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PubMed1979

The effects of H1 and H2 receptor antagonism on the response of monkey skin to intradermal histamine, reverse-type anaphylaxis, and passive cutaneous anaphylaxis.

The effects of H1 and H2 receptor anatagonists on models of allergic reactions in monkey skin have been studied. Intradermal histamine is markedly inhibited by H1 receptor antagonists but not by H2 receptor antagonists in the doses used. However, the combination of both receptor antagonists gives greater inhibition than that seen with H1 receptor blockade alone. Reverse-type anaphylaxis is also markedly inhibited by H1 but not H2 receptor antagonists. Passive cutaneous anaphylaxis (PCA) is likewise inhibited by H1 receptor antagonism, but not by H2 receptor antagonism. The combination of the two inhibitors leads to a complete inhibition of this PCA response. The data suggest that the addition of an H2 receptor antagonist may potentiate the effect of H1 blockade alone.

Anaphylaxis↗
PubMed1978

Release of mediators of anaphylaxis: inhibition of prostaglandin synthesis and the modification of release of slow reacting substance of anaphylaxis and histamine.

1 When isolated perfused lungs from sensitized guinea-pigs were challenged with antigen, histamine, slow reacting substance of anaphylaxis (SRS-A) and prostaglandin-like substances were released into the effluent. 2 Treatment of the lungs before and during challenge with indomethacin (0.5--10 microgram/ml), sodium aspirin (1--10 microgram/ml), sodium meclofenamate (0.1--1 microgram/ml) or ketoprofen (0.5--5 microgram/ml) inhibited the release of prostaglandins while increasing the output of histamine and SRS-A between three- and five-fold. 3 Diethylcarbamazine (0.2--1 mg/ml) reduced the release of SRS-A and histamine but increased the amount of prostaglandin-like substances produced. 4 Eicosatetraynoic acid (10 microgram/ml) inhibited formation of prostaglandins but did not modify release of histamine and SRS-A. 5 The results with non-steroid anti-inflammatory drugs and diethylcarbamazine suggest that prostaglandins, or some other product of the cyclo-oxygenase system, depress the anaphylactic release of SRS-A and histamine.

5,8,11,14-Eicosatetraynoic Acid↗
PubMed1991

Current review of anaphylaxis and its relationship to asthma.

Anaphylaxis is the most dramatic of hypersensitivity reactions with a two-fold relationship with asthma, in the immediate and late phases and drugs and immunotherapy may be triggers. There are many causes of anaphylaxis, with IgE-mediated reactions, especially those to some foods very common. Drug reactions are next most common, especially to beta-lactam antibiotics, sulphonamides, Dilantin and aspirin. Exercise-induced anaphylaxis is well documented and may be exacerbated by food. Careful examination of the etiology of anaphylaxis is essential. Anaphylaxis may occur during immunotherapy and skin testing and every physician who uses these techniques must have available for immediate use appropriate remedial measures. In a study of 25 patients three distinct clinical patterns were seen, uniphasic, biphasic and protected degree of anaphylaxis. Latex is now known to be responsible for immediate anaphylaxis, as well as Type IV and is found in a variety of clinical situations, including surgery. The world-wide AIDS epidemic has caused much greater use of latex with a concomitant rise in risk of anaphylaxis.

Adrenergic beta-Antagonists↗
PubMed1991

Glafenine-associated anaphylaxis as a cause of hospital admission in The Netherlands.

