time of a constant number of cross bridges that cycle at a lower frequency or 2) the decline in energy expenditure caused by the slowing of cross-bridge cycling is sufficient to mask the increase caused by the recruitment of additional cross bridges.


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

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