Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 1985 Oct;17(4):673-85.

The muscle coat of the lower esophageal sphincter in patients with achalasia and hypertensive sphincter. An electron microscopic study

  • PMID: 4078952

The muscle coat of the lower esophageal sphincter in patients with achalasia and hypertensive sphincter. An electron microscopic study

M S Faussone-Pellegrini et al. J Submicrosc Cytol. 1985 Oct.

Abstract

The muscle coat of the lower esophageal sphincter (LES) of seven patients with achalasia and three patients with a hypertensive sphincter has been studied with the electron microscope. In these pathological conditions the ultrastructural pictures differ both from normal and from one another. In achalasia, the LES muscle wall components (nerve endings, smooth muscle cells, interstitial cells of Cajal and connective tissue) are altered, but, while all the nerve endings and interstitial cells are affected, only a few smooth muscle cells are damaged. The severity of the alterations is more pronounced in the older patients. On the contrary, there is no damage of the muscle wall components in the hypertensive sphincter, whereas an increase in the cytoplasmic organelles (smooth endoplasmic reticulum and mitochondria) has been found in all interstitial cells and in some smooth muscle cells. Moreover, the ultrastructural picture of the hypertensive sphincter does not seem to change with patients' age. Since the LES components specifically altered in achalasia are the nerve endings and the interstitial cells of Cajal, they are regarded as principally responsible for the altered motility. On the contrary, the ultrastructural picture of the hypertensive sphincter suggests an enhancement of the activity of the activity of all the interstitial cells and of some smooth muscle cell; therefore, we consider the hyperfunction of these cells as the cause of this esophageal motor disorder.

PubMed Disclaimer

Similar articles

Cited by

Publication types