Induction Of Anaphylactic Shock Research Articles

EFFECT OF POST MORTEM INTERVAL TOWARD Β-TRYPTASE AND CHYMASE EXPRESSION OF ANAPHYLACTIC HEART MAST CELLS

Background: The effects of post mortem interval on tryptase levels are unclear and have been challenging to quantify due to limited and at times contradictory research. Purpose: Analyze the effects of Post Mortem Interval (PMI) due to anaphylactic shock on the expression of β-tryptase and mast cell chymase in the heart organ. Method: This type of research was an experimental study with a randomized block design (RBD) with the same subjects and a time series for 24 hours, using 5 (five) rabbits. The measurement of β-tryptase and chymase expression was based on immunohistochemical IRS (immunoreactive score) in the heart organs of rabbits experiencing anaphylactic shock sensitization and induction of anaphylactic shock using ovalbumin. Result: Based on the results of statistical tests using univariate analysis, there was a relationship between the length of death (post mortem interval) and the expression of mast cells β-Tryptase and cardiac chymase (p-value = 0.006) and chymase (p-value = 0.002) with (p-value <0.05). The effective test time with β-tryptase markers using cardiac organs was prone to long death time of 0 - 15 hours. The effective check-up time with chymase markers using the heart organ was at a long time of death of 9 hours. Conclusion: The results of the study showed that tryptase and chymase could be used as markers of anaphylactic shock.

Chitosan-coated PLGA nanoparticles for transcutaneous immunization: Skin distribution in lysozyme-sensitized mice

The effect of transcutaneous immunization was studied using a combined system of poly(DL-lactide-co-glycolide) (PLGA) nanoparticles and iontophoresis (IP). Both hen egg-white lysozyme (HEL)-loaded PLGA nanoparticles coated with chitosan hydroxypropyltrimonium chloride and their fluorescent nanoparticles were prepared using an antisolvent diffusion method. Their mean volume diameters were 87.6 ± 38.9 nm and 84.9 ± 27.6 nm, respectively. It was suggested from the results of the ex vivo skin accumulation study using fluorescent nanoparticles that the HEL released from the nanoparticles to the skin surface was efficiently delivered to antigen-presenting cells. HEL-specific IgG1 and IgG2a titers were determined in an in vivo percutaneous immunoreactivity study using lysozyme-sensitized mice. As results, the group using nanoparticles and IP showed 1.33 times higher HEL-specific IgG1 titer than a sham treatment group. The HEL-specific IgG2a titer was 1.36 times higher in the nanoparticles and IP group than in the HEL solution and IP group. It was suggested from the quantification results of total IgE in serum that the combined use of PLGA nanoparticles and IP reduced the total IgE concentration. The level of cytokines may have decreased due to Th1 cell activation and relative suppression of Th2 cells. The cytokine level is presumed to be reduced by activation of Th1 cells and relative suppression of Th2 cells. The histamine amount in plasma and rectal temperature after the induction of anaphylactic shock using lysozyme-sensitized mice were also studied, which indicates that the combined use of PLGA nanoparticles and IP may provide the same therapeutic effect as an injection.

4-Aminopyridine, A Blocker of Voltage-Dependent K+ Channels, Restores Blood Pressure and Improves Survival in the Wistar Rat Model of Anaphylactic Shock.

Anaphylactic shock is associated with severe hypotension. Potassium channel blockers, such as 4-aminopyridine, induce vasoconstriction. The objective of this study was to test the ability of 4-aminopyridine to restore blood pressure and increase survival in anaphylactic shock. Experimental study. Physiology laboratory. Adult male Wistar rats. Rats were sensitized with ovalbumin (1 mg SC), and anaphylactic shock was induced by IV injection of ovalbumin (1 mg). Experimental groups included non-allergic rats (NA) (n = 6); allergic rats (Controls) (n = 6); allergic rats treated with 4-aminopyridine (4-aminopyridine) (1 mg/kg) (n = 6); and allergic rats treated with epinephrine (EPI) (10 µg/kg) (n = 6). Treatments were administered 1 minute after induction of anaphylactic shock. Mean arterial blood pressure, heart rate, and survival were measured for 60 minutes. Plasma levels of histamine, leukotriene B4, prostaglandin E2, prostaglandin F2, pH, and HCO3 were measured. Mean arterial blood pressure was normal in the NA group; severe hypotension and high mortality were observed in controls; normalization of mean arterial blood pressure, heart rate, and increased survival were observed in 4-aminopyridine and EPI groups. All allergic 4-aminopyridine-treated rats survived after the induction of anaphylactic shock. Histamine level was higher in controls and the 4-aminopyridine group but reduced in the EPI group. Prostaglandin E2 increased in controls and EPI group and decreased in 4-aminopyridine group; prostaglandin F2 increased in controls but decreased in 4-aminopyridine and EPI groups. Leukotriene B4 decreased in 4-aminopyridine and EPI groups. Metabolic acidosis was prevented in the 4-aminopyridine group. Our data suggest that voltage-dependent K+ channel inhibition with 4-aminopyridine treatment restores blood pressure and increases survival in the Wistar rat model of anaphylactic shock. 4-aminopyridine or related voltage-dependent K channel blockers could be a useful additional therapeutic approach to treatment of refractory anaphylactic shock.

