23 Preventive Phytotherapy of Anaphylaxis and Allergic Reactions Elaine A. Cruz 1 , Michelle F. Muzitano 1 , Sonia S. Costa 2 and Bartira Rossi-Bergmann 3 1 Faculdade de Farmacia, Macae Campus, 2 Nucleo de Pesquisa de Produtos Naturais, 3 Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Brazil 1. Introduction Anaphylactic shock is an extreme and life-threatening allergic reaction that requires immediate action to prevent death from airway and blood pressure collapse. The acute management comprises the use of epinephrine (adrenaline), the first-line medication of choice, and H1-antihistaminic drugs in doses that will depend on the severity of symptoms, in order to preserve the airway function and maintain the blood pressure and oxygenation at acceptable levels (Kemp & Lockey, 2002). On the other hand, long-term management comprises identification of precipitants (e.g.: Medications, foods, latex, insect venom) and their avoidance, and also immunotherapy. One of the main mediators that are released and associated the many anaphylactic symptoms is histamine. H1-antihistamines are commonly used to relieve anaphylactic cutaneous symptoms such as itching, flushing, and urticaria, but play little role in the relief of bronchospasm or gastrointestinal symptoms, and fail to relieve upper airway edema or hypotension. Moreover, in usual doses, antihistamines alone do not prevent the explosive release of histamine and other mediators of inflammation from mast cells and basophils that culminate in the anaphylactic shock. Since bronchospasm, hypotension and edema are not reversed immediately with antihistamines, a rapid administration of epinephrine is required to revert these symptoms. It has potent life-saving β-1 adrenergic vasoconstrictor effects on the small arterioles and precapillary sphincters leading to decreased mucosal edema, thereby preventing and relieving upper airway obstruction, and also to increased blood pressure, thereby preventing and relieving shock. (Kemp et al, 2008). Its strong effect on β-1 adrenergic receptors activation lead to increased rate and force of cardiac contractions, while activation of β-2 adrenergic receptors leads to increased bronchodilation and decreased release of histamine, tryptase, and other mediators of inflammation from mast cells and basophils (T.C. Westfall & D.P. Westfall, 2006). The adverse effects of epinephrine therapy involve pallor, headache (β -1 adrenergic receptors), palpitations (β-1 adrenergic receptors), tremor, vasodilation, increased release of mediators (β-2 adrenergic receptors) and anxiety (central CNS stimulation) that altogether