In 1981 generalized anaphylaxis was registered on 166 occasions in Dutch general and academic hospitals. Clinical details of 120 of those patients revealed that in 107 anaphylaxis was either probable (n = 90) or possible (n = 17), whereas in 13 cases some other reaction than anaphylaxis had occurred. The series of confirmed cases contained 46 men and 61 women, with mean ages of 47 y and 48 y, respectively. There was a complete recovery in 102 patients and two patients died. Hypotension was present in 79 cases (74%), dyspnoea in 34 cases (32%) and a skin reaction, mainly urticaria, erythema or angioedema, was mentioned in 62 cases (58%). Most cases of anaphylaxis were drug-induced (76%), the main causes being the analgesic glafenine and contrast media. Glafenine was mentioned as the cause in 36% of all admissions for drug-induced anaphylaxis. Only 3.7% of cases had been reported to the voluntary reporting scheme of the Netherlands Centre for Monitoring of Adverse Reactions to Drugs. On the basis of reimbursement data, the risk of developing severe anaphylaxis to glafenine was estimated at 11.7-19.3-fold relative to indomethacin, and 13.4-20.2-fold relative to oral penicillins.

Adolescent↗
PubMed1992

The effect of three novel thromboxane A2 receptor antagonists (S-1452, AA-2414 and ONO-3708) on the increase in pulmonary pressure caused by Forssman anaphylaxis in guinea-pigs.

The effects were studied of three novel thromboxane A2 (TXA2) receptor antagonists (S-1452, AA-2414 and ONO-3708) on the increase in pulmonary pressure caused by Forssman anaphylaxis in guinea-pigs. Three TXA2 antagonists at doses of between 1 and 10 mg/kg administered orally 1 h before the challenge clearly inhibited the pulmonary pressure increase. At a dose of 10 mg/kg, all three antagonists inhibited the pulmonary pressure increase caused by leukotriene D4 (LTD4) and U-46619, but not that caused by histamine. The decrease in peripheral platelet counts caused by Forssman anaphylaxis was also clearly inhibited by the three TXA2 antagonists. However, the decreased peripheral leukocyte counts were unaffected by the three agents. The decrease in serum complement activity (CH50) was inhibited by S-1452 and AA-2414 at a dose of 10 mg/kg. In bronchoalveolar lavage fluid (BALF), significant increases in eosinophils and neutrophils were observed after Forssman anaphylaxis. Three TXA2 antagonists at a dose of 10 mg/kg (except for AA-2414 on eosinophils) did not affect the changes of leukocyte counts in BALF. Moreover, increases in the TXB2 and 6-keto-PGF1 alpha levels of the BALF brought about by Forssman anaphylaxis were unaffected by the three TXA2 receptor antagonists. Histamine and LTD4 were not changed in the BALF after Forssman anaphylaxis. These results indicate the efficacy of TXA2 receptor antagonists on the increase in pulmonary pressure caused by Forssman anaphylaxis in guinea-pigs by direct antagonism to released TXA2.

6-Ketoprostaglandin F1 alpha↗
PubMed1991

[The so-called "idiopathic" anaphylaxis: allergic and pseudo-allergic reactions].

The anaphylaxis that is called idiopathic (A.I.) forms less than 1% of the publications that are concerned with anaphylaxis. The clinical picture associates all the symptoms of anaphylaxis, with particular frequency of Quincke's laryngeal oedema. A vital risk is supposed. No abnormal biological factor can be found. There is an associated, variable pathology in 20% of subjects, 58% are atopic. A.I. effects women more--69%. Quincke's hereditary angioneurotic oedema, the carcinoid syndrome, and the capillary hyperpermeability syndrome, paroxysm with monoclonal gammopathy, systemic mastocytosis must be eliminated as well as false anaphylaxis. The authors review the exceptional causes that may not be considered: drug anaphylaxis, to foods, hymenoptera, effort anaphylaxis, to hydatic antigens, to toboggans, to progesterone. Pathogenic hypotheses incriminate sensitization to unknown allergens, functional anomalies of mastocytes, heterogeneity of IgE. Addition of allergic and non-allergic factors is possible. Release of mediators other than histamine is one hypothesis proposed, to account for the inefficiency of anti H1. Prevention requires avoidance of aspirin, non-steroid anti-inflammatory drugs and beta blockers. Basic treatment is always corticosteroids, with anti H1 and sympathomimetic amines where the A.I. is severe.

Adrenal Cortex Hormones↗
PubMed1991

PAF induces rat plasma extravasation and releases eicosanoids during anaphylaxis.

