Transient Lower Esophageal Sphincter Relaxation in Morbid Obesity

2009 ◽  
Vol 19 (5) ◽  
pp. 595-600 ◽  
Author(s):  
J. H. Schneider ◽  
M. Küper ◽  
A. Königsrainer ◽  
B. Brücher
2014 ◽  
Vol 51 (2) ◽  
pp. 102-106 ◽  
Author(s):  
Michel Santos PALHETA ◽  
José Ronaldo Vasconcelos da GRAÇA ◽  
Armênio Aguiar dos SANTOS ◽  
Liziane Hermógenes LOPES ◽  
Raimundo Campos PALHETA JÚNIOR ◽  
...  

ContextThe rectal distension in dogs increases the rate of transitory lower esophageal sphincter relaxation considered the main factor causing gastroesophageal reflux.ObjectivesThe aim of this study was evaluate the participation of the nitrergic pathway in the increased transitory lower esophageal sphincter relaxation rate induced by rectal distension in anesthetized dogs.MethodsMale mongrel dogs (n = 21), weighing 10-15 kg, were fasted for 12 hours, with water ad libitum. Thereafter, they were anesthetized (ketamine 10 mg.Kg-1+ xylazine 20 mg.Kg-1), so as to carry out the esophageal motility evaluation protocol during 120 min. After a 30-minute basal period, the animals were randomly intravenous treated whith: saline solution 0.15M (1ml.Kg-1), L-NAME (3 mg.Kg-1), L-NAME (3 mg.Kg-1) + L-Arginine (200 mg.Kg-1), glibenclamide (1 mg.Kg-1) or methylene blue (3 mg.Kg-1). Forty-five min after these pre-treatments, the rectum was distended (rectal distension, 5 mL.Kg-1) or not (control) with a latex balloon, with changes in the esophageal motility recorded over 45 min. Data were analyzed using ANOVA followed by Student Newman-Keuls test.ResultsIn comparison to the respective control group, rectal distension induces an increase in transitory lower esophageal sphincter relaxation. Pre-treatment with L-NAME or methylene blue prevents (P<0.05) this phenomenon, which is reversible by L-Arginine plus L-NAME. However, pretreating with glibenclamide failed to abolish this process.ConclusionsTherefore, these experiments suggested, that rectal distension increases transitory lower esophageal sphincter relaxation in dogs via through nitrergic pathways.


2001 ◽  
Vol 120 (5) ◽  
pp. A632
Author(s):  
Guoxiang Shi ◽  
John E. Pandolfino ◽  
Raymond J. Joehl ◽  
James G. Brassuer ◽  
Peter J. Kahrilas

2005 ◽  
Vol 288 (4) ◽  
pp. G671-G676 ◽  
Author(s):  
John E. Pandolfino ◽  
Guoxiang Shi ◽  
Qing Zhang ◽  
Peter J. Kahrilas

This study aimed to determine the interactions between closely paired swallow-induced primary peristalsis (PP) and air injection-induced secondary peristalsis (SP). Ten subjects (7 men, 18–42 yr) were studied using a catheter, including two sleeves (upper and lower esophageal sphincters), a midesophageal infusion port, and seven esophageal and two pharyngeal recording sites. Ten iterations of PP and SP were induced by 5-ml water swallows and 20-ml intraesophageal air injections, respectively. Thereafter, the interactions between PP and SP, separated by 1- to 12-s intervals, were studied in all four possible sequences: paired swallows, swallow preceded by air injection, air injection preceded by swallow, and paired air injections. Tracings were analyzed for lower esophageal sphincter relaxation, presence and integrity of peristalsis, and event interaction. Eight subjects with success rates of both ≥90% PP and ≥80% SP were analyzed (PP 97 ± 2%, SP 90 ± 3%). During paired PP interactions and SP followed by PP, the first sequence was inhibited by the second with intervals < 4–6 s. However, no inhibition of the first peristaltic sequence was found in either PP followed by SP trials or SP followed by air injection. In contrast to swallowing or proximal esophageal distention, air injection into the lumen of the midesophagus does not inhibit an ongoing peristaltic event. Being that the elicitation of SP in the smooth muscle esophagus is intramurally mediated, this suggests that deglutitive inhibition is a centrally mediated phenomenon rather than an intrinsic property of peristalsis.


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