Misunderstanding of ATP involvement in inflammation and stages of inflammation

Abstract

a specific detector of large increases in [eATP], such as those that occur on cell death`. Necrotic cells are considered to expel ATP.1,5 The applied concentration exceeded the physiological amount of 1μmol / ml full blood hundred-fold. Even in one of the latest publication 2012 of the New York Academy of Sciences researchers still believe that ATP is secreted by necrotic cells.6 Even though a publication by Welsch7 as early as 1994 in detail described the ATP content in the MCA and penumbra area after occlusion and reperfusion of the middle cerebral artery7 the apprehension is still propagated. From the pathophysiological point of view the release of ATP from necrotic tissue is not acceptable. These cells have undergone necrosis in the wake of total ATP depletion. The neuronal unit consists of endothelial cells, astrocytes, and neurons. In 1999 Magistretti published that neurons mainly metabolize lactate and are widely devoid of the glycolytic pathways.8 Whereas the astrocytes engage the endothelial cells by their processes and neurons the latter do not have access to the capillary system.9 Neurons do not metabolize glucose for energy production and therefore cannot produce ATP by glycolysis. Instead they are fed with lactate by astrocytes to meet metabolic demand and are extremely vulnerable to lack of oxygen.8