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B Tuchweber

Publications and source records attributed to B Tuchweber.

At least 181 records · Page 10Linked to original sources
PubMed1966

Effect of lead acetate on the susceptibility of rats to bacterial endotoxins.

Selye, H. (Université de Montréal, Montreal, Canada), B. Tuchweber, and L. Bertók. Effect of lead acetate on susceptibility of rats to bacterial endotoxins. J. Bacteriol. 91:884-890. 1966.-A single, normally well-tolerated, intravenous injection of lead acetate increases the sensitivity of the rat to the endotoxins of various gram-negative bacteria about 100,000 times above normal. Under the conditions of these experiments, the mortality and organ changes normally produced by the intravenous injection of 100 mug of Escherichia coli endotoxin were essentially the same as those obtained by use of 1 nanogram in lead-sensitized rats. The sensitizing effect of lead acetate for E. coli endotoxin is greatest when the two agents are given simultaneously. However, considerable sensitization is still detectable when endotoxin is injected up to 1 hr before or 7 hr after sensitization with lead. No sensitization was noted when the endotoxin was administered 24 hr before or after lead acetate. Under our experimental conditions, the minimal dose of lead acetate which could still induce significant sensitization to E. coli endotoxin was 1 mg per 100 g of body weight. Although lead acetate induces a high degree of susceptibility to various endotoxins, other reticuloendothelial blocking agents did not acquire unusual toxicity after pretreatment with lead. Finally, none of the other metals or reticuloendothelial blocking agents tested could duplicate the pronounced decrease in endotoxin resistance induced by lead acetate.

Acetates↗
PubMed1965

An experimental obliterating thromboangiitis limited to the posterior part of the body.

After a brief outline of the principles involved in the production of thrombohemorrhagic phenomena (THP) with special organotropic localizations, an experimental technique is described which permits the production of acrocyanosis and thrombohemorrhagic lesions largely limited to the posterior part of the body. This phenomenon can be consistently produced by certain combinations of THP elicitors, anaphylactoid agents and noradrenaline (NA). The most effective combination among those tested is thorium dextrin (Th-Din) plus tannic acid plus NA. Several drugs can decisively influence the course of this reaction. Most otable among these are Neo-Antergan (an antihistaminic) which sensitizes for the production of the aboral THP, while heparin (presumably through its anticoagulant effect) and Dibenamine (presumably through its antiadrenergic action) offer virtually complete protection. When only Th-Din plus tannic acid is given, there develops an intense but reversible cyanosis in the hind paws and tail; additional treatment with NA induces obliterating thromboangiitis with hemorrhages and gangrene. None of hese changes are produced by Th-Din, tannic acid or NA alone. Evidently, here, e are dealing with pluricausal experimental diseases whose possible relationship to Raynaud's disease, thromboangiitis obliterans and anaphylactoid purpura is briefly discussed.

Animals↗