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Endotoxin inactivation in plasma from septic patients: An in vitro study
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AbstractPatients with suspected septicemia were screened for endotoxemia with a quantitative chromogenic assay. In some patients endotoxin concentrations were within the range of healthy controls. Eleven of these were patients on intensive care with severe, culture‐verified, gram‐negative infections in blood or other foci. One possible explanation for this paradoxical absence of endotoxin is increased plasma inactivation. In order to test this hypothesis, endotoxin was added to platelet‐rich plasma from these patients to give a concentration of 100 ng/l, and serial quantitative determinations were made for 2 hours. Plasma from 11 healthy individuals served as controls. In the first sample, measured immediately after addition of endotoxin, a mean of 97.3 ng/l was recovered in plasma from healthy individuals and only 75.8 ng/l in the septic plasma (p<0.05). When kept on ice, these concentrations were maintained, while at +37‡C they decreased rapidly at rates that were equal in both septic and control plasmas. In a corresponding study in platelet‐free plasma, it was found that the platelets could not account for this inactivation. The results demonstrate the possibility of immediate endotoxin inactivation in plasma from patients with sepsis, probably caused by chemical binding.
Title: Endotoxin inactivation in plasma from septic patients: An in vitro study
Description:
AbstractPatients with suspected septicemia were screened for endotoxemia with a quantitative chromogenic assay.
In some patients endotoxin concentrations were within the range of healthy controls.
Eleven of these were patients on intensive care with severe, culture‐verified, gram‐negative infections in blood or other foci.
One possible explanation for this paradoxical absence of endotoxin is increased plasma inactivation.
In order to test this hypothesis, endotoxin was added to platelet‐rich plasma from these patients to give a concentration of 100 ng/l, and serial quantitative determinations were made for 2 hours.
Plasma from 11 healthy individuals served as controls.
In the first sample, measured immediately after addition of endotoxin, a mean of 97.
3 ng/l was recovered in plasma from healthy individuals and only 75.
8 ng/l in the septic plasma (p<0.
05).
When kept on ice, these concentrations were maintained, while at +37‡C they decreased rapidly at rates that were equal in both septic and control plasmas.
In a corresponding study in platelet‐free plasma, it was found that the platelets could not account for this inactivation.
The results demonstrate the possibility of immediate endotoxin inactivation in plasma from patients with sepsis, probably caused by chemical binding.
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