Methylene Blue and Epinephrine

Severe hypotension resulting from anaphylactic shock may be refractory to epinephrine and impair cerebral oxygenation and metabolism contributing to anaphylactic shock morbidity and mortality. Refractoriness to epinephrine could be corrected by nitric oxide pathway inhibitors such as methylene blue. To compare the systemic and regional (brain and skeletal muscle) effects of epinephrine and methylene blue given alone or in combination in a rat model of anaphylactic shock. Prospective laboratory study. University laboratory. Male Brown-Norway rats (n = 60). After sensitization and induction of anaphylactic shock by ovalbumin, animals received either vehicle (ovalbumin group) or a 3-mg/kg methylene blue bolus (methylene blue group) or epinephrine (epinephrine group) or both (methylene blue-epinephrine group). Sensitized control rats received only vehicle and no ovalbumin (control group). Mean arterial pressure, cardiac output, cerebral blood flow, skeletal muscular oxygen partial pressure, cerebral oxygen partial pressure, skeletal muscular, and cerebral interstitial lactate/pyruvate ratio were measured. Cleaved caspase 3 and hypoxia-inducible factor-1α expression were analyzed in the cerebral cortex by Western blot. Without treatment, rats died rapidly within 15 mins from a decrease in cardiac output and mean arterial pressure, whereas treated rats survived until the end of the experiment. Methylene blue alone extended survival time but without significant improvement of hemodynamic variables and tissue perfusion and did not prevent neuronal injury. Epinephrine restored partially systemic hemodynamic variables and cerebral perfusion preventing glutamate-induced excitotoxicity. Compared with epinephrine alone, the methylene blue-epinephrine association avoided neuronal excitotoxicity and had an additive effect both on hemodynamic variables and for prevention of brain ischemia. Neither treatment could significantly restore cardiac output or prevent muscular compartment ischemia and microvascular leakage. Anaphylactic shock is associated with severe impairment of cerebral blood flow despite correction of arterial hypotension. Epinephrine must still be considered as the first-line vasoconstrictive agent to treat anaphylactic shock. The epinephrine-methylene blue association was the most effective treatment to prevent cerebral ischemia and could be used in anaphylactic shock refractory to epinephrine.

Effects of Plant Water-Soluble Polysaccharides on the Production of Immunoglobulins E and G1 by Lymphocytes of Mice Sensitized with Ovalbumin

Were studied the effects of water-soluble plant polysaccharides isolated from pharmacopoeic raw material on anaphylactic shock and production of IgE and IgG1 by lymphocytes from mice immunized with ovalbumin. Course treatment with polysaccharides from coltsfoot, sweet flag, clover, Artemisia, marigold, and elecampane reduced animal mortality after induction of anaphylactic shock. In addition, injection of these substances reduced serum concentrations of IgE and IgG1. These substances can be regarded as promising agents for the treatment of IgE-dependent diseases (atopic dermatitis, asthma, atopic rhinitis, urticaria, food allergies, etc.).

Anaphylactic shock in neuropsychoimmunological research.

Anaphylaxis appears to be an excellent experimental model for investigating the interactions between central nervous system (CNS) and immune system. Both afferent and efferent regulatory pathways of anaphylactic response are well characterized. The potent mediators of anaphylactic shock, such as histamine and serotonin, are at the same time neurotransmitters, acting in the CNS, and regulators/modulators of the immune system, since receptors for these substances exist on the membrane of the cells of the immune system. In this article the results of studies on the relationship between anaphylaxis and CNS, performed by both pioneers and contemporary investigators, are briefly reviewed. Recent experiments done in our laboratory are presented, which showed that (a) anaphylactic shock can be induced by intracerebroventricular administration of the shocking dose of antigen; (b) rats can learn to associate the induction of anaphylactic shock with neutral stimuli from the environment; and (c) stress in the form of electric tail-shocks reduces the intensity of anaphylactic shock.

