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PubMed1960

Evidence for a lethal endotoxemia as the fundamental feature of irreversibility in three types of traumatic shock.

The data here reported (Table I) show that a toxin is present in the blood of animals with two types of irreversible hypovolemic shock. These data also show that although blood volume therapy does not correct the hypovolemia because of continuing loss of plasma at the site of injury, the major factor in the progressive decline and death is the endotoxemia rather than the hypovolemia. This is also true of severe and prolonged hemorrhagic shock that is irreversible to transfusion. The data also show that even when there is bacterial activity at the site of injury, the pool of endotoxin in the intestine is the chief source of the circulating endotoxin. In all three types of shock, the endotoxemia develops because persisting hypovolemic shock renders the RE system unable to destroy the endotoxin. The demonstration of an endotoxemia as the cause of irreversibility and death in three types of traumatic shock caused by three different agents suggests that a single pathophysiological mechanism accounts for the phenomenon of irreversibility in all types of traumatic shock.

Animals↗

PubMed1960

On the relation of the size of the intraintestinal pool of endotoxin to the development of irreversibility in hemorrhagic shock.

Additional evidence is presented affirming the role of the intestinal pool of endotoxin in producing irreversibility in prolonged hemorrhagic shock. The fact that coliform-free rabbits tolerate exposure to a degree and duration of hemorrhagic shock which is lethal for rabbits that possess the normal flora, and that these tolerant rabbits lose their tolerance when E. coli are introduced into the gut several hours before inducing shock, demonstrate the critical importance of the size of the pool of endotoxin. That there is a proportionality between the size of the pool of endotoxin and the tolerance of hemorrhagic shock is suggested by the survival rate of several series of coliform-free rabbits fed E. coli by gavage. The rate was less the more firmly the E. coli were reestablished in the flora. The presence of the usual number of coliform bacteria in the intestinal flora does not mean the presence of the usual amount of endotoxin in these bacteria. The amount of endotoxin depends not only on the size of the population, but also, as our own experience demonstrates, on the particular ecological factors extant at any particular time which govern the amount of endotoxin elaborated by any given strain or strains of coliform bacteria.

Bacteria↗

PubMed1961

Pathogenesis of experimental shock. II. Absence of endotoxic activity in blood of rabbits subjected to graded hemorrhage.

A series of biological test reactions was used in order to establish the presence of bacterial endotoxins in the blood of rabbits during the progression of hemorrhagic shock. 1. When the shocked animal was used as the test object, it was not possible to induce either the generalized Shwartzman reaction or the dermal Shwartzman phenomenon with exogenous endotoxin (S. enteritidis or E. coli) as one of the two provocative factors. 2. Epinephrine instilled into the skin of rabbits either before, during, or after an episode of hemorrhagic shock did not result in the hemorrhagic skin reaction which occurs in the presence of as little as 1 microg of endotoxin intravenously. 3. Passive transfer from a donor in the irreversible phase of shock of 20 to 25 ml of blood into a primed recipient (B.P. at 40 mm Hg for 1 hour) was uniformly lethal. 4. Similar amounts of blood from such shocked donor failed upon intravenous injection to elicit a protective hemorrhagic reaction in skin sites which were infiltrated with 100 microg of epinephrine. In the same animals 1 microg of endotoxin added to the blood samples caused a positive dermal response. 5. Blood was taken from rabbits which had been pretreated with S. enteritidis endotoxin and then subjected to hemorrhagic shock (35 mm Hg for 2 hours). Such samples upon passive transfer produced positive skin reactions in epinephrine sites but were not lethal to the primed test recipient used in these studies. It is concluded that the contribution of bacterial endotoxemia to the genesis of hemorrhagic shock remains to be determined.

Animals↗

PubMed1961

Pathogenesis of experimental shock. III. A lethal factor in the blood of rabbits following occlusion of the superior mesentric artery.

Donor rabbits were subjected to shock by occlusion of the superior mesenteric artery (SMAO shock). Portal blood was collected from these animals at certain intervals after release of the arterial ligature. Infusion of this blood into sub-lethally hemorrhaged rabbits caused the death of half of the tested animals; a mortality incidence which closely matched the per cent mortality in rabbits shocked by SMA occlusion alone. Blood from sham-operated donor animals did not prove lethal when infused into hemorrhage-prepared rabbits. Infusion of SMAO shock plasma did not result in the death of recipient animals, even though the whole blood source of the plasma had proven to be lethal upon infusion into hemorrhage-prepared rabbits. Moreover, following pretreatment of donor animals with a non-absorbable antibiotic per os, the number of actively reproducing bacteria in the intestinal fluids was reduced to less than 0.1 per cent of normal; nevertheless, the incidence of passive transfer of lethality from shocked donors receiving this pretreatment was not consistently reduced. Furthermore, when SMAO shock portal blood was tested for the presence of bacterial endotoxin by the sensitive dermal epinephrine reaction, although some blood samples demonstrated lesion-provoking activity, there was no correlation between this activity and the lethal properties of the blood samples. In seeking an explanation for the production of dermal epinephrine lesions by non-lethal shock blood, a positive correlation was demonstrated between the lesion-provoking activity of portal blood and the serotonin content of intestinal tissues of rabbits shocked by SMA ligation. In addition, small amounts of serotonin were shown to be capable of provoking dermal epinephrine reactions in rabbits, under the same conditions used to test the lesion-provoking activity of portal blood. It was therefore concluded that: (a) a toxic factor(s) is present in the portal blood of SMAO-shocked rabbits; (b) that this factor(s) is not likely to be a bacterial endotoxin; and (c) that the occasional provocation of a dermal epinephrine reaction by portal blood from SMAO-shocked rabbits, a property heretofore exclusively attributed to the presence of endotoxin in shock blood, can be entirely explained on the basis of elevated levels of serotonin in this blood.

Animals↗

PubMed1961

Involvement of adrenergic factors in the effects of bacterial endotoxin.

The possible involvement of adrenergic mechanisms in the effects of Escherichia coli endotoxin was investigated in several preparations. Appropriate pretreatment of rabbits with E. coli endotoxin significantly increased pressor responses to epinephrine and norepinephrine as compared to untreated controls. Exposure of isolated rabbit aorta strips to E. coli endotoxin in a medium containing whole blood or cellular constituents of blood significantly increased the response to epinephrine. Endotoxin had no effect on responses to epinephrine in ritro when plain Krebs-Ringer solution was used. Pretreatment with reserpine or phenoxybenzamine (dibenzyline) protected rabbits and mice against the acute lethal effects of E. coli endotoxin. The time period intervening between reserpine or dibenzyline administration and challenge by endotoxin precluded a direct antiendotoxic action of these agents. In addition, incubation of dibenzyline with endotoxin in vitro, under conditions which would favor reaction, did not decrease the toxicity of the latter. These results indicate that peripheral adrenergic mechanisms are intimately involved in the effects of E. coli endotoxin and support the concept that deleterious effects of endotoxin in shock probably are due to exaggeration of existing vasoconstriction in an already compromised organism.

Adrenergic Agents↗

PubMed1958