Anaphylactoid oedema

The egg-white anaphylactoid reaction is accompanied by haemoconcentration and hypothermia [243, 247, 248], both of which are probably a consequence of the increased vascular permeability and oedema of the Reaction. The adrenal cholesterol, circulating eosinophil count and blood concentration of corticosteroids remain unchanged after egg-white is administered to rats. The adrenal ascorbic acid, however, is significantly decreased, but this does not correlate with the severity of the anaphylactoid oedema [641, 642]. Other studies show that there is a reduction of the adrenal medullary catecholamines during the egg-white reaction and these amines may condition the resistance of the rats to the effects of egg-white [392]. 

Several workers have noted that rats sometimes failed to respond with a characteristic anaphylactoid oedema when injected with egg-white [171, 248, 401, 402, 447] or dextran [263, 344, 345, 361, 411, 464, 605] however, it was Harris and West [275] who first differentiated between rats which occasionally failed to show an oedema response and those animals which never responded. These workers found that out of 832 Wistar albino rats injected systemically with egg-white or dextran, no fewer than 162 failed to show the characteristic symptoms of the anaphylactoid reaction. Moreover, procedures such as adrenalectomy or hypoglycaemia which were known to potentiate the reaction failed to facilitate the response in the resistant animals. Despite subsequent research effort no physiological, biochemical or immunological difference between these 2 types of rat has yet been isolated which will explain this lack of reactivity to egg-white and dextran. 

Other evidence shows that histamine is not the main mediator in the anaphylactoid reaction. For example, the injection of histamine itself does not elicit all the symptoms which are typical of an anaphylactoid response [171]. Moreover, egg-white and dextran elicit a full anaphylactoid oedema in rats whose skin histamine has been reduced to about 9% of the control values by compound 48/80 pretreatment [371]. Depletion studies with the antibiotic polymyxin B sulphate indicate that a maximum release of skin histamine, with little change of the tissue 5-hydroxytryptamine, does not modify the egg-white or dextran reactions [485]. Not all antihistamines inhibit the anaphylactoid reaction [90, 187, 248, 463, 464, 487, 530], and it is possible that the antihistamines found by earlier workers to inhibit the reaction possessed non-specific effects and especially anti-5-hydroxytryptamine activity [61,137, 203, 489]. 

There are 3 known plasma kinins, namely the nonapeptide bradykinin or kallidin-9 [154, 157, 158, 363, 364, 473, 523], lysyl-bradykinin or kaUidin-10 [499,665] and methionyl-lysyl-bradykinin [155,159,556]. These pharmacologically active polypeptides behave simlarily, although quantitative differences exist between them [141, 156, 412]. Bradykinin increases vascular permeability in the rat after intradermal injection [82,107,167,633] and also after sub-plantar injection into the paw [110, 210, 389, 601], and as such plasma kinins are potential mediators of the anaphylactoid oedema. 

G.Gabbiani, Action of Cyproheptadine on Generalized and Local Anaphylactoid Oedema, Int. Archs Allergy appl. Immun. 33, 568-575 (1968). 

R.Veilleux, Anaphylactoid Oedema Produced in Rats by Certain Dextrins, Br. J. Pharmac. Chemother. 21, 235-237 (1963). 

C.V. Winder, J.Wax and M. A.Been, Rapid Foot Volume Measurements on Unanesthetized Rats, and the Question of a Phenylbutazone Effect on Anaphylactoid Oedema, Archs int. Pharmacodyn. Th r. 112, 174-187 (1957). 

Beauquier B +, Encephale (French) 24, 62 Anaphylactoid reactions/Anaphylaxis Angi oedema... 

Anaphylactoid reactions/Anaphylaxis Angi oedema Bullous dermatitis Dermatitis... 

Acute generalized exanthematous pustulosis (AGEP) (2001) Chu CY+, Dermatology 202(2), 141 Anaphylactoid reactions/Anaphylaxis Angi oedema Erythema... 

