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J FINE

Publications and source records attributed to J FINE.

At least 37 records · Page 2Linked to original sources
PubMed1962

The role of the sympathetic nervous system in the generalized Shwartzman reaction.

Unilateral denervation of the renal pedicle was performed in a series of rabbits. 5 to 21 days later two intravenous injections of E. coli endotoxin were given 18 hours apart. In seven rabbits the generalized Shwartzman reaction developed in the non-denervated kidney. Four of the seven denervated kidneys did not show the reaction, and in the remaining three only a mild reaction was present. From these and previous observations we conclude that an intact sympathetic nervous system as well as endotoxin from the intestine, are necessary for the production of the generalized Shwartzman reaction.

Animals↗
PubMed1960

In vivo detoxification of endotoxin by the reticuloendothelial system.

Evidence is presented that The normal RES extracts endotoxin from the circulation and inactivates it very rapidly. When the RES has been damaged, whether by a blockading agent, such as thorotrast, or by a reversible degree of hemorrhagic shock, it cannot extract more than a small per cent of the amount of the endotoxin the normal system can extract. Of that fraction of endotoxin which is extracted, very little is detoxified. An organ like the kidney, which does not contain a significant amount of RE tissue, does not extract more than an insignificant percentage of the injected amount, and therefore does not detoxify endotoxin. Since dephosphorylation is a process concurrent with detoxification, and does not occur in an organ which does not extract or inactivate a significant amount of injected endotoxin, it is probable that this process is an indirect index of detoxification. Within the time limits of these experiments, plasma alone does not inactivate endotoxin.

Bacteria↗
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↗
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↗