Role of endotoxins and bile acids in the pathogenesis of septic circulatory shock.
It has long been known that the toxic effects of endotoxins under experimental conditions can be induced only when they are administered parenterally. However, in naturally occurring enteroendotoxemic diseases (e. g. septic and intestinal ischemic shocks) the endotoxins--which are produced by gram negative members of intestinal flora-, absorb from the intestinal tract to the blood circulation and can elicit pathological processes. It is an important distinction between natural and experimental endotoxin shock. If the common bile duct of rats were chronically cannulated a significant amount of perorally administered endotoxin was absorbed into the blood. This endotoxin shock can be prevented by bile acids. The physiological surfactants, the bile acids, are important facts in the defense of macroorganisms against endotoxins (physico-chemical defense). The production and passage of bile acids depend from the function of liver and the cholecystokinine (CCK) synthesis of small intestine wall. If the bile (bile acid) content of the intestinal canal decreases the endotoxin can translocate to the body and elicits toxic symptoms. So most important parts of defense against endotoxins in natural conditions are the CCK and bile acids. The consequence of damage of liver (place of bile acid synthesis) or small intestine (place of CCK synthesis) is the absorption of endotoxins.
Bertók
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Frédéric Joliot-Curie National Research Institute for Radiobiology and Radiohygiene, Budapest, Hungary.
D000042:Absorption; D000284:Administration, Oral; D000818:Animals; D001427:Bacterial Toxins / Q000009:adverse effects / Q000493:pharmacokinetics; D018988:Bacterial Translocation; D001646:Bile / Q000737:chemistry; D001647:Bile Acids and Salts / Q000737:chemistry / Q000378:metabolism / Q000502:physiology*; D002766:Cholecystokinin / Q000096:biosynthesis; D003135:Common Bile Duct / Q000502:physiology; D019446:Endotoxemia / Q000150:complications / Q000378:metabolism; D004731:Endotoxins / Q000008:administration & dosage / Q000009:adverse effects / Q000493:pharmacokinetics / Q000502:physiology*; D016905:Gram-Negative Bacterial Infections / Q000378:metabolism / Q000503:physiopathology; D007263:Infusions, Parenteral; D007408:Intestinal Absorption; D007421:Intestine, Small / Q000378:metabolism; D007422:Intestines / Q000098:blood supply / Q000382:microbiology; D007511:Ischemia / Q000209:etiology; D008099:Liver / Q000502:physiology; D051381:Rats; D012772:Shock, Septic / Q000209:etiology* / Q000378:metabolism / Q000503:physiopathology
D001427:Bacterial Toxins; D001647:Bile Acids and Salts; D004731:Endotoxins; D002766:Cholecystokinin