Leger and Masson [401] examined the possibility that the inflammatory anaphylactoid reaction in rats results from an acute deficiency of biotin however, pretreatment with biotin did not alter the incidence or the severity of the oedema produced by egg-white. 

Individuals with hereditary angioneurotic oedema lack serum CT-esterase inhibitor, the inhibitor of the activated first component of hemolytic complement. During an acute episode of this disorder circulating CT-esterase, which is a permeability-increasing factor in human skin, is markedly increased [57, 97, 140, 142, 219, 332]. It is unlikely that a similar mechanism is involved in the anaphylactoid reaction in rats as reactivity is not an absolute phenomenon [32-34, 274]. The final inflammatory mediator(s) of the reaction is, therefore, available for release in both reactor and non-reactor rats. This implies that the trigger mechanism or some intermediary step in the reaction is different in the two types of rat. 

HT is relatively more potent than histamine in increasing vascular permeability in the rat [61, 137, 414, 485, 487, 534, 578, 581]. Parratt and West [482-490] extensively studied the significance of the presence of the substantial amounts of both 5-HT and histamine in the skin and subcutaneous tissues of the rat, and the importance of their release from these sites during the anaphylactoid reaction. Polymyxin B sulphate released more than 90% of the histamine in the rat skin but less than 20% of its 5-HT on the other hand, reserpine released more than 90% of the 5-HT but only small amounts of the histamine. Pretreatment with reserpine, but not with polymyxin B sulphate, effectively inhibited both the egg-white and dextran anaphylactoid reaction. Further evidence for an important role of 5-HT in the anaphylactoid reaction was obtained when it was found that after an intraperitoneal injection of egg-white or dextran 5-HT, but not histamine, was present in the oedema fluid associated with the subcutaneous tissues on the dorsal side of the foot. 

The plasma kinin precursor may pass into the inflamed regions as a result of the increased vascular permeability produced by primary mediators of the anaphylactoid reaction. Activation of kininogen might then occur through dilution in oedema fluid or by contact with damaged and foreign tissue surfaces. Moreover, the pH of inflamed interstitial fluid and exudate is slightly acid [195, 422, 450-452, 546] and kininase activity may thus be inhibited [149, 700]. Such conditions would favour the accumulation of released kinins at interstitial... 

Although the anaphylactoid reaction in normal rats is characterized by gross peripheral oedema a shock-like condition, often resulting in death from haemorrhage in the small intestines, occurs when rats pretreated with thyroxine are injected with egg-white or ovomucoid in contrast, the severity and incidence of the egg-white anaphylactoid reaction is reduced in thyroidectomized animals [401, 404, 670]. The potentiating action of the thyroid hormone may be related to actions in reducing intestinal histaminase and increasing the level of tissue histamine and 5-hydroxytryptamine [220, 481], or to an increased sensitivity of tissues and blood vessels to the release of these 2 amines [491]. 

The administration of egg-white, ovomucoid, dextran or compound 48/80 to adrenalectomized rats produces a state of severe shock characterized by marked oedema, piostration, cyanosis and often death [89, 90, 120, 122, 243, 246-248, 250, 259, 298, 306, 401, 425, 447, 559, 563, 640]. The reason for this potentiated anaphylactoid response is unknown however, histaminase activity is reduced after adrenalectomy [342] which results in an elevation of tissue histamine [51, 434, 527, 613]. Moreover, adrenalectomy increases the sensitivity of rats to histamine [296, 354, 432, 650, 695] and to 5-hydroxytryptamine [103, 202, 286], 2 amines released during the anaphylactoid reaction. 

The egg-white and dextran reactions are inhibited in rats pretreated with alloxan [151, 702] but insulin restores the normal anaphylactoid response [5, 217, 218]. Tolbutamide is inactive in this latter respect, but this hypogly-caemic drug aggravates the reaction in normal rats [8, 305] possibly by releasing endogenous insulin. Insulin itself increases the rate of onset and the intensity of the oedema and also lowers the activity-threshold for egg-white and dextran in normal animals [9-11, 213, 217, 218, 514, 539, 540], but these potentiated... 

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