In the pathophysiology of many different diseases, proinflammatory disease processes repeatedly seem to represent a basic principle. Proinflammation, as any biologic process, has the capacity of exerting negative effects, since its components are toxic and autotoxic. Since proinflammation is a common phenomenon and is, capable of executing negative ‘side effects’, it is understandable and plausible why it seems to be involved in many different disease states. The different clinical manifestations of proinflammation (different diseases) may actually represent a common and consistent pathophysiological entity that is not separable by its molecular implications. Simultaneously, preconditioning protection counter-intuitively may rely on the same molecular process involving nitric oxide as a chemical messenger.

Keywords: Morphine - pharmacology, Nitric Oxide - metabolism, Models, Biological, Mitochondria - metabolism, Inflammation, Immune System - physiology, Humans, Dopamine - metabolism, Catecholamines - metabolism, Animals, Nitric Oxide Synthase Type II - metabolism, Signal Transduction