Abstract
All definitions of various forms of shock, also those induced by gram-negative bacteria respectively their endotoxins, include the alterations of the microcirculation as an essential component.
In regard to the initial phase of endotoxemia we found in all species studied, that alterations of the microvascular bed are the first detectable changes besides the drop in leukocytes and platelets.
The endothelial cells increase in volume and deviations. This deviation of endothelial cells induces, besides the increase in permeation of plasma into the tissue, a direct contact of the content of the vessels with the basement membrane. Using the Texture Analysis System morphometric results of the endothelial cells confirm the vitalmicroscopic observations. Endothelial cells cultured from human umbilical veins react with contractions after application of histamine and with degranulation after exposure to endotoxin.
Also degranulation of periadventitial mast cells occurs early in the initial phase after endotoxin. In the hamster cheek pouch and the mesentery of the guinea pig local application of complement activated by endotoxin provokes degranulation of mast cells. Isolated complement fractions C3a and C5a have the same effect.
In the status of tolerance against lethal doses of endotoxins induced by a detoxified endotoxin the endotoxin-caused alterations of the microcirculation described fail to occur. This fact provides additional evidence of the significance of the microvasculatory disturbances in the starter mechanism of the endotoxic effects.
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