PubMed Health⌕ Search

Biomedical subjects

B W ZWEIFACH

Publications and source records attributed to B W ZWEIFACH.

At least 37 records · Page 2Linked to original sources
PubMed1961

Alterations in the oxidative metabolism of rats with induced tolerance: in vitro study of diaphragm.

Oxidative metabolism of diaphragms from endotoxin- and trauma-tolerant rats was investigated, utilizing the reduction of tetrazolium salt. It was found that diaphragms from normal and stress-tolerant animals did not differ in "oxidative performance" (activity in the absence of the redox dye phenazine methosulfate). However, diaphragms from tolerant animals exhibited a highly significant enhancement in "oxidative potential" (activity in the presence of phenazine methosulfate). This change was apparently not precipitated by adjustments in circulatory dynamics, nor was it related to reticuloendothelial stimulation. The suggestion is made that the effects observed may develop through the secondary release of endogenous epinephrine. Evidence is presented suggesting that the enhancement of "oxidative potential" exhibited by the parenchymal tissues of tolerant animals represents an adaptation in metabolism whereby pools of potentially oxidizable foodstuffs are stockpiled.

Animals↗
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

Some effects of proteolytic inhibitors on tissue injury and systemic anaphylaxis.

A study was made of the development of various forms of local and systemic injury in animals treated with inhibitors of proteolytic activity. The agents used were tosylarginine methyl ester (TAME), epsilon aminocaproic acid (EACA), and soybean trypsin inhibitor (SBTI). 1. Hemorrhagic necrosis in the skin of the rabbit following intradermal epinephrine in combination with bacterial endotoxin (either intravenous or local) was clearly suppressed by EACA, TAME, and SBTI, given systemically. Tosylarginine (TA) was ineffective. 2. No effect was observed on the classical Shwartzman reaction, the local Arthus phenomenon, or inflammation induced by xylene. 3. The lethal effects of systemic anaphylaxis in the mouse, acute endotoxemia in the rat and mouse, and drum shock in the rat are suppressed by EACA and TAME. 4. There was no effect on the generalized Shwartzman phenomenon in the rabbit and on anaphylaxis in the guinea pig. 5. The effects of EACA or TAME on the injury reactions under investigation were not due to a pharmacological or chemical action on vascular behavior per se. 6. The data provide corroborative evidence for a proteolytic step in injury phenomena which may be mediated through some common activation system. 7. The working hypothesis is advanced that local or systemic stress through the release of epinephrine may result in an increase of a circulating activator of proteolysis and that this in turn may give rise to the release of vasoactive substances,-possibly histamine, serotonin, or a polypeptide.

Anaphylaxis↗
PubMed1960

Inactivation of bacterial exotoxins and endotoxin by iron. In vitro studies.

After incubation with various agents in vitro, the lethal effects of aqueous solutions of Cl. perfringens alpha toxin, C. diphtheriae toxin, and E. coli endotoxin were tested in mice, guinea pigs, and rabbits, respectively. Iron, copper, cysteine, ascorbic acid, and versene counteracted the lethal effects of alpha toxin in mice, while magnesium, manganese, zinc, and citrate did not. Iron also counteracted the lethal effects of diphtheria toxin in guinea pigs. After incubation of endotoxin with iron, its lethal effects and tissue-necrotizing actions in rabbits were counteracted. However, the pyrogenic properties of the toxin were not affected. The solubilities of perfringens alpha toxin and diphtheria toxin were markedly reduced after incubation with detoxifying metals, and resolubilization of these toxins with chelators resulted in partial restoration of toxicity. Addition of versene to detoxified endotoxin also resulted in partial recovery of lethal effectiveness. The inactivation of bacterial toxins by iron under in vitro conditions is not specific to this metal, is a reversible process, and may be due to desolubilization, reduction, or to competition by the metal for sites on the toxin normally bound by other cations in vivo. Although no evidence is presented in this paper to support the view that there is a relationship between the inactivation of endotoxin and the storage iron in the reticuloendothelial system of shocked animals, the observation of an in vitro inactivation of endotoxin by inorganic iron warrants consideration of such a mechanism.

Animals↗