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PubMed1958

Wound shock.

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Humans↗
PubMed1956

On the nature of parabiosis intoxication: shock as the precipitating cause.

Spinal transection of one of a parabiotic pair of rats is immediately followed by a state indistinguishable in visual and hematologic characteristics from spontaneous "parabiosis intoxication." The transected rat develops erythremia, hyperhemoglobinemia, and an increased hematocrit count; whereas the twin concurrently shows anemia characterized by a decrease in hemoglobin, erythrocyte count, and hematocrit reading, and often also lipemia. These findings are ascribed to whole blood transfusion of one rat by the other followed by adjustments compensatory to the resulting distortion in the respective blood volumes. It is suggested that parabiosis intoxication is a manifestation of this same process and is not due, as has been contended, to an immune response.

Anemia↗
PubMed1957

The relationship between the vascular manifestations of shock produced by endotoxin, trauma, and hemorrhage. I. Certain similarities between the reactions in normal and endotoxin-tolerant rats.

The vascular effects of lethal doses of E. coli endotoxin, as observed in the mesentery of the rat, resemble the reactions of traumatic and hemorrhagic shock in the following respects: a profound inhibition of arteriolar and precapillary reactivity to topical epinephrine occurs after an initial stage of hyperreactivity; the small veins show failure to relax completely following constrictor doses of epinephrine; and the terminal vessels develop an unusual sensitivity to fluctuations in temperature of the fluid irrigating the tissue. Rats in which tolerance to bacterial endotoxin is induced, by repeated doses given daily, become highly resistant to the lethal effects of both drum trauma and hemorrhagic shock. However, rats in which the adaptation to traumatic shock is produced by repeated exposure to drum trauma, do not develop a significant degree of tolerance to lethal doses of endotoxin. The injection of small non-lethal doses of bacterial endotoxin during non-lethal episodes of trauma or hemorrhage, leads to the development of irreversible shock and death. The bearing of these findings on the problem of the relationship between endotoxin and traumatic shock is discussed.

Animals↗
PubMed1957

The relationship between the vascular manifestations of shock produced by endotoxin, trauma, and hemorrhage. II. The possible role of the reticulo-endothelial system in resistance to each type of shock.

In studies designed to establish the interrelationship between bacterial endotoxins and the vascular sequelae of hemorrhagic and traumatic shock, the effect of factors known to influence the phagocytic behavior of the reticulo-endothelial system (RES) were investigated. Measures which induced a so called "blockade" of the RES were uniformly associated with an exacerbation of the vascular effects of the endotoxin of E. coli. Such pretreatment also counteracted the cross-tolerance induced by endotoxins against the lethal effects of hemorrhage or drum trauma. The vascular reactions characteristic of irreversible hemorrhagic shock could be simulated by a combination of pretreatment with carbon or proferrin and the infusion of small doses of E. coli endotoxin. An increase in the phagocytic activity of the RES, induced by repeated injections of certain colloids, was associated with an enhanced tolerance of shock. Measurement of carbon clearance values indicated that although an augmented phagocytic capacity was present in rats with induced tolerance to bacterial endotoxins, the development of resistance to trauma was not associated with a comparable change in the phagocytic function of the RES.

Animals↗
PubMed1958

Irreversible hemorrhagic shock in germfree rats.

Evidence has been provided that a state of irreversible hemorrhagic shock can be induced in a bacteria-free environment in rats reared under germfree conditions. The response to bleeding, the duration of the hypotensive episode and the pathological changes were the same in the germfree and in normal stock rats. The findings are interpreted as evidence opposed to the concept that bacteria or bacterial products are implicated, as primary factors, in the pathogenicity of shock.

Animals↗
PubMed1960

On the absorption of bacterial endotoxin from the gastro-intestinal tract of the normal and shocked animal.

Coliform-free rabbits fed P(32) labeled E. coli 0111B(4) prior to the induction of experimental hemorrhagic shock were shown to have a substantial amount of the type-specific 0111B(4) antigen in the circulating blood, liver, and spleen, whereas normal rabbits fed the same amount of these bacteria and held under identical conditions, but not exposed to shock, have the antigen within the liver, and occasionally in the kidney, but not in the blood. That the antigen recovered from the blood and tissues was derived from this specific strain of bacteria was demonstrated by the use of the hemagglutination inhibition reaction, by the absence of cross-reacting antigens in appropriate control animals, and by agreement in the amount of antigen as estimated by two different technics. Transport of bacterial endotoxin across the intestinal membrane appears to be achieved primarily by passive diffusion. The accumulation of biologically active endotoxin in the blood and tissues of the shocked animal appears to be due to a reduction in the detoxifying potential of the reticulo-endothelial system, and not to a greater than normal absorption of endotoxin from the intestine. The absence of toxicity in the specific antigen extracted from normal liver demonstrates that the degradation of endotoxic potency can be achieved without altering the chemical integrity of the polysaccharide moiety of the molecule. The implications of the hypothesis that there is a continuous but fluctuating absorption of bacterial endotoxin from the intestine are briefly discussed, and the contribution of free circulating bacterial endotoxin of intestinal origin to the fate of the shocked animal is noted.

Animals↗