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Background: Oesophagus is a muscular tube that transports food and liquids by coordinated contraction of its muscular lining led by stimuli from the nerve plexus. Its muscularis proper layer consists of muscle cells, connective tissue and myenteric plexus. The aim of our histomorphometric study was to reveal detailed characteristics of this layer, cell number, volume, orientation, properties of myenteric plexus as well as changes related to aging. Materials and methods: Oesophagus tissue samples from 17 male cadavers were taken from the cranial and thoracic parts. Samples were divided in 2 groups: younger (ages 21–45) and older (ages 66–78). The tissue was routinely processed, embedded and serially sectioned. Sections were stained with Masson-Goldner and Cresyl-violet dyes. Digital images were analysed with the image analysis software. Statistics were performed with SPSS software. Results: The average thickness of the cranial part of the oesophageal wall and muscularis proper was 2590 µm and 1197 µm, respectively in the younger and 2453 µm and 1144 µm in the older group. Overall volume of the muscle tissue was slightly larger in the thoracic part, and in the younger group compared to the cranial part and the older group. The average number of the striated muscle cells per 100 µm in the cranial part was 771.5 and 749.7 in the younger and the older group, respectively. Striated cells were significantly less present only in the lower thoracic part of the oesophagus. In the older group, smaller striated muscle cells dominated over the larger ones. In the younger group, majority of the striated muscle cells were mid-sized. The thickness of the circular layer of muscularis proper was more affected by aging than the longitudinal one. Ganglion cells number was lower in the older group, but plexus area was unchanged. Conclusions: Aging affects muscularis proper and myenteric plexus of the oesophagus. Major differences can be observed in the striated muscle cells size, volume of the circular layer and number of the ganglionic cells in the myenteric plexus. (Folia Morphol 2013; 72, 3: 223–229)
Gastro-esophageal reflux disease (GERD) is the result of the acid contents regurgitation back from the stomach into the esophagus. According to the endoscopic findings, GERD can be divided into two main forms: non-erosive (NERD) and erosive reflux esophagitis. The pathogenesis of GERD is associated with the impaired function of the antireflux barrier. Disturbances of the autonomic nervous system (ANS), especially parasympathetic part of the ANS, may be also involved in the pathogenesis of this disease. The aim of our study was to establish the parasympathetic activity in patients with reflux esophagitis and in patients with symptomatic endoscopically negative reflux. Working hypothesis was the question, whether the possible parasympathetic activity disturbances, which are observed in all GERD patients, may be regarded as the primary or secondary to the esophagitis. All the participants (20 pts. with NERD, 20 pts. with reflux esophagitis and 20 healthy controls) underwent esophageal manometry, 24-hour ambulatory pH-monitoring, resting heart rate variability (HRV) recording and the deep breathing (DB) test with the continuous HRV recording. The results of the spectral analysis both of the short-term, resting HRV recordings and DB-evoked revealed the disturbances of the main power spectra components - LF and HF in both groups of patients in comparison with the control group. In our opinion, the observed HRV spectra changes in both groups of patients support the hypothesis that not only is the parasympathetic activity impairment associated with the pathogenesis of GERD but it is also the primary factor contributing to the pathophysiological mechanism of reflux.
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Helicobacter pylori infection in pathogenesis of gastroesophageal reflux disease

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Gastroesophageal reflux disease (GERD) refers to the very common and constantly increasing conditions where reflux of gastric contents into the esophagus leads to development of characteristic symptoms. The esophagus, LES and stomach can be envisioned as single functional unit controlled by neuro-hormonal factors. The abnormalities that contribute to GERD can start in any component of this unit, resulting particularly from disturbances in their control system. It is extremely important to identify factors and mechanisms leading to functional failure of this system so that causative therapy can be effectively applied. The key-role has been attributed to parasympathetic dysfunction, which may adversely affect motor activity of this area by increasing transient LES relaxation number and impairing LES pressure, esophageal acid clearance and motility of the proximal stomach. Recently, numerous investigations have been performed to elucidate the role of Helicobacter pylori (Hp) infection in GERD pathogenesis with the most concern given to its potency to increase gastric acid secretion. However, it appeared that this infection leads to much more complex changes in gastric mucosa including modification of afferent neural signals and specific gastric hormones release. Plasma ghrelin level is low in subjects infected and increases significantly after eradication. Since ghrelin, beside potency to increase gastric secretion has strong prokinetic action on LES functional unit, this phenomenon together with impaired vagal control may contribute to the Hp infection or eradication - related GERD development. Thus, ghrelin and vagal activity could be the missing links that partially explains relationship between GERD and Hp infection.
