Effects of hemorrhage, hypoxia, and intravascular coagulation on bacterial clearance and translocation

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This study was undertaken to discover if impaired blood clearance functions and killing capacity of the reticuloendothelial system contribute to the high occurrence rate of septic complications after shock, trauma, and thermal injury.


Prospective, randomized, controlled trial.


Experimental laboratory in a university teaching hospital.


Thirty-three standard-breed rabbits of either sex.


Defined numbers of Escherichia coli (1.3 x 108 colony-forming units were injected intravenously 60 mins after induction of hypoxia, standardized by defined reduction of oxygen uptake (60% to 75% of baseline) induced by hy-poventilation (n = 6) or hemorrhage (n = 6), after complete defibrination caused by the snake toxin, ancrod (n = 6), and after 60 mins without intervention (controls, n = 6). At 180 mins after bacterial injection, the animals were killed and tissue samples of liver, kidney, spleen, and lung were collected for microbiological examinations.

Measurements and Main Results:

Bacterial elimination from the blood and distribution pattern of viable bacteria in liver, spleen, kidney, and lung were investigated in hemorrhagic, hypoxic, and defibrinated rabbits. Compared with controls, there was a distinct alteration of the elimination kinetics of bacteria from the circulating blood in the experimental groups. First, the initial counts of viable E. coli were up to 300% (p < .05) higher in the defibrination, hemorrhage, and hypoxia groups than in controls. Second, greater numbers of E. coli were found in the blood for a significantly (p < .001) longer period, coupled with up to four times higher counts in organ homogenates in the hemorrhagic and defibrinated group (p < .01) and more than 100 times higher counts than control values in the hypoxic animals (p < .001).


Hemorrhage, hypoxia, and intravascular coagulation induce impaired bacterial clearance from the blood that is associated with altered organ distribution patterns, thus reflecting dysfunction of the reticuloendothelial system. (Crit Care Med 1993; 21:1758–1764)

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