Untersuchungen über den Mechanismus der Blutdruckwirkung des Anaphylatoxins bei Katzen und Meerschweinchen

Bodammer, G.

doi:10.1007/978-3-662-39718-3_17

Cited by 3 publications

(2 citation statements)

References 5 publications

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“…As we have shown, noradrenaline is liberated by AT, and this effect is mepyramine-resistant. Findings of Bodammer [1969] and H icks and Sackeyfio [1972] strongly support the idea that, besides adrenaline release from the adrenal me dulla, an activation of sympathetic neurons occurs in AT shock.…”

Section: Discussionsupporting

confidence: 63%

Investigations on the Catecholamine Release in Anaphylactic, Anaphylatoxin, and Histamine Shock of Guinea Pigs

Bundschu¹,

Bernauer²,

Filipowski³

1973

Int Arch Allergy Immunol

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(1) Antigen, in sensitized guinea pigs, produced a dose-dependent increase of the serum adrenaline concentrations, whereas the noradrenaline levels were not enhanced significantly. (2) The anaphylactic adrenaline release was diminished, but not prevented, by high doses of the antihistamine mepyramine. (3) Rat serum anaphylatoxin, in non-sensitized animals, provoked a significant increase in both the adrenaline and noradrenaline concentrations. Mepyramine abolished the adrenaline release, but not the noradrenaline release. (4) Histamine, in non-sensitized guinea pigs, also caused a dose-dependent adrenaline release, which was partially resistant to mepyramine.

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Section: Discussionsupporting

confidence: 63%

Investigations on the Catecholamine Release in Anaphylactic, Anaphylatoxin, and Histamine Shock of Guinea Pigs

Bundschu¹,

Bernauer²,

Filipowski³

1973

Int Arch Allergy Immunol

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“…in vivo, C5a-desArg and even C3a-desArg has considerable po tency [20,21], Under these conditions, helper factors may assist in the effects [22], Many of the biological actions of anaphylatoxins are rather indirect, and require the cooperation of more than one target cell and of cell-derived mediators. Smooth muscle contraction is partially mediated by mast cell-derived histamine [23], by prostaglan dins and by leukotrienes [24], Various smooth muscle organs are certainly con tracted by C5a independent of histamine [25,26]; however, a clearly direct response to C5a has as yet been demonstrated in one target only -isolated muscle cells from toad stom ach [27], Vascular smooth muscle may be contracted [24,[28][29][30] or relaxed [31,32] depending on the type of blood vessel. This could be due to the involvement of second mediators released in different ratios, and then causing different net effects.…”

mentioning

confidence: 99%

Anaphylatoxins: Possible Roles in Disease

Vogt¹

1986

Complement

116

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Anaphylatoxins, in particular C3a and C5a, have various biological activities which suggest a role as mediators of inflammatory reactions: they cause contraction of smooth muscle, histamine release, increase in capillary permeability, adhesion of leukocytes to vascular endothelium, leukocyte chemotaxis, and aggregation of platelets and leukocytes. Most of these effects are supported by the cooperation of other mediators, in particular arachidonic acid derivatives which may be produced by anaphylatoxin-stimulated cells, e.g. leukocytes or endothelium. In vivo effects of the complement peptides depend very much on the site of their generation: intravascular release in the general circulation leads to adverse symptoms such as adult respiratory distress syndrome and shock lung, mainly due to leukocyte activation, aggregation and their accumulation in lung vessels. Intravascular release may be induced by certain drugs, and by contact of blood with the surfaces of bypass or dialysis apparatus. Induction of local inflammatory and defense reactions requires release of anaphylatoxins in tissue spaces. Tissue fluid differs quantitatively from blood plasma in its concentration of complement components. This raises some problems of how efficient concentrations of C3a and C5a can be attained at the site of a lesion to generate a chemotactic gradient capable of attracting blood leukocytes.

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