An inhibitor of nitric oxide production, N Gnitro-L-arginine-methyl ester, improves survival in anaphylactic shock

Induction of anaphylactic shock in mice by i.v. antigen challenge (bovine serum albumin, 100 mg) or i.v. treatment with the mast cell degranulator compound 48/80 resulted in 80 and 90% mortality rate, respectively. Inhibition of nitric oxide (NO) synthesis from L-arginine by co-injection of the L-arginine analog N Gnitro-L-arginine methyl ester (L-NAME, 30 mg/kg) reduced the mortality rate by 40 and 20% in the antigen- and compound 48/80-induced shock models. Treatment with 60 mg/kg L-NAME reduced the mortality rate by 60% in these shock models. This beneficial effect was reversed by addition of L-arginine (120 mg/kg) but not D-arginine (120 mg/kg). These results suggest NO production as a possible mechanism involved in the pathophysiology of anaphylactic shock.

Anaphylactic shock-induced conditioned taste aversion: II. Correlation between taste aversion and indicators of anaphylactic shock

Previous studies (V. J. Djurić, B. M. Marković, M. Lazarević, & B. D. Janković, 1987, in B. D. Janković, B. M. Marković, & N. H. Spector (Eds.), Neuroimmune interactions, pp. 561–568, New York: New York Acad. Sci.; B. M. Marković, V. J. Djurić, M. Lazarević, & B. D. Janković, 1988, Brain Behav. Immun. 2, 11–23) have shown that rats learn to associate the taste of saccharin with the induction of anaphylactic shock, thus exhibiting conditioned taste aversion (CTA) toward an otherwise preferred saccharin solution. The present experiment investigates the effect of unconditioned stimulus intensity (the amount of antigen used for the induction of shock) on CTA. Rats were sensitized to ovalbumin and subjected to a conditioning trial in which the conditioned stimulus (CS; saccharin solution given orally) signaled the presentation of the unconditioned stimulus (US; shocking doses of ovalbumin ranging from 0.5 to 3 mg given intraperitoneally). Behavioral signs, hematocrit, and rectal temperature were used for evaluation of anaphylactic shock. Twenty-four hours after the conditioning trial, rats were subjected to a two-bottle preference test between saccharin solution and water. Multiple regression statistical analysis revealed significant correlations among saccharin preference ratio, dose of antigen used for the induction of shock, behavioral signs of shock, rise in hematocrit, and fall in rectal temperature. A dose-dependent relation among saccharin preference ratio and physiological indicators of shock suggests that conditioned anaphylactic shock-induced avoidance behavior is functionally related to homeostatic factors involved in immune reactivity.

STUDIES ON EXPERIMENTAL THERAPY OF ANAPHYLACTIC SHOCK IN DOGS.

Abstract1. Treatment with blood transfusion or arterenol perfusion set up 3-6 min. after induction of anaphylactic shock in dogs, protected animals from dying in acute phase, but did not decrease total mortality rate, since a significant number of the treated animals died in the following hours.2. Arterenol perfusion applied in the same way in animals treated with phenergan before challenge, as well as perfusion with arterenol, adrenaline, and phenergan in animals not previously treated with the antihistaminic, prevented animals from dying in acute phase and increased significantly the number of survivors.3. Treatment with adrenaline and phenergan by intramuscular route, as well as perfusion with hypertensin, only or in association with phenergan, did not not, always prevent animals form dying in acute phase and did not significantly increase the number of survivors.4. Death in anaphylactic shock in dogs does not represent a direct, effect, to the biochemical lesions induced in cells by the antigen-antibo...

Allergic reactions to hyaluronidase.

Summary and ConclusionsIt has been demonstrated by hemagglutination inhibition tests as well as by induction of anaphylactic shock that a commercial hyaluronidase preparation contained a small but ...

Serum histaminase during rabbit anaphylaxis.

1. Studies on the blood histamine and the serum histaminase were made in a series of 19 rabbits before and after the induction of anaphylactic shock. 2. In all but one, a reduction of the blood histamine was produced following anaphylaxis. This confirms previous observations. 3. An increase in the serum histaminase activity was noted in all animals except the one in which there was no reduction of the blood histamine. 4. These findings support the view that the rapid disappearance of blood histamine which occurs during anaphylaxis in this species may be due in part to an activation of histaminase.

Observations on Induction of Anaphylactic Shock by the Specific Carbohydrates of Type-I Pneumococcus

Further comparative studies of the soluble specific substance of Avery and Heidelberger and of the specific “cellular carbohydrate”1 by means of the experimental induction of anaphylactic shock have given additional information regarding the antigenic activities of these preparations. Avery and Tillett2 induced fatal anaphylactic shock in passively sensitized guinea pigs with the homologous soluble specific substance of the pneumococcus, and Enders3 reported that antiserum, after precipitation with soluble specific substance, still sensitized guinea pigs to his “A” substance but not to the soluble specific substance. This report records experiments with the type-I specific substances injected intracardially into guinea pigs which had been passively sensitized with type-I antipneumococcus rabbit serum 24 or 48 hours previously.The minimum amount of immune serum necessary to sensitize guinea pigs so that fatal shock developed when they were injected intracardially with soluble specific substance was always ...