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This review was designed to show the role of expression of cyclooxygenase (COX)-1 and COX-2 in the cancerogenesis of esophagus, stomach and colon. Unlike COX-1, which is expressed in the normal esophageo-gastro-colonic mucosa, COX-2 was found to be expressed mainly in the pre-cancer changes in the mucosa including Barrett's esophagus, Helicobacter pylori (H. pylori)-induced gastritis and inflammatory changes in colonic mucosa. In Barrett's esophagus, prostaglandins (PGs) derived from upregulated COX-2 contribute to the progression of low-grade to high-grade dysplasia and finally to cancer. In chronic gastritis induced by chronic H. pylori infection, overexpression of COX-2 is probably induced by inflammatory cytokines, growth factors, especially gastrin and reactive oxygen species leading to mutagenesis and subsequent metaplasia, dysplasia and cancer formation. The imbalance between cell proliferation and apoptosis caused mainly by products of COX-2 leads to cancerogenesis. Similarly, in colorectal cancer the overexpression of COX-2, possibly induced by the action of growth promoting factors including progastrin and gastrin and overexpression of survivin contribute to the colorectal cancerogenesis that could be, at least in part, amended by the treatment with specific COX-2 inhibitors. We conclude that: 1) COX-2-derived PGs play a key role in the tumorogenesis in the gastrointestinal tract; 2) The tumor-promoting effect of PGs may be attributed to their ability to stimulate cell proliferation and migration, to inhibit the apoptosis and to increase angiogenesis and invasiveness; 3) In accordance to the proposed major role of COX-2 in cancerogenesis, selective COX-2 inhibitors have been shown in numerous studies to exhibit strong chemopreventive effect on the development of gastrointestinal cancers.
Activity of cancer procoagulant (CP) was studied in blood serum of 90 patients with cancer of lung, breast, oesophagus and colorectum, and of 15 healthy people. The activity of CP was determined by the coagulation method. Sera of patients with cancer showed higher mean activity of CP than sera of healthy control. Of the 90 cancer patients 78 were identified correctly by this test as having cancer (sensitivity 85%). In the case of lung and colorectal cancers the higher CP activity was observed the more advanced was the clinical stage of cancer, and the test was positive in 100%. After radical removal of malignant tumor of lung, decreased CP activity was found.
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Acid-sensing protective mechanisms of duodenum

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The proximal duodenal mucosa, exposed to frequent pulses of gastric acid, is functionally "leaky", increasing the importance of defense mechanisms such as the mucus gel layer, cellular acid/base transporters, bicarbonate secretion, and mucosal blood flow. Our laboratory has used a unique in vitro perfused microscopic system to measure thickness of the adherent mucus gel (MGT), intracellular pH (pHi), bicarbonate secretion, and mucosal blood flow in anesthetized rats. Exposure to pulses of luminal acid, mimicking the rapid physiologic shifts of luminal pH, increases MGT and blood flow, and induces cellular bicarbonate loading, the latter followed by augmented bicarbonate secretion. The mechanism by which the epithelium senses luminal acid includes capsazepine-inhibitable vanilloid receptors, presumably similar to the vanilloid receptor TPVR-1. CFTR, the cAMP-regulated anion channel mutated in the disease cystic fibrosis, plays an essential role in duodenal bicarbonate secretion. Our data are consistent with the hypothesis that cellular bicarbonate loading is an important means of preserving epithelial pHi during luminal acid challenge. Increased MGT may damp rapid shifts of luminal pH. Enhanced mucosal blood flow plays a significant role in the removal of back-diffusing acid. These neurally coordinated systems act coherently to defend the vulnerable duodenal epithelial cells from concentrated gastric acid.
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