Systemic anaphylaxis is a shock-like and often fatal state whose onset occurs within minutes of a type I hypersensitive reaction. This was the response observed by Portier and Richet in dogs after antigenic challenge. Systemic anaphy-laxis can be induced in a variety of experimental animals and is seen occasionally in humans. Each species exhibits characteristic symptoms, which reflect differences in the distribution of mast cells and in the biologically active contents of their granules. The animal model of choice for studying systemic anaphylaxis has been the guinea pig. Anaphylaxis can be induced in guinea pigs with ease, and its symptoms closely parallel those observed in humans.
Active sensitization in guinea pigs is induced by a single injection of a foreign protein such as egg albumin. After an incubation period of about 2 weeks, the animal is usually challenged with an intravenous injection of the same protein. Within 1 min, the animal becomes restless, its respiration becomes labored, and its blood pressure drops. As the smooth muscles of the gastrointestinal tract and bladder contract, the guinea pig defecates and urinates. Finally bronchiole constriction results in death by asphyxiation within 2-4 min of the injection. These events all stem from the systemic vasodilation and smooth-muscle contraction brought on by mediators released in the course of the reaction. Postmortem examination reveals that massive edema, shock, and bronchiole constriction are the major causes of death.
Systemic anaphylaxis in humans is characterized by a similar sequence of events. A wide range of antigens have been shown to trigger this reaction in susceptible humans, including the venom from bee, wasp, hornet, and ant stings; drugs, such as penicillin, insulin, and antitoxins; and seafood and nuts. If not treated quickly, these reactions can be fatal. Epi-nephrine is the drug of choice for systemic anaphylactic reactions. Epinephrine counteracts the effects of mediators such as histamine and the leukotrienes by relaxing the smooth muscles and reducing vascular permeability. Epinephrine also improves cardiac output, which is necessary to prevent vascular collapse during an anaphylactic reaction. In addition, epinephrine increases cAMP levels in the mast cell, thereby blocking further degranulation.
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