scholarly journals Pacemaker shift in the gastric antrum of guinea‐pigs produced by excitatory vagal stimulation involves intramuscular interstitial cells

2002 ◽  
Vol 541 (3) ◽  
pp. 917-928 ◽  
Author(s):  
G. D. S. Hirst ◽  
E. J. Dickens ◽  
F. R. Edwards
Keyword(s):  
Guinea Pigs ◽  
Vagal Stimulation ◽  
Interstitial Cells ◽  
Gastric Antrum ◽  
Pacemaker Shift

Gastrointestinal myoelectric activity in conscious guinea pigs

1985 ◽  
Vol 249 (1) ◽  
pp. G92-G99 ◽  
Author(s):  
J. J. Galligan ◽  
M. Costa ◽  
J. B. Furness
Keyword(s):  
Small Intestine ◽  
Guinea Pigs ◽  
Mammalian Species ◽  
Gastric Antrum ◽  
Slow Waves ◽  
Cycle Period ◽  
Myoelectric Activity ◽  
Phase 3 ◽  
Fed State ◽  
Intestinal Slow Waves

Myoelectric activity was recorded from the gastric antrum and small intestine of conscious, unrestrained guinea pigs using bipolar Ag-Ag chloride electrodes that had been previously implanted under pentobarbital sodium/Innovar anesthesia. In fasted guinea pigs, the migrating myoelectric complex (MMC) was recorded from the small intestine and was observed to propagate aborally at a speed that declined with distance from the pylorus (range of speeds of the front of phase 3: 17.5 cm/min in the duodenum to 4.1 cm/min in the ileum). The complex was not disrupted by feeding but occurred less frequently in the freely fed state (82-min cycle period in the fasted state versus 139 min in the fed state). The complex started in the duodenum and was accompanied by a brief (6.3 +/- 0.9 min) period of inhibition of antral myoelectric activity. Slow waves were also recorded from the gastric antrum (10.3 +/- 1.3/min) and the small intestine. The frequency of intestinal slow waves was uniform along the length of the bowel (26.2 +/- 1.3/min in the duodenum to 24.7 +/- 1.3/min in the ileum). It is concluded that the guinea pig is similar to other mammalian species, so far examined, in its pattern of gastrointestinal myoelectric activity.

scholarly journals Acute Cholecystitis Reduces Interstitial Cells of Cajal in Porcine Gallbladder Through Decreased mRNA Synthesis

2018 ◽  
Vol 47 (2) ◽  
pp. 535-544 ◽  
Author(s):  
Zhen-peng Huang ◽  
Hu Qiu ◽  
Bao-ping Yu
Keyword(s):  
Acute Cholecystitis ◽  
Guinea Pigs ◽  
Interstitial Cells Of Cajal ◽  
Interstitial Cells ◽  
Motility Disorder ◽  
Gallbladder Motility ◽  
Control Group ◽  
Mrna Levels ◽  
Duct Ligation ◽  
Cells Of Cajal

Background/Aims: Acute cholecystitis is a common gastrointestinal disorder, often characterized by acute cholecystitis with gallbladder motility disorder. Interstitial cells of Cajal (ICCs) are the pacemaker cells of gut motility in the gastrointestinal tract. Disruption of ICC function is related to motility disorders. The aim of this study was to explore the cellular and molecular mechanisms of ICCs in acute cholecystitis and after the resolution of acute inflammation. Materials and Methods: Fifty adult guinea pigs were randomly divided into five groups: a sham-administered group (control group); two groups that were intraperitoneally administered an anti-polyclonal neutrophil (PMN) antibody 24 h before common bile duct ligation (CBDL); and two groups of guinea pigs that were subjected to CBDL without receiving the PMN antibody. Guinea pigs that underwent CBDL were held for 24 h or 48 h after surgery before being subjected to laparotomy and cholecystectomy. Immunohistochemistry, TUNEL assays, western blotting, and real-time PCR were performed to determine ICC morphology and density, to detect ICC apoptosis, and to examine stem cell factor (SCF) and c-kit protein expression and SCF and c-kit mRNA levels, respectively. Results: Both hematoxylin-eosin staining and histological inflammation scores in the PMN groups were lower than those in the control groups (P < 0.01). No differences were observed in ICC morphology between groups. During acute cholecystitis, ICCs numbers were reduced. Conversely, the density of ICCs increased after inflammation was relieved (P < 0.01). In addition, SCF and c-kit protein and mRNA expression levels decreased during acute cholecystitis (P < 0.05) and increased after inflammation was relieved (P < 0.05). Furthermore, ICC apoptosis increased during acute cholecystitis and decreased after resolution of acute cholecystitis (P < 0.01). Conclusions: In acute cholecystitis, ICC injury may be related to gallbladder motility disorder.

