Document Detail

Mechanics and hemodynamics of esophageal varices during peristaltic contraction.
MedLine Citation:
PMID:  15361363     Owner:  NLM     Status:  MEDLINE    
Our hypothesis states that variceal pressure and wall tension increase dramatically during esophageal peristaltic contractions. This increase in pressure and wall tension is a natural consequence of the anatomy and physiology of the esophagus and of the esophageal venous plexus. The purpose of this study was to evaluate variceal hemodynamics during peristaltic contraction. A simultaneous ultrasound probe and manometry catheter was placed in the distal esophagus in nine patients with esophageal varices. Simultaneous esophageal luminal pressure and ultrasound images of varices were recorded during peristaltic contraction. Maximum variceal cross-sectional area and esophageal luminal pressures at which the varix flattened, closed, and opened were measured. The esophageal lumen pressure equals the intravariceal pressure at variceal flattening due to force balance laws. The mean flattening pressures (40.11 +/- 16.77 mmHg) were significantly higher than the mean opening pressures (11.56 +/- 25.56 mmHg) (P < or = 0.0001). Flattening pressures >80 mmHg were generated during peristaltic contractions in 15.5% of the swallows. Variceal cross-sectional area increased a mean of 41% above baseline (range 7-89%, P < 0.0001) during swallowing. The peak closing pressures in patients that experience future variceal bleeding were significantly higher than the peak closing pressures in patients that did not experience variceal bleeding (P < 0.04). Patients with a mean peak closing pressure >61 mmHg were more likely to bleed. In this study, accuracy of predicting future variceal bleeding, based on these criteria, was 100%. Variceal models were developed, and it was demonstrated that during peristaltic contraction there was a significant increase in intravariceal pressure over baseline intravariceal pressure and that the peak intravariceal pressures were directly proportional to the resistance at the gastroesophageal junction. In conclusion, esophageal peristalsis in combination with high resistance to blood flow through the gastroesophageal junction leads to distension of the esophageal varices and an increase in intravariceal pressure and wall tension.
Larry S Miller; Joseph K Kim; Qing Dai; Jyothi Mekapati; James Izanec; Chan Chung; Ji-Bin Liu; Andrew Sanderson; Matt Bohning; Josh Desipio; Jasneet Gandegok; Justin J Harberson; Carson Schneck; Mark A Nicosia; Vinod Thangada; Beje Thomas; Brian Copeland; Elan Miller; Aaron Miller; Naji Ahmed; James G Brasseur
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  American journal of physiology. Gastrointestinal and liver physiology     Volume:  287     ISSN:  0193-1857     ISO Abbreviation:  Am. J. Physiol. Gastrointest. Liver Physiol.     Publication Date:  2004 Oct 
Date Detail:
Created Date:  2004-09-13     Completed Date:  2004-11-06     Revised Date:  2004-11-17    
Medline Journal Info:
Nlm Unique ID:  100901227     Medline TA:  Am J Physiol Gastrointest Liver Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  G830-5     Citation Subset:  IM    
Dept. of Gastroenterology, Temple Univ. Hospital, 3401 North Broad St., Philadelphia, PA 19140, USA.
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MeSH Terms
Esophageal and Gastric Varices / physiopathology*,  ultrasonography
Esophagus / blood supply*,  physiology*
Middle Aged
Models, Anatomic
Muscle Contraction / physiology*
Peristalsis / physiology*

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