Cardiac Arrest and Neuroprotection by Methylene Blue

Abstract

After the onset of cardiac arrest, global ischemia activates the glia and the complement system with the release of cytokines by neurons. The pro-inflammatory cascade is initiated by the expression of adhesion molecules, polymorphonuclear leukocyte chemotaxis, and the reactive oxygen species production. As a result, there is an increase in vascular permeability, blood clotting activation, platelet activation, and vasoconstrictors release, contributing to the regional flow reduction. Cerebral edema increased blood-brain barrier (BBB) permeability and neurological damage are seen early in ischemia-induced by cardiac arrest. The positive nitric oxide synthase (NOS) regulation is associated with an increase in nitric oxide (NO) production that induces the BBB breakdown. It has been suggested that pretreatment with pharmacological agents can reduce excess NO or oxidative stress, decreasing the interruption of BBB permeability caused by ischemia/reperfusion injury. Methylene blue (MB), a nontoxic dye and scavenger cleaner, recently proved to be a potential aid in the resuscitation of cardiac arrest, attenuating oxidative, inflammatory, myocardial, and neurological lesions.