Cerebral protection in experimental cardiopulmonary resuscitation (with special reference to the effects of methylene blue)

作者：Adriana Miclescu · 发表于：Acta Anaesthesiologica Scandinavica · 年份：2009 · DOI：10.1111/j.1399-6576.2009.02182.x · 被引用次数：1 · 研究领域：Cardiac Arrest and Resuscitation、Anesthesia and Neurotoxicity Research、Cardiac Ischemia and Reperfusion

Although survival rates are increasing, brain injury continues to be a leading cause of death after cardiac arrest (CA).Permanent brain damage after CA is determined by limited tolerance to ischemia from CA and cardiopulmonary resuscitation (CPR), as well as the unique cerebral response to reperfusion after return of spontaneous circulation (ROSC).A major pathway leading to neurotoxic cascade and neuronal injury after CA involves the increased presence of reactive oxygen and nitrogen species generated during ischemia and reperfusion.The magnitude of cerebral oxidative injury induced by free radicals increased with the duration of CA (Paper I).Nitric oxide (NO), a free radical responsible for the formation of reactive nitrogen species, is increased during global ischemia from CA and reperfusion (Paper IV).Hypothetically, the administration of a drug that counteracts the overproduction of NO and also acts as a scavenger of oxygen free radicals might be warranted in order to reduce the damage caused by nitrosative and oxidative stress.For these purposes we used methylene blue (MB), an old dye that has been used in medicine for almost half a century, and an experimental pig model of 20 min of ventricular fibrillation (VF) to reflect a clinical scenario of ischemia/reperfusion injury.Administration of MB added to a hypertonic-hyperoncotic solution (MBHSD) that was started during CPR and continued for 50 min after ROSC increased short-term survival by decreasing myocardial damage, ...