Peptone Shock Research Articles

Biologically Active Components and Properties of Bordetella perfussis

This chapter discusses the biologically active components and properties of Bordetella pertussis. A variety of biological effects are observed in experimental animals following injection of phase I Bordetella pertussis cells or products. It includes sensitization to the lethal effects of the pharmacological agents histamine and serotonin as well as to nonspecific stresses such as cold and peptone shock; unresponsiveness to the induction of hyperglycemia by epinephrine, which has been attributed to the causation of a β-adrenergic blockade; leukocytosis with predominating lymphocytosis; adjuvanticity with respect to both antibody production—including reaginic antibody ( IgE )—and cell-mediated immunity; and direct, acute toxic effects which are in general related to either a distinct heat-labile toxin or to heat-stable lipopolysaccharide endotoxin. In addition, components of B. pertussis can be shown to induce striking effects in in vitro systems. Paradoxically, while clinical pertussis has become of decreasing importance where effective vaccines are routinely used; there has been an increased interest in the biological activities of B. pertussis.

Course of experimental peptone shock following preliminary administration of DOCA

Course of experimental peptone shock following preliminary administration of DOCA

Properties of the immunogenic and sensitizing activities of Bordetella pertussis in mice: I. Enhancement of peptone shock

The capacity of pertussis vaccine to enhance peptone shock in mice paralleled the immunogenic and histamine-sensitizing activities in fractionation and was similarly labile to heat and to tryptic degradation. It is, therefore, suggested that the immunogen itself may be responsible for these sensitizing activities. Elicitation of heightened susceptibility to peptone shock by the administration of a beta-adrenergic blocking agent, propranolol, would suggest that pertussis vaccine may induce this effect, as had earlier been reported and is presently confirmed, with histamine, via autonomic nervous pathways. Several significant differences were found, however, between pertussis-mediated hypersensitivity to histamine and to peptone, including degree of sensitivity engendered, mouse strain specificity, and duration of symptoms.

Permeability of the blood-brain barrier to P32 in peptone shock

Permeability of the blood-brain barrier to P32 in peptone shock

CHARACTERISTIC DISTRIBUTION OF MAST CELLS IN DOG LIVER. A CONSIDERATION ON THE MECHANISM OF ANAPHYLACTIC SHOCK.

Paraffin sections of the liver of the dog in various ages were stained by aldehydefuchsin plus GOLDNER's trichrome stain in order to investigate the distribution of mast cells.The mast cells of the liver are concentrated along the branches of hepatic veins which are provided with periodically arranged constrictor muscles. Flattened mast cells adhere to the endothelial lining of the vessels. The relation of endothelial and mast cell layers is so close that sometimes it is impossible to distinguish one from the other. The lining up of mast cells in the hepatic vein branches seems to be accomplished within one month after birth, during which time the vessels come to be provided with the constrictor muscles. The interlobular veins, branches of the portal vein, are completely lacking in such juxta-endothelial mast cells.The specific distribution of mast cells presented in this work seems to explain the mechanism of the well-known symptoms of the dog in anaphylactic and peptone shock. The mast cells in the hepatic vein branches are believed to react promptly to the shock substances administered by releasing histamine which must cause, on one hand, the spasm of the constrictor muscles and the following blood congestion in the same vessels and, on the other hand, elevation of the endothelial permeability which facilitates the escape of a liquid component of the blood into the accompanying lymphatics connected to the thoracic duct.

Hexadimethrine and protamine as antiheparin agents. An experimental comparison after totalbody perfusion in dogs.

There have been several reports on the effectiveness of protamine and hexadimethrine (Polybrene) in neutralizing the effects of heparin. Parkin and Kvale¹showed in rabbits with no extracorporeal circulation that clotting times returned to normal at a 1.5:1 dose of protamine to heparin in 5 minutes. In 1953, Preston and Parker²reported on the effects of hexadimethrine on the clotting time in peptone shock and in experimental radiation injury. They found that in the normal animal 7.5 mg. hexadimethrine neutralized 10 mg. of heparin in vivo. In peptone shock, when the coagulation time was prolonged to 56 minutes or more, hexadimethrine in doses of 0.9 to 2.2 mg. per kilogram restored the coagulation time to approximately control levels within a few minutes. In vitro studies showed that the shortest clotting time occurred when the amount of protamine and heparin exactly neutralized each other. If either was in excess,

Further studies on the role of proteases in the allergic reaction.

