A Computer Yodel Of The Migrating Myoelectric Complex

Author(s):  
B.L. Bardakjian ◽  
K. Ahmed
2008 ◽  
Vol 3 (2) ◽  
pp. 84-91 ◽  
Author(s):  
I. Nilsson ◽  
T. Svenberg ◽  
B. Wallin ◽  
G. Hedenborg ◽  
P. M. Hellström

1992 ◽  
Vol 421 (5) ◽  
pp. 492-496 ◽  
Author(s):  
W. Janssens ◽  
H. Vandenbogaerde ◽  
Ph. Caenepeel ◽  
J. Janssens ◽  
G. Vantrappen

1982 ◽  
Vol 82 (6) ◽  
pp. 1395-1402 ◽  
Author(s):  
L. Bueno ◽  
J. Fioramonti ◽  
V. Rayner ◽  
Y. Ruckebusch

1992 ◽  
Vol 262 (6) ◽  
pp. G1121-G1126 ◽  
Author(s):  
B. Bonaz ◽  
L. Martin ◽  
E. Beurriand ◽  
M. Manier ◽  
J. Hostein ◽  
...  

The role of the locus ceruleus (LC) in the control of migrating myoelectric complex (MMC) was investigated in rats with lesions induced by injections of 6-hydroxydopamine (6-OHDA). Control animals received the vehicle alone. MMC was recorded in conscious rats chronically fitted with electrodes. After 6-OHDA was injected into the LC, lesions of the LC were total, partial (mostly rostral), or ineffective. The MMC period was significantly longer in animals with a total or partial lesion but was unchanged in animals with an ineffective lesion. No lesion of other brain noradrenergic nuclei was observed. The longer MMC period is comparable to that obtained after intracerebroventricular injection of 6-OHDA, which is responsible for a more diffuse destruction of brain noradrenergic systems, including LC itself. Bilateral lesions of the central tegmental tract, which carries ascending noradrenergic axons from the medullary and pontine cell groups outside the LC, do not alter the MMC cycle. Consequently, the LC is most likely the major brain noradrenergic candidate for modulating the MMC pattern in rats.


1983 ◽  
Vol 244 (1) ◽  
pp. G13-G19
Author(s):  
R. B. Scott ◽  
T. Y. El-Sharkawy ◽  
N. E. Diamant

1989 ◽  
Vol 67 (11) ◽  
pp. 1437-1441 ◽  
Author(s):  
M. Maric ◽  
D. G. Gall ◽  
R. B. Scott

The aim of this study was to determine if the altered jejunal motility previously demonstrated in this animal model of food protein-induced intestinal anaphylaxis is (a) a localized (the jejunal site of challenge), or a generalized response of the small intestine, and (b) associated with more rapid aboral transit of intraluminal contents. Hooded–Lister rats, 100–150 g in weight, were sensitized by intraperitoneal injection of 10 μg egg albumin. Control rats were sham-sensitized. On day 7 rats were surgically prepared with six bipolar electrodes from duodenum to ileum and (or) a jejunostomy tube was positioned at the ligament of Treitz. On day 14, after an 18-h fast, recordings of myoelectric activity were obtained from four sensitized animals with electrodes from duodenum to ileum during a control period for 45 min after saline challenge and for 45 min after antigen challenge. Control (n = 25) and sensitized (n = 31) animals with only a jejunostomy had Na251CrO4 instilled through the jejunostomy in 0.5 mL of saline, with or without egg albumin, either during a fast or after a standard meal. Propulsion of isotope through the small bowel was allowed to progress for 15 min, the animals were sacrificed, and their gut was removed for division into eight equal segments of small intestine, cecum, and remaining colon. The radioactivity of each segment was determined in a gamma counter. Jejunal antigen challenge of sensitized animals was associated with diarrhea and disruption of the migrating myoelectric complex at electrode sites from duodenum to ileum, while placebo challenge caused neither diarrhea (p < 0.01) nor disruption of the migrating myoelectric complex (p < 0.05). In both the fasted and fed states, the geometric centre of transit was significantly (p < 0.05) greater in sensitized animals challenged with antigen than in control animals challenged with placebo or antigen, or in sensitized animals challenged with placebo. Food protein-induced intestinal anaphylaxis induces a generalized alteration of small intestinal motility not limited to the region of antigen exposure and is associated with an increased rate of aboral transit.Key words: intestine, intestinal transit, anaphylaxis, food allergy.


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