The effects of anaphylaxis on vascular protein extravasation in selected tissues and on the release of prostaglandins in the peritoneal cavity were studied in sensitized rats. Extravasation of Evans blue dye was used as a measure of vascular permeability. Specific antigen challenge increased by 279, 297, 328, 250, and 192% the protein extravasation in the trachea, upper and lower bronchi, pancreas, and duodenum, respectively, but did not modify significantly the vascular permeability of the lung parenchyma, heart, liver, and kidney. Extravasation of Evans blue dye also was increased by 43-fold in the peritoneal cavity. Pretreatment of the animals with indomethacin (10 mg/kg) did not modify significantly the protein extravasation of the trachea, upper and lower bronchi, pancreas, and duodenum induced by anaphylaxis. Pretreatment with a mixture of mepyramine (3 mg/kg) and methysergide (2.5 mg/kg) reduced by 62, 66, and 40% the protein extravasation in the trachea, upper bronchi, and peritoneal cavity, respectively, in similar conditions. The PAF antagonist BN-52021 (5 mg/kg) very strongly reduced the protein extravasation elicited by anaphylaxis in the trachea, upper and lower bronchi, pancreas, and duodenum by 72, 87, 82, 67, and 85%, respectively, and by 53% in the peritoneal cavity. Anaphylaxis also increased the concentrations of thromboxane B2 and leukotriene B4 in the peritoneal exudates, but prostaglandin E2 levels were not affected. Pretreatment with BN-52021 reduced by 29 and 75% the level of thromboxane B2 and leukotriene B4 in the exudates. These results suggest that PAF, histamine, and serotonin mediate the protein extravasation associated with anaphylaxis, whereas prostaglandins are likely to play a minor role in this reaction.

Anaphylaxis↗
PubMed1992

Changes in cell-mediated immune responses after experimentally-induced anaphylaxis in dogs.

Experimentally-induced type 1 hypersensitivities were induced in normal dogs to either ovalbumin or Ascaris antigen. In vitro and in vivo cell-mediated immune responses were measured before sensitization and again at 1 and 6 days after induction of anaphylaxis by intravenous challenge with antigen. Histamine-modulated lymphocyte functions, such as histamine-induced suppression, histamine co-mitogen induced blastogenesis and the in vivo cutaneous responses to intradermally injected mitogens decreased post anaphylaxis. Spontaneous suppression of the autologous mixed-lymphocyte reaction increased post anaphylaxis. Lymphocyte blastogenic response to Concanavalin A (Con A) decreased at 6 (but not at 1) days post anaphylaxis probably due to a mediator other than histamine. Blastogenesis of 24 h preincubated cells by suboptimal concentration of Con A, declined post anaphylaxis, but Con A-induced suppression was not significantly altered. Dogs with atopic dermatitis have some altered cell-mediated immune responses. Altered histamine-induced and spontaneous suppression, histamine suppression of mitogenesis and decreased contact sensitivity observed in this experimental type 1 hypersensitivity mimicked that of atopic dogs. Increased cutaneous response to mitogens observed in atopic dogs was not reproduced in the type 1 hypersensitive dogs. These findings suggest some of the altered cell-mediated immune functions observed in dogs with atopic dermatitis result from type 1 hypersensitivity. The other abnormalities may be intrinsic to the atopic state.

Anaphylaxis↗
PubMed1990

Characterization of cardiovascular events mediated by platelet activating factor during systemic anaphylaxis.