Protease activity was measured through the hydrolysis of synthetic amino acid esters in body fluids and tissues of guinea pigs, rats, mice, and humans. Significant in vitro activation was observed in serum and lung slices of sensitized guinea pigs on addition of the specific antigen. Increased proteolytic activity was also seen in reverse anaphylaxis. More marked activation occurred when guinea pig serum was treated with peptone and guinea pig or rat serum was treated with agar. Protease activation was demonstrated in specimens of human skin under the influence of a poison ivy extract or croton oil added in vitro. Urinary protease activity of guinea pigs increased significantly during the first hours of anaphylactic shock and very markedly in peptone shock. Peptone shock, elicited in mice pretreated with H. pertussis, was accompanied by a considerable increase in protease activity in the peritoneal fluid as compared with non-pretreated mice which were insensitive to peptone. Proteolytic activity resulting from the activation procedures was due to a number of proteases. The dominant substrate affinity and inhibition patterns suggest that serum and urine proteases are similar to but not identical with plasmin. Anaphylactic activation exhibited patterns different from those resulting from the action of anaphylactoid agents. Tissue enzymes are either of cathepsin- or chymotrypsin-type or mixtures of both. Some of the activated enzymes, although remarkably effective in hydrolyzing amino acid esters, show no activity on protein substrates. This does not justify, however, their designation as "esterases." They probably belong to the class of specific proteases acting only on a single or a small number of functionally significant protein substrates. There is at present sufficient evidence to prove not only that protease activation does occur in anaphylaxis and anaphylactoid conditions but also that it is an important component of the chain of reactions leading to the allergic response.

Peptone shock in the pertussis-sensitized mouse

The susceptibility of pertussis-sensitized mice to fatal shock varies with each peptone preparation. The peptone containing the greatest amount of histamine produced the highest mortality rate. It was confirmed that Bacto-Peptone, with relatively little histamine content, was without appreciable effect. The mechanism of death is probably neither the exogenous histamine administered nor the histamine or serotonin engendered but a combination of these and other factors, still unknown.

Endocrine management of selected cases of allergy based on enzymatic mechanism of sensitization.

The discrepancies in the rationale of the antigen-antibody conjugation being the basic mechanism of allergy make an understanding of the problem of allergy more difficult; the contradictory findings which are often encountered in the antigen-antibody reaction make this theory unacceptable. Nonetheless, the majority of allergists still accept it as a working theory of the allergic reactions. It will be pertinent to mention a few of the contradictions: A constant and predictable anaphylactic response to the first injection of certain antigens (e.g., peptone shock in dogs, 76,77 or intravenous injection of human γ-globulins into humans 47 ) makes the concept of antigen-antibody interaction a logical impossibility because specific antibodies are not present at this stage. The presence of allergic diseases in persons with agammaglobulinemia who are unable to manufacture antibodies has been observed repeatedly. 52,53,75,153 Allergic reactions occur so commonly that they might be looked upon as physiopathologic responses which exist in

犬のPeptoneショック及びアナフィラキシー・ショックにおける二次的活性物質の検索

犬のPeptoneショック及びアナフィラキシー・ショックにおける二次的活性物質の検索

Disturbances of vascular permeability in shock (electrophoretic investigation of protein composition of the lymph in development of peptone shock)

Peptone shock is developed in 5 minutes following the intravenous injection of peptone. There is an acute decrease in the blood pressure. There were no changes in the protein concentration and in the relationship between the protein fraction of the blood serum. A pronounced increase of the lymph flow with increased concentration of the protein in the lymph of the thoracic duct was noted. The average value of the protein concentration before the introduction of peptone equalled 3.5, m±0.11 g%; following peptone introduction it was 4.7, m±0.2 g%: (P<0.01).

