Anaphylactic shock in the albino rat

Sanyal, R. K.; West, G. B.

doi:10.1113/jphysiol.1958.sp006037

Cited by 93 publications

(78 citation statements)

References 13 publications

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“…Anaphylactic shock in rats injected with the vaccine at the time of sensitization was so severe that all 8 animals died within 2 hr with typical haemorrhagic lesions in the intestines (Sanyal & West, 1958a). This result contrasts markedly with that of mild shock found in 8 rats when there was no vaccine present.…”

Section: Resultscontrasting

confidence: 53%

The Relationship of the Blood Sugar Level to the Severity of Anaphylactic Shock

Sanyal

West

1967

British Journal of Pharmacology and Chemotherapy

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Section: Resultscontrasting

confidence: 53%

The Relationship of the Blood Sugar Level to the Severity of Anaphylactic Shock

Sanyal

West

1967

British Journal of Pharmacology and Chemotherapy

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“…Mediators released were dependent on the immunoglobulins involved. As our experiments with eviscerated animals showed, mediators released from the intestine, considered to be the primary 'shock' organ of anaphylaxis in the rat (Sanyal & West, 1958;West, 1959), did not contribute to anaphylactic bronchoconstriction. The mediators which produce bronchoconstriction in vivo are probably released from the lungs themselves.…”

Section: Discussionmentioning

confidence: 91%

Mediators of Passive Lung Anaphylaxis in the Rat

Farmer¹,

Richards²,

Sheard³

et al. 1975

British J Pharmacology

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1 Passive lung anaphylaxis (PLA) was investigated in rats sensitized by the intravenous injection of high titre reaginic antiserum prepared in rats. 2 The effect of various pharmacological antagonists on anaphylactic bronchoconstriction in vivo were examined. An antihistamine (mepyramine), a kallikrein inactivator (aprotinin) or a prostaglandin synthesis inhibitor (aspirin) did not inhibit PLA, whereas an anti-5-hydroxytryptamine agent (methysergide) and an anti-slow reacting substance-A agent (FPL, 55712) significantly reduced the response. 3 Isolated perfused lungs taken from sensitized rats released, on challenge with the sensitizing antigen, histamine, 5-hydroxytryptamine, slow reacting substance of anaphylaxis (SRS-A) and prostaglandins, but no rabbit aorta contracting substance (RCS). 4 Disodium cromoglycate inhibited both anaphylactic bronchoconstriction in vivo and the anaphylactic release of mediators in vitro. Inhibition in vivo was dose-related. 5 Mediators from the intestine, the primary shock organ of anaphylaxis in the rat, did not contribute to the lung response. 6 Vagal reflex pathways were found not to be important in PLA in vivo. 7 The relationship between the mediators released following antigen challenge of passively sensitized rat lung in vitro and passive lung anaphylaxis in vivo is discussed.

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“…Whereas kininogen levels in the liver are reduced, those in the intestinal wall are increased. The target organ in rat anaphylaxis is the small intestine (Sanyal & West, 1958) where haemorrhagic lesions and sloughing of the mucosal wall are particularly prominent. These results support the hypothesis that there are two phases in anaphylaxis in the rat-an early phase in which a kinin is a mediator and a late phase which involves other mediators.…”

Section: Discussionmentioning

confidence: 99%

“…Histamine does not appear to play a major role in this type of shock as the specific antihistamine drug, mepyramine, fails to protect the animal. 5-Hydroxytryptamine also may not be involved, although its toxicity like those of bradykinin and histamine is greatly increased during the period of maximal sensitization (Sanyal & West, 1958).We have now examined the effects of another group of antagonists on the severity of anaphylactic shock in the rat, and then studied changes in the kinin and kininogen levels in certain body fluids and tissues during anaphylaxis. …”

mentioning

confidence: 99%

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Further evidence for the involvement of kinin in anaphylactic shock in the rat

Starr

West

1969

British J Pharmacology

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1. Sodium phenylbutazone, soya bean trypsin inhibitor, or the concomitant administration of ascorbic acid and mepyramine protected rats against anaphylactic shock at 10 days after sensitization but gave no protection against anaphylaxis at 20 days. 2. During anaphylactic shock in rats at 10 days after sensitization, the plasma bradykinin and bradykininogen levels, as well as those in the intestinal lumen and peritoneal cavity, were markedly raised. 3. The results support the hypothesis that there are two phases in anaphylaxis in the rat-an early phase in which bradykinin is a mediator and against which phenylbutazone or soya bean trypsin inhibitor or the mixture of ascorbic acid and mepyramine, give protection, and a late phase which does not involve bradykinin.During anaphylaxis in the rat bradykinin is formed and released in large quantities (Dawson, Starr & West, 1966). Histamine does not appear to play a major role in this type of shock as the specific antihistamine drug, mepyramine, fails to protect the animal. 5-Hydroxytryptamine also may not be involved, although its toxicity like those of bradykinin and histamine is greatly increased during the period of maximal sensitization (Sanyal & West, 1958).We have now examined the effects of another group of antagonists on the severity of anaphylactic shock in the rat, and then studied changes in the kinin and kininogen levels in certain body fluids and tissues during anaphylaxis. MethodsGroups of ten or more male or female Wistar albino rats weighing 120-150 g were obtained from Fison's Ltd (Holmes Chapel). They were allowed free access to food and water.

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Anaphylactic shock in the albino rat

Cited by 93 publications

References 13 publications

The Relationship of the Blood Sugar Level to the Severity of Anaphylactic Shock

The Relationship of the Blood Sugar Level to the Severity of Anaphylactic Shock

Mediators of Passive Lung Anaphylaxis in the Rat

Further evidence for the involvement of kinin in anaphylactic shock in the rat

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