The physical and chemical characteristics of Enterosgel define its absorptive and protective properties: • The solid porous structure of the gel-forming matrix determines absorption capacity by the molecular
adsorption mechanism and allows predominantly adsorbing medium molecular weight toxic substances and metabolites (e.g.
bilirubin and products of
protein breakdown). • Due to its gel-like consistency: • it absorbs high-molecular-weight toxic substances by the mechanism of co-precipitation in the gel (e.g.
bacterial toxins); • it shows protective properties — its elastic gel-like particles form a layer on the surface of mucous membranes. This layer protects mucous membranes from various damaging factors, and its protective properties are manifested universally — in the intestine, and on the surface of the mucous membranes of other organs. It absorbs toxic substances produced in the gastrointestinal tract, as well as toxic substances entering the gastrointestinal tract from the environment (e.g.,
ethyl alcohol). It also prevents reabsorption of toxic substances and metabolites excreted into the intestinal lumen from the blood, as well as getting into the intestine with bile. In an
in vitro experiment, it reduced the production of staphylococcal
enterotoxin and inhibited the growth of
Staphylococcus aureus. It reduced malonic dialdehyde formation and increased integral antiradical activity in toxic liver damage
in vivo. Due to adsorption in the gastrointestinal tract, it helps reduce blood sugar and
glycated hemoglobin levels, eliminate lipid distress syndrome, including diabetic dyslipidemia, improves energy processes in liver tissues in experimental diabetes. Enterosgel (PMSPH) firmly binds and excretes pathogenic bacteria and
rotaviruses. Highly viscous PMSPH particles cover mucosal areas and protect them from the damaging effects of bacterial toxins and various active chemical compounds (e.g., deconjugated bile salts that damage the mucosa of the gastrointestinal tract). Enterosgel has a pronounced ability to absorb lipopolysaccharide molecules. Large molecules of lipopolysaccharide are co-precipitated in the gel and excreted from the body.
Lipopolysaccharide (LPS), which has extremely high biological activity, can be found in the outer wall of all
Gram-negative bacteria and is released only when the bacterium is destroyed, and is also known as
endotoxin (the prefix endo- means inside, inside the bacterium). The distal section of the intestine is the main reservoir of Gram-negative microflora and lipopolysaccharides. Normally, only a small amount of endotoxin enters the bloodstream because the intestinal wall works as a barrier and limits the inflow of endotoxin into the bloodstream. Most (94%) of the endotoxin entering the bloodstream undergoes detoxification in the liver. However, a small amount of endotoxin bypasses the liver and enters the systemic bloodstream, maintaining physiological concentration of endotoxin in the blood (physiological endotoxinemia). The process of endotoxin entering the bloodstream can be intensified by various lesions of the intestinal mucosa and by dysbacteriosis, which is accompanied by translocation of bacteria and products of their life activity into the small intestine and as a result of antibiotic-induced death of Gram-negative microflora and the release of large amounts of endotoxin. It should be particularly emphasized that various stressful situations (severe seizures, burns, trauma, etc.) cause damage to the mucous membrane of the gastrointestinal tract. This damage occurs due to redistribution of energy and structural resources of the body, i.e. transfer from systems not involved in adaptation to the stress factor to systems providing adaptation. An increase in the concentration of endotoxin in the blood exceeding the physiological norm leads to a pathological condition known as endotoxin aggression. Endotoxin aggression is a universal factor in the pathogenesis of human diseases, the development of which is caused by an excess of endotoxin entering the general bloodstream and a lack of endotoxin-binding systems. Excess endotoxin causes endothelial damage in the microcirculatory vessels of the intestinal mucosa and leads to the development of mucosal ischemia. This, in turn, causes further damage to the mucosa and a weakening of the intestinal barrier. Reduction of endotoxin back to physiological levels in the blood prevents damage to the vascular wall and restores impaired blood supply to the intestinal mucosa and eliminates mucosal ischemia. The latter, in turn, contributes to its regeneration and restoration of the barrier function of the intestinal mucosa. The positive effect of using Enterosgel (PMSPH) is primarily aimed at preserving/restoring the intestinal barrier, restoring the physiological level of endotoxin and breaking the vicious circle caused by damage to the mucous membrane. This inhibits the development of endotoxin aggression.
Notes Figure 1:
As a result of insufficiency of the intestinal barrier, the concentration of LPS in the blood flow of the mucous membrane increases, which leads to disruption of microcirculation and ischemia of the mucous membrane, its damage and further development of intestinal barrier insufficiency. Endotoxin aggression develops. Figure 2:
The use of Enterosgel (PMS PH) reverses the course of events: the level of LPS decreases, microcirculation processes in the intestinal mucosa are restored, and so are the intestinal mucosa and the functions of the intestinal barrier (more). == Effects on the human ==