Previous studies have shown that an anaphylactic reaction in the isolated perfused heart is characterized by drastic coronary constriction, arrhythmias, and severe impairment of contractility. In vivo anaphylaxis is associated with myocardial ischemia and rapid cardiovascular failure. Recently, not only histamine but also platelet activating factor (PAF) has been implicated in cardiac manifestation of anaphylaxis. The present study was designed to separate the effects of PAF from those of histamine on cardiovascular function during systemic anaphylaxis. In guinea pigs, sensitization was produced by subcutaneous (s.c.) application of ovalbumin. Fourteen days after sensitization, the effects of an intravenous (i.v.) infusion of ovalbumin were tested in anesthetized artificially ventilated guinea pigs. The renewed application of the antigen induced severe cardiac dysfunction. Within 3 min, cardiac output (CO) had already decreased by 90% and left ventricular end-diastolic pressure (LVEDP) increased significantly, indicating left ventricular pump failure. Concurrently, ECG recordings uniformly showed signs of acute myocardial ischemia. In addition, arrhythmias occurred in terms of atrioventricular block. After 4 min, blood pressure (BP) rapidly decreased. All animals died within 10 min. Pretreatment with the H1-receptor antagonist mepyramine (1 mg/kg i.v.) in combination with the H2-receptor antagonist cimetidine (10 mg/kg i.v.) delayed onset of myocardial ischemia, arrhythmias and cardiac pump failure. After 10 min, however, LV contractility and BP steadily decreased, leading to severe hypotension within 30 min. If the selective PAF antagonist WEB 2086 (1 mg/kg i.v.) was administered in addition to cimetidine and mepyramine, myocardial ischemia and LV contractile failure were markedly inhibited further. In contrast, pretreatment with WEB 2086 alone had no beneficial effects on the anaphylactic cardiovascular changes. Therefore, we conclude that histamine is the predominant mediator during the early phase of systemic anaphylaxis whereas PAF-mediated effects are involved in cardiac dysfunction during the protracted late phase of anaphylaxis.

Anaphylaxis↗
PubMed1991

Efficacy of ketotifen in corticosteroid-dependent idiopathic anaphylaxis.

To assess the potential benefit of ketotifen in the treatment of patients with corticosteroid-dependent idiopathic anaphylaxis, ketotifen was administered in an open trial to nine patients with idiopathic anaphylaxis who required maintenance prednisone for control of their disease. A double-blind trial was not done for reasons of patient safety. After a period of management with prednisone and establishment of the minimal dose of prednisone that controlled idiopathic anaphylaxis, ketotifen was initiated and cautious reduction of prednisone was attempted. The prednisone requirement was not altered in two patients, but prednisone was either substantially reduced or terminated in seven patients. Of these seven, three patients developed recurrent symptoms of idiopathic anaphylaxis after tapering and discontinuation of ketotifen, and ketotifen had to be resumed. The statistical analysis of prednisone reduction was highly significant (P less than .004) and we conclude ketotifen was of significant benefit in seven of nine patients with corticosteroid-dependent idiopathic anaphylaxis.

Adult↗
PubMed1979

Pulmonary anaphylaxis and the kallikrein-kinin system.

The kallikrein-kinin system has been thought to participate in the pathogenesis of anaphylaxis. Kallikrein, released from lungs, has been postulated to contribute to cardiovascular collapse. Further to test the hypothesis, we examined for the occurrence of a kallikrein-like enzyme in guinea pig lungs and examined for release of such an enzyme by isolated, perfused lungs of guinea pig sensitized to and challenged with egg albumin. In addition, we treated guinea pigs with the bradykinin potentiating agents, BPP9a and SQ 14,225. In parallel experiments, we examined for effects of non-steroidal anti-inflammatory agents on the supposition that prostaglandin-related substances may mediate or modulate actions of kinins during anaphylaxis. A plasma kallikrein-like enzyme was found in lung homogenates and occurred in concentrations greater than that of plasma itself. Similarly, a store of kininogen occurs in lungs. However, using a sensitive radioassay for kallikrein-like enzymes, we were unable to confirm that antigenic challenge of sensitized lungs causes the release of enzyme into pulmonary venous effluent. Further, we were unable to modify the acute course of anaphylaxis by pretreatment of guinea pigs with bradykinin potentiating agents. However, indomethacin and aspirin at 20-40 mg/kg were found to greatly increase the severity of pulmonary anaphylaxis in terms of increased resistance to ventilation and increased numbers of lung hemorrhages. Paradoxically, aspirin or sodium salicylate at 80-100 mg/kg prevents the characteristic rise of insufflation pressure and the formation of lung hemorrhages.

