Methylene Blue in the Treatment of Anaphylaxis

Since the mid-1970s of the last century, the presence of H1 and H2 receptors in the pulmonary and systemic circulation has been described, illustrating the importance of histamine in anaphylactic shock (ASh) mediation, since when released and transported by the bloodstream, it can produce an effect on the entire cardiovascular system, in addition to other tissues where histaminergic receptors can also be found. One of the hypotheses that could explain the important vasodilatory effect of histamine in ASh is that histamine binds to H1 receptors in the vascular endothelium, activating the nitric oxide (NO) production, one of the relaxing factors derived from the endothelium, which diffuses to vascular smooth muscle and activates the guanosine 3′5′-cyclic monophosphate (cGMP) production, resulting in vasodilation. Histamine can also bind to H2 receptors present in vascular smooth muscle, activating the adenosine 3′5′-cyclic monophosphate (cAMP) production pathway that also results in vasodilation. Thus, the vasodilation resulting from the activation of the cGMP and cAMP pathways synergistically contribute to the development and maintenance of the characteristic ASh hypotension. Therefore, treatment of Ash with MB is an option as rescue therapy.