Catecholamine release during anaphylactic shock in guinea pigs

Bernauer, W.; Hagedorn, Manfred; Filipowski, P.

doi:10.1007/bf01002344

Cited by 18 publications

(5 citation statements)

References 16 publications

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“…The blood was transferred into conical tubes where it remained 20 min for coagulation at room temperature. This procedure does not lead to a loss of catecholamines, as shown earlier [Bernauer et al, 1971], The blood was then centrifuged for 30 min at 3,000 rpm, and the serum was transferred into glass-stoppered tubes.…”

Section: Methodsmentioning

confidence: 99%

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: Methodsmentioning

confidence: 99%

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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“…This is compatible with a resting plasma catecholamine concentration of the order of 10 -9 M [2]. In protracted anaphylaxis in the guinea pig, plasma adrenaline concentrations may rise to 10 -7 M [12]. Such concentrations may contribute to multiple beneficial effects: reduced bronchospasm, reduced pulmonary and coronary vasoconstriction and decreased mediator release [57,58].…”

Section: Sympathomimetie Agentsmentioning

confidence: 73%

Auto-modulation of release of pharmacological mediators of immediate (type I) hypersensitivity. A review

1977

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IntroductionVarious chemical agents (pharmacological mediators) are released from sensitized tissue following exposure to specific antigen. These mediators include: histamine, serotonin, slowreacting substance of anaphylaxis, catecholamines, kallikreins and kinins, platelet activating factor, several chemotactic factors and prostaglandins. The release of a combination of these substances provides evidence for the existence of the 'Type I' anaphylactic reaction: the tissue mast cells and circulating leukocytes being the principal targets of the antigen-antibody interactions.Numerous substances are known to inhibit the anaphylactic release of histamine and SRS-A. This review will be concerned with the intrinsic regulation of release of mediators by autonomic neuro-transmitters (e.g. catecholamines and cholinesters) and autacoids (e.g. histamine, serotonin and prostaglandins). It has become clear that positive and negative feedback mechanisms by these endogenous chemical substances by means of the intermediary (second messenger) cyclic nucleotides provide important means for the intrinsic modulation of Type I allergic manifestations in animals and patients. We have discussed the evidence for autoregulation of anaphylactic mediator release and the receptor mechanisms involved.

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“…Disodium cromoglycate (DSCG) increased the tissue cAMP only in sensitized but not in non-sensitized lungs.A similar inverse relationship existed in all our experimental condi tions between the tissue cAMP levels and the anaphylactic histamine re lease as was demonstrated by other authors in different test systems [Lichtenstein, 1971;Orange et al, 1971].The present study was done to learn whether catecholamine concen trations in the range of 10~9 to 1CL7 m, as found in the blood plasma of normal and anaphylactic guinea pigs [Piper et al, 1967;Bernauer et al, 1971 ;Bundschu et al, 1973], are sufficient to increase cAMP levels and to inhibit the anaphylactic histamine release in guinea pig lung tissue.We determined the activity of the adenylcyclase in chopped lung tissue from guinea pigs actively sensitized against ovalbumin, according to Krishna et al [1968]. The lung samples were preincubated for 2 h with 0.24 //Ci14C-adeninc and incubated for 15 min with isoprénaline, ad renaline, or noradrenaline.…”

mentioning

confidence: 75%

The Effect of Glucocorticoids and Catecholamines on Cyclic AMP and Allergic Histamine Release in Guinea Pig Lung

Schmutzler¹,

Freundt²

1975

Int Arch Allergy Immunol

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Catecholamine release during anaphylactic shock in guinea pigs

Cited by 18 publications

References 16 publications

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

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

Auto-modulation of release of pharmacological mediators of immediate (type I) hypersensitivity. A review

The Effect of Glucocorticoids and Catecholamines on Cyclic AMP and Allergic Histamine Release in Guinea Pig Lung

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