Anaphylaxis↗
PubMed1992

Relationship between mast cell degranulation and jejunal myoelectric alterations in intestinal anaphylaxis in rats.

The effects of two degranulators of mast cells and intestinal anaphylaxis on jejunal myoelectric activity were compared in rats fasted for 15 hours. Attempts to antagonize the motility changes were performed using antagonists of histamine and serotonin and a cyclooxygenase and lipoxygenase inhibitor. Hooded Lister rats were chronically fitted with electrodes implanted in the jejunal wall. A group of rats was sensitized to egg albumin and challenged 14 days later by intraduodenal infusion of antigen. Sensitized animals had serum titers greater than or equal to 1:64. The other group was administered with mast cells degranulators. Both 48/80 (1 mg/kg), a degranulator of connective mast cells, and bromolasalocid (2 mg/kg), acting on connective and mucosal mast cells, induced a phase of total spiking inhibition followed by a progressive irregular spiking activity until the recovery of migrating myoelectric complex pattern (about 3 hours after injection). In contrast, antigen challenge disrupted the migrating myoelectric complex pattern, which was replaced by a peculiar pattern characterized by propagated spike burst, lasting 98 +/- 11.3 minutes. Chlorpheniramine (1 mg/kg) antagonized only the inhibitory phase induced by degranulators and was ineffective on the intestinal anaphylaxis-induced motor changes. Methysergide (1 mg/kg) and indomethacin (5 mg/kg) significantly reduced the degranulator effects as well as the anaphylaxis-induced alterations of intestinal motility. It is concluded that anaphylaxis-induced motor disturbances are relevant to mucosal mast cell degranulation involving 5-hydroxytryptamine and arachidonic acid derivative products, whereas histamine release appears to be a minor component.

Anaphylaxis↗
PubMed1975

Uptake of catecholamines in guinea pig lung: influence of cortisol and anaphylaxis.

UNLABELLED: Effects of cortisol and anaphylaxis on the uptake of catecholamines (CA) in the guinea pig lung have not been investigated previously. Sensitized and healthy animals were randomly killed, catheters were inserted into the pulmonary artery and vein, and the preparation was perfused with Tyrode. Half of the animals received 50 mg. of cortisol 2 hours before the procedure. H3-epinephrine (E) or norepinephrine (NE), 10 ng. per milliliter, was infused for 6 minutes. Infusion was started 15 seconds prior to challenge with ovalbumin or NaCl. Total -H3 and NE(E)-H3 were determined in the lung homogenates. Results showed (1) 6 to 14 per cent of circulating CA were retained by the lung. (2) In healthy animals cortisol inhibited NE uptake by 35 per cent and E uptake by 15 per cent. (3) Anaphylaxis increased NE and E accumulation by 10 and 19 per cent, respectively. (4) Regardless of experimental conditions approximately 40 per cent of NE and 30 per cent of E taken up were recovered unchanged. IN CONCLUSION: (1) There is significant uptake of CA in the lung. (2) One of the mechanisms of therapeutic effect of cortisol in asthma might be its inhibitory effect on CA uptake. (3) Increased CA accumulation during anaphylaxis could be beneficial by increasing the local concentration of amines, or detrimental by decreasing availability of CA, depending on the uptake site and cell type and degree of subsequent metabolism. (4) Cortisol and anaphylaxis per se appear not to change degradation of CA.

Anaphylaxis↗
PubMed1976

Hypersensitivity to histamine and systemic anaphylaxis in mice with pharmacologic beta adrenergic blockade: protection by nucleotides.