scholarly journals Xiangbinfang granules enhance gastric antrum motility via intramuscular interstitial cells of Cajal in mice

2021 ◽  
Vol 27 (7) ◽  
pp. 576-591
Author(s):  
Qi-Cheng Chen ◽  
Zhi Jiang ◽  
Jun-Hong Zhang ◽  
Li-Xing Cao ◽  
Zhi-Qiang Chen
Keyword(s):  
Interstitial Cells Of Cajal ◽  
Interstitial Cells ◽  
Gastric Antrum ◽  
Cells Of Cajal

Vagal effects on sinoatrial and atrial conduction studied with epicardial mapping in dogs: the influence of pacemaker shifts on the measurement of sinoatrial conduction time

1985 ◽  
Vol 63 (2) ◽  
pp. 113-121 ◽  
Author(s):  
Hidehiko Watanabe ◽  
Jean-Benoît Perry ◽  
Pierre Pagé ◽  
Pierre Savard ◽  
Réginald Nadeau
Keyword(s):  
Conduction Velocity ◽  
Vagal Stimulation ◽  
Superior Vena ◽  
Vena Cava ◽  
Right Atrial ◽  
Conduction Time ◽  
Atrial Conduction Time ◽  
Pacemaker Shift ◽  
Atrial Conduction Times ◽  
Recording Electrodes

The influence of pacemaker shifts on sinoatrial conduction time (SACT) was studied by investigating the effects of vagal stimulation on SACT and atrial conduction in anesthetized open-chest dogs. Isochronal maps were drawn from unipolar electrograms simultaneously recorded at 60 epicardial sites on the right atrial free wall and the inferior and superior vena cava. Vagal stimulation caused atrial conduction velocity to increase from 0.99 ± 0.10 m/s (mean ± SD) to 1.23 ± 0.23 m/s (p < 0.01), and the pacemaker to shift to lower positions along the superior vena cava – right atrial junction. As a result of the changes, the distances and the atrial conduction times from the stimulating and recording electrodes to the pacemaker site varied, and hence, the SACT values obtained indirectly by premature atrial stimulation varied. The isochronal maps were used to measure the atrial conduction times from stimulating to recording electrodes (a), from stimulating electrode to pacemaker site (b), and from pacemaker site to recording electrode (c). Indirect SACT was lengthened by vagal stimulation from 43 ± 16 to 64 ± 22 ms (p < 0.02). After correcting by subtracting the atrial conduction time (b + c − a), these values became 26 ± 6 ms (control) and 40 ± 11 ms (vagal stimulation) (p < 0.01). SACT values measured directly from the electrograms were 27 ± 7 ms (control) and 42 ± 10 ms (vagal stimulation) (p < 0.01). Corrected indirect SACTs were closer to direct SACTs than were the uncorrected indirect SACTs. It was concluded that (i) vagal stimulation induced pacemaker shift, increased atrial conduction velocity, and prolonged SACT; (ii) constant atrial pacing induced a pacemaker shift toward the stimulating electrode; and (iii) atrial conduction time must be taken into account to correctly estimate SACT.

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