The Elastic Fibre System in the Veins of the Human Lower Oesophagus

Carvalho, Cláudio Antonio Ferraz de

doi:10.1159/000146371

Cited by 4 publications

(2 citation statements)

References 8 publications

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“…However, TreSting increases rather abruptly about Lo. Morphological data have suggested a low compliance of the veins in the human lower oesophagus owing to a reduced amount of elastin at the expense of the less compliant elaunin fibres (DeCarvalho 1987). This is in contrast to the results of the present study, but might be explained by a curly arrangement of the collagen fibres (Stromberg & Wiederhielm 1969).…”

Section: -2contrasting

confidence: 99%

Mechanical properties of isolated human oesophageal submucosal veins

Madsen

Tøttrup

Forman

et al. 1991

Acta Physiologica Scandinavica

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The mechanical properties of isolated human oesophageal submucosal veins were investigated. The veins were without tone or spontaneous activity and possessed a high compliance, tolerating a stretch of several hundred per cent of the length at which the vessels were first able to contract with only minor increases in passive tension. The veins were capable of producing active tension when the length exceeded 30% of L0 (the length at which maximum wall tension (T0) was developed when activated by 124 mM K(+)-solution). The veins from the oesophageal body (OB) had a higher L0 than the veins from the gastrooesophageal junction (GOJ) (1180 microns vs 820 microns) and T0 was correspondingly higher (1.1 mN/mm vs. 0.6 mN/mm). However, there was no significant difference in the calculated effective transmural pressure (P) at the two locations. Noradrenaline induced contractions in all preparations tested with a maximum response equivalent to the tension achieved after stimulation with 124 mM K(+)-solution, pD2 values for noradrenaline in vessels from the oesophageal body and the gastroesophageal junction were 7.03 +/- 0.28 (mean +/- SEM) and 7.15 +/- 0.20, respectively. The present model seems suitable for future studies of human oesophageal submucosal veins from the oesophageal body and the gastrooesophageal junction.

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Section: -2contrasting

confidence: 99%

Mechanical properties of isolated human oesophageal submucosal veins

Madsen

Tøttrup

Forman

et al. 1991

Acta Physiologica Scandinavica

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“…Oxytalan fibers consist of microfibril bundles with a diameter of 10 nm composed of various glycoproteins, including fibrillin. They are found in the zonule of Zinn in the eyes, in periodontal ligaments, esophageal submucosa, and certain places of the skin, where they connect the elastic system to the basal lamina (FERRAZ DE CARVALHO and KÖNIG JUNIOR, 1982;FERRAZ DE CARVALHO, 1987;INOUE, HARA and SATO, 2012;BALDWIN, SIMPSON, STEER et al, 2013;JUNQUEIRA and CARNEIRO, 2013).…”

Section: Resultsmentioning

confidence: 99%

Untitled

2017

J Morphol Sci

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Introduction: Marfan syndrome (OMIM #154700) was described for the first time in 1896 by Antoine Bernard-Jean Marfan. It is characterized by its autosomal dominant inheritance pattern, affects 1:5000 of those born alive, and involves the gene that codifies the structural protein fribrillin-1. Fibrillin-1 is critical for the formation of the elastic system backbone and for the negative regulation of the cytokine transforming growth factor beta 1 (TGF-β1). In the syndrome this fibrillar component causes the degeneration of the fibers of the elastic system, which no longer sequesters matrix TGF-β, causing disorganization of the collagen fibers and vascular smooth muscles. The disease affects mainly the cardiovascular system, cardiovascular problems being the main cause of death. This is because arteries have large amounts of elastic fibers that rupture in an adverse process, causing mainly dissections and aneurisms, which have been better clarified in experimental studies with mice. Objective: The objective of this study was to conduct an etiopathogenic and molecular review to describe the advances in the understanding of blood vessel dysmorphism in the syndrome, especially of the aorta. Materials and Methods: For this purpose the literature of the last 35 years was extensively reviewed. Conclusion: The origin of the aortic dysmorphism in the syndrome stems from a number of events that begin with the mutation of the gene fibrillin-1, causing fragmentation of the aortic elastic fibers. Excess cytokine TGF-β increases the amount of metalloproteinases and of vascular smooth muscle cell apoptosis, leading to matrix remodeling and increasing the susceptibility of the vessel to an aneurysm or dissecting process.

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