T1383 Acotiamide Hydrochloride (Z-338), a Novel Gastroprokinetic Agent, Restores Delayed Gastric Emptying and Feeding Inhibition Induced By Restraint Stress in Rats

2008 ◽  
Vol 134 (4) ◽  
pp. A-543
Author(s):  
Koichi Seto ◽  
Takahiro Sasaki ◽  
Kokichi Katsunuma ◽  
Nobuyoshi Kobayashi ◽  
Koichiro Tanaka ◽  
...  
2009 ◽  
Vol 37 (01) ◽  
pp. 45-55 ◽  
Author(s):  
Kenji Imai ◽  
Hajime Ariga ◽  
Toku Takahashi

Acupuncture may modulate the imbalance of the autonomic nervous system. It is well known that restraint stress delays gastric emptying via inhibiting parasympathetic activity and/or stimulating sympathetic activity in rats. We have previously shown that electroacupuncture (EA) improves delayed gastric emptying induced by restraint stress in rats. To investigate whether the beneficial effect of EA on delayed gastric emptying is associated with its modulatory effects on autonomic nervous activity, we utilized spectral analysis of heart rate variability (HRV). In rats, the power in the low frequency (LF; 0.04–1.0 Hz) and high frequency (HF; 1.0–3 Hz) band of HRV represent sympathetic and parasympathetic activities, respectively. Electrocardiography (ECG)-electrodes were implanted on the subcutaneous tissues of the back. One week after the surgery, ECG was recorded before, during and after the restraint stress loading in a conscious state. EA (10 Hz) was applied at bilateral acupuncture points [ST-36 (lower leg) or BL-21 (back)] during restraint stress loading. In response to restraint stress, heart rate and LF component were increased, suggesting the increased activity of sympathetic tone. EA at ST-36 significantly reduced the elevated heart rate and LF, compared to that of control group. EA at ST-36 also significantly increased HF component after finishing the stress loading. In contrast, EA at BL-21 had no significant effect on the heart rate, LF and HF. It is suggested that EA at ST-36 stimulates parasympathetic activity and inhibits sympathetic activity under the restraint stress in rats.


2006 ◽  
Vol 290 (3) ◽  
pp. R616-R624 ◽  
Author(s):  
Yukiomi Nakade ◽  
Daisuke Tsuchida ◽  
Hiroyuki Fukuda ◽  
Masahiro Iwa ◽  
Theodore N. Pappas ◽  
...  

Central corticotropin-releasing factor (CRF) plays an important role in mediating restraint stress-induced delayed gastric emptying. However, it is unclear how restraint stress modulates gastric motility to delay gastric emptying. Inasmuch as solid gastric emptying is regulated via antropyloric coordination, we hypothesized that restraint stress impairs antropyloric coordination, resulting in delayed solid gastric emptying in conscious rats. Two strain gauge transducers were sutured onto the serosal surface of the antrum and pylorus, and postprandial gastric motility was monitored before, during, and after restraint stress. Antropyloric coordination, defined as a propagated single contraction from the antrum to the pylorus within 10 s, was followed by ≥20 s of quiescence. Restraint stress enhanced postprandial gastric motility in the antrum and pylorus to 140 ± 9% and 134 ± 9% of basal, respectively ( n = 6). The number of episodes of antropyloric coordination before restraint stress, 2.4 ± 0.4/10 min, was significantly reduced to 0.6 ± 0.3/10 min by restraint stress. Intracisternal injection of the CRF type 2 receptor antagonist astressin 2B (60 μg) or guanethidine partially restored restraint stress-induced impairment of antropyloric coordination (1.6 ± 0.3/10 min, n = 6). The restraint stress-induced augmentation of antral and pyloric contractions was increased by astressin 2B and guanethidine but abolished by atropine, hexamethonium, and vagotomy. Restraint stress enhanced postprandial gastric motility via a vagal cholinergic pathway. Restraint stress-induced delay of solid gastric emptying is due to impairment of antropyloric coordination. Restraint stress-induced impairment of antropyloric coordination might be mediated via a central CRF pathway.


2012 ◽  
Vol 142 (5) ◽  
pp. S-300
Author(s):  
Hiroshi Taniguchi ◽  
Kenji Imai ◽  
Sazu Yoshimoto ◽  
Chie Ogasawara ◽  
Kokoro Hino ◽  
...  

2010 ◽  
Vol 22 (11) ◽  
pp. 1181-1186 ◽  
Author(s):  
R. Babygirija ◽  
J. Zheng ◽  
M. Bülbül ◽  
D. Cerjak ◽  
K. Ludwig ◽  
...  

2013 ◽  
Vol 144 (5) ◽  
pp. S-542
Author(s):  
Shunsuke Ohnishi ◽  
Shuichi Muto ◽  
Koji Nakagawa ◽  
Chiharu Sadakane ◽  
Yayoi Saegusa ◽  
...  

2009 ◽  
Vol 296 (5) ◽  
pp. R1358-R1365 ◽  
Author(s):  
Jun Zheng ◽  
Anthony Dobner ◽  
Reji Babygirija ◽  
Kirk Ludwig ◽  
Toku Takahashi

In our daily life, individuals encounter with various types of stress. Accumulation of daily life stress (chronic stress) often causes gastrointestinal symptoms and functional gastrointestinal diseases. Although some can adapt toward chronic stress, the adaptation mechanism against chronic stress remains unknown. Although acute stress delays gastric emptying and alters upper gastrointestinal motility, effects of chronic stress on gastric motility still remain unclear. We investigated the effects of acute (single stress) and chronic (repeated stress for 5 consecutive days) stress on solid gastric emptying and interdigestive gastroduodenal contractions in rats. It is well established that acute restraint stress inhibits solid gastric emptying via central corticotropin-releasing factor (CRF). To investigate whether the sensitivity to CRF is altered following chronic stress, CRF was administered intracisternally. Ghrelin is involved in regulating gastric emptying and upper gastrointestinal motility in rodents. The changes in plasma active ghrelin levels and mRNA expression in the stomach were studied following chronic stress. To evaluate the effects of chronic stress on the hypothalamus-pituitary-adrenal (HPA) axis, plasma corticosterone levels were also measured. Delayed gastric emptying observed in acute stress was completely restored following chronic stress. Acute stress abolished gastric phase III-like contractions, without affecting duodenal phase III-like contractions in the interdigestive state. Impaired gastric phase III-like contractions were also restored following chronic stress. Plasma ghrelin levels and ghrelin mRNA expression were increased significantly after chronic stress. Intracisternal injection of CRF delayed gastric emptying and impaired gastric motility in rats who received chronic stress. Plasma corticosterone concentrations were no more elevated following chronic stress. The restored gastric emptying following chronic stress was antagonized by the administration of ghrelin receptor antagonists. The adaptation mechanism may involve upregulation of ghrelin expression and attenuation of the HPA axis. In contrast, the sensitivity to central CRF remained unaltered following chronic stress in rats.


2002 ◽  
Vol 282 (1) ◽  
pp. G34-G40 ◽  
Author(s):  
Mulugeta Million ◽  
Céline Maillot ◽  
Paul Saunders ◽  
Jean Rivier ◽  
Wylie Vale ◽  
...  

Human urocortin (hUcn) II is a new member of the corticotropin-releasing factor (CRF) family that selectively binds to the CRF2receptor. We investigated the CRF receptors involved in mediating the effects of hUcn II and human/rat CRF (h/rCRF) on gut transit. Gastric emptying, 4 h after a solid meal, and distal colonic transit (bead expulsion time) were monitored simultaneously in conscious rats. CRF antagonists were given subcutaneously 30 min before intravenous injection of peptides or partial restraint (for 90 min). hUcn II (3 or 10 μg/kg iv) inhibited gastric emptying (by 45% and 55%, respectively) and did not influence distal colonic transit. The CRF2 peptide antagonist astressin2-B blocked hUcn II action. h/rCRF, rat Ucn, and restraint delayed gastric emptying while accelerating distal colonic transit. The gastric response to intravenous h/rCRF and restraint was blocked by the CRF2 antagonist but not by the CRF1 antagonist CP-154,526, whereas the colonic response was blocked only by CP-154,526. None of the CRF antagonists influenced postprandial gut transit. These data show that intravenous h/rCRF and restraint stress-induced delayed gastric emptying involve CRF2 whereas stimulation of distal colonic transit involves CRF1. The distinct profile of hUcn II, only on gastric transit, is linked to its CRF2 selectivity.


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