enerbol and Inflammation

The successive pathophysiological mechanisms that develop in the interstitium of tissