As the function of the gastrointestinal tract is to a large degree mechanical, it has become increasingly popular to acquire distensibility data in motility research based on various parameters. Hence it is important to know on which geometrical and mechanical assumptions the various parameters are based. Currently, compliance and tone derived from pressure-volume curves are by far the most often used parameters. However, pressure-volume relations obtained in tubular organs must be carefully interpreted as they provide no direct measure of luminal cross-sectional area and other variables useful in plane stress and strain analysis. Thus, erroneous conclusions concerning tissue distensibility may be deduced. Other parameters, such as wall tension, stress and strain, give more useful information about mechanical behaviour. Distensibility data procure significance in fluid mechanics and in the study of tone, peristaltic reflexes, and mechanoreceptor kinematics. Such data are needed for the determination of the interaction between stimulus, electrical responses in neurons and the mechanical behaviour of the gut. Furthermore, from a clinical perspective, investigation of visco-elastic properties is important because GI diseases are associated with growth and remodelling. For example, prestenotic dilatation, increased collagen synthesis, dysmotility and altered distensibility are common features of obstructive diseases. The purpose of this review is to discuss the physiological and clinical importance of acquiring biomechanical data, distensibility parameters and interpretation of these results and their associated errors. We will also discuss some aspects of the relationship between morphology, growth and biomechanics. Finally, we will outline a number of techniques to study the mechanical properties of the GI tract.
In patients with chest pain and normal cardiac and esophageal evaluations, impedance planimetry of the esophagus reproduces pain and is associated with a 50% lower sensory threshold for pain, a 50% lower threshold for reactive contractions, and reduced esophageal compliance.
P, Drewes AM, Gregersen H. The functional lumen imaging probe (FLIP) for evaluation of the esophagogastric junction. Am J Physiol Gastrointest Liver Physiol 292: G377-G384, 2007. First published August 31, 2006; doi:10.1152/ajpgi.00311.2006.-There is a need for new methods to study the dynamics of the esophagogastric junction (EGJ). The aims were to verify the efficacy and usefulness of a "functional lumen imaging probe" (FLIP) for the evaluation of the EGJ. Eight healthy volunteers (6 men), median age 26 (21-35) yr, and two achalasia patients underwent the FLIP procedure. The EGJ was located by manometry. The FLIP measured eight cross-sectional areas (CSAs) 4 mm apart together with the pressure inside a saline-filled cylindrical bag. The data showed the geometric profile of the EGJ reconstructed in a video animation of its dynamic activity. A plot of curve-fitted data for the smallest CSA vs. pressure after balloon distension indicated that the pressure increased from 18 cmH 2O at a CSA of 38 mm 2 to a pressure of 37 cmH2O at a CSA of 230 mm 2 for the healthy controls. In one achalasia patient (unsuccessfully treated with dilations), the CSA never rose above the minimal measurable value despite the pressure increasing to 50 cmH2O. In another achalasia patient (successfully treated with dilations), the pressure only reached 15 cmH2O despite opening to a CSA of 250 mm 2 . In conclusion, FLIP represents the first dynamic technique to profile the function and anatomy of the EGJ. The method can be used practically to evaluate difficult cases of EGJ dysfunction and may provide a role in evaluating patients before and after therapies for diseases affecting the EGJ such as achalasia and gastroesophageal reflux disease. esophagus; competence; distensibility; cross-sectional area; functional imaging THE LOWER ESOPHAGEAL SPHINCTER (LES) is not solely responsible for impeding the flow between the esophagus and the stomach. The crural diaphragm encircles ϳ2 cm of the esophagogastric junction (EGJ), and the sling or oblique fibers of the stomach also contribute to the mechanism (15, 21). Esophageal and gastric motility, pressures in the abdominal and thoracic cavities, and the exact location of the EGJ all play a role in defining its function. The anatomy and behavior of the EGJ also change with time and body posture (20). The EGJ is a very dynamic mechanical structure. A lot of knowledge about the anatomy of the EGJ has been assembled over the last 40 years, but much of our limited understanding of the behavior has been related to manometric studies. Intraluminal pressure recording is the current gold standard for determining the motility characteristics of the esophagus. Although manometry provides useful information on the location of the EGJ and on phasic motility within the lumens of the digestive tract, it may be more restrictive in what it can tell us about sphincteric regions and their dynamics.Two classic diseases involving the EGJ are gastroesophageal reflux disease (GERD) and achalasia. Achalasia is an esophageal ...
Visceral hyperalgesia/allodynia can be induced experimentally and assessed quantitatively by the newly introduced multi-modal psychophysical assessment approach. The significant changes of the experimentally evoked referred pain patterns and of the nociceptive reflex evoked from a distant somatic structure indicate that even short-lasting visceral hyperalgesia can generate generalised sensitisation.
Vascular smooth muscle cells (VSMCs) have critical functions in vascular diseases. Haemodynamic factors are important regulators of VSMC functions in vascular pathophysiology. VSMCs are physiologically active in the threedimensional matrix and interact with the shear stress sensor of endothelial cells (ECs). The purpose of this review is to illustrate how haemodynamic factors regulate VSMC functions under two-dimensional conditions in vitro or three-dimensional co-culture conditions in vivo. Recent advances show that high shear stress induces VSMC apoptosis through endothelial-released nitric oxide and low shear stress upregulates VSMC proliferation and migration through platelet-derived growth factor released by ECs. This differential regulation emphasizes the need to construct more actual environments for future research on vascular diseases (such as atherosclerosis and hypertension) and cardiovascular tissue engineering.
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