Production of peptone shock in mice following administration of H. pertussis vaccine.

SummaryPopulations of ABC and Swiss-Webster male and female mice were found to be resistant to peptone, but an increased susceptibility to peptone with a lethal outcome could be produced by prior treatment with pertussis vaccine. Mice rendered susceptible to peptone with pertussis vaccine could be protected with the antihistaminic agent, Benadryl, with chlorpromazine and with cortisone. The possible role of histamine in the increased susceptibility of mice to peptone, produced by pertussis vaccine, has been discussed.

Heparin content of thoracic duct lymph following shock in dogs.

Anaphylactic or peptone shock causes a release of heparin which is present in greater concentrations in lymph obtained from the thoracic duct than in either arterial or hepatic venous blood. Frequently heparin is present only in thoracic duct lymph following such shock. The evidence indicates that the source of this heparin is the liver and that during shock its passage from liver to blood is mainly by means of the thoracic duct. Heparin is not released into thoracic duct lymph or blood during a histamine or hemorrhage induced shock.

Release of histamine in hepatectomized dogs during anaphylactic, peptone and tryptic shock.

IT is well known that in dogs the liver is the main source of the histamine released during certain types of shock, such as anaphylactic and peptone shock1. However, shock can be obtained in hepatectomized dogs2 and some evidence, particularly recent work by Feldberg and Schachter3, indicates that under certain conditions tissues other than the liver release relatively large amounts of histamine.

Effect of roentgen irradiation and other types of injurious agents on capillaries.

SummaryBy means of a microinjection method it was possible to measure the fragility of mesenteric capillaries of the frog. Roentgen irradiation, heparin injection, trypsin and peptone shock increase the fragility of the capillaries. The increased capillary fragility appears to be a consequence of a liberation of heparin into the circulation of the animals, due to the irradiation or shock treatments.

Action of peptone on mast cells of the dog.

ALTERATIONS of mast cells in the liver of dogs submitted to peptone shock were described by Wilander1; Jaques and Waters2 have confirmed Wilander's results and found similar changes of the mast cells in anaphylactic shock. These alterations have been related by these authors to heparin liberation.

Mucolytic enzyme systems XIX. Comparison of hyaluronidase inhibitor and heparin levels in serum.

SummaryThe effects of peptone shock (with and without block of the reticuloendothelial system by India ink), and administrations of desoxycorticosterone on the nonspecific hyaluronidase inhibitor and heparin concentrations in the blood serum of rabbits at intervals before and after the treatments were observed. A general parallelism was noted in the direction of the changes produced in both serum factors, but variations were observed with respect to the magnitude and time of change. In vitro experiments were carried out on the effect of janus green, thionin, toluidene blue, safranin, neutral violet, neutral red, and aureomycin on the serum inhibitor and on hyaluronidase. A general correlation was observed between the anti-heparin action of these substances and their anti-inhibitor effects.

Shock Phenomena and Thrombin Inactivation

IT is known experimentally that changes in blood-clotting occur under shock. In general, the blood takes longer to coagulate in anaphylactic and peptone shock, while in histamine shock the observations made have been rather uncertain. To clear up the question, we have used the method worked out by Gerendas1,2 for investigating thrombin inactivation.

Comparison of Atropine and Tripelennamine in Treatment of Peptone Shock in Dogs

Conclusions1) One gram/kg body weight of Witte's peptone administered intravenously in a 20% solution, proved fatal in dogs anesthetized with sodium pentobarbital.2) Atropine sulfate, 2.0 mg/kg prevented death from peptone.3) Pyribenzamine, 10.0 mg/kg, afforded better protection than atropine as determined by rapidity of recovery of blood pressure.4) The rapidity of recovery of blood pressure was not greater in those animals receiving both pyribenzamine and atropine than in those receiving pyribenzamine alone.5) These findings support the theory that acetylcholine is concerned in the production of peptone shock, although histamine plays a more important role.

Activation of Serum Protease in Peptone Shock.

Activation of Serum Protease in Peptone Shock.