The effects of exogenous nucleotides on the histamine hypersensitivity of pharmacologically beta-blocked mice were investigated. Female HLA-SW (ICR) mice, 27-29 gm, were injected intraperitoneally with 20 to 100 mug of propranolol 45 min before intraperitoneal challenge with 1 mg histamine. These animals had a mortality which averaged approximately 80%. At various time intervals before histamine, doses of from 0.5 to 12 mumoles of nucleotides were administered intravenously. Noncyclic nucleotides, adenosine, adenosine 5'-monophosphate (AMP), and guanosine 5'-monophosphate (GMP) showed clear, dose-response protection against histamine death of propranolol-treated mice when they were given 45 to 90 min before histamine. Cyclic AMP showed significant protection only when it was given at a dose of 8 mumoles 45 to 90 min before histamine, and lower or higher doses gave equivocal or no protection. Cyclic GMP WAS Not protective at any dose tested. Propranolol treatment also produced enhanced sensitivity to passive systemic anaphylaxis. Mice were passively sensitized by intraperitoneal injection of mouse anti-egg albumin antibody 6 hr before intravenous challenge with 0.5 mg egg albumin. The mortality from anaphylaxis in the group treated with 20 mug propranolol 45 min before antigen challenge increased to 83%, while that of the group not given propranolol was only 10%. Nucleotides were given intravenously 45 min before antigen challenge. The nucleotides that protected mice from death due to histamine challenge also protected them from death due to systemic anaphylaxis. These protective nucleotides were the same nucleotides that had been reported previously to be protective against Bordetella pertussis-induced hypersensitivity to histamine and anaphylaxis.

Adenosine↗
PubMed1975

Mediators of passive lung anaphylaxis in the rat.

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.

Anaphylaxis↗
PubMed1992

Platelet activating factor and systemic anaphylaxis in Nippostrongylus brasiliensis-sensitized rats: differential effects of PAF antagonists.

1. The effects of two platelet-activating factor (PAF) antagonists, WEB 2086 and BN 52021, in reducing the changes in extravasation (Evans blue technique) and blood flow (radiolabelled microsphere method) to various organs and tissues following anaphylactic shock in the Nippostrongylus brasiliensis-sensitized rat were investigated. 2. Both antagonists attenuated anaphylaxis-induced increases in plasma protein leak in the trachea, stomach and small intestine, although they did not block extravasation in the colon and kidneys. 3. Anaphylaxis-induced decreases in blood flow to the adrenals were effectively antagonized by WEB 2086, although this antagonist did not reverse blood flow decreases to any other tissues. BN 52021, on the other hand, did not alter anaphylaxis-induced decreases in blood flow to the adrenals, but effectively prevented dramatic decreases in blood flow to the large and small bowel and spleen. 4. Anaphylactic shock produced marked reduction in blood pressure that was partly reversed by WEB 2086, whereas BN 52021 effectively blocked the decreases in cardiac output. 5. Thus, PAF is responsible for some of the haemodynamic and extravasation of protein changes associated with systemic anaphylaxis in the rat, although the differential inhibition observed with the two antagonists suggests that PAF alters vascular responsiveness through different mechanisms in selected tissues.

Anaphylaxis↗
PubMed1991

Antibodies to toluene diisocyanate in patients with and without dialysis anaphylaxis.

In a majority of patients with anaphylaxis to dialysis, ethylene oxide has been identified as an etiologic agent. In a significant minority of patients sustaining such reactions, the antigen remains unidentified. Conflicting results have been published with regard to isocyanates as a possible antigen. The authors studied 19 hemodialysis patients with anaphylaxis in whom IgE against ethylene oxide-human serum albumin (ETO-HSA) was not identified (Group 1) and 25 peritoneal dialysis patients without anaphylaxis (Group 2). IgE against toluene diisocyanate-human serum albumin (TDI-HSA) was found in one patient in Group 1, and a similar incidence of IgG against TDI-HSA in Group 1 (16%) and Group 2 (12%) was noted. The results do not suggest that IgE against TDI-HSA is an important cause of dialysis anaphylaxis.

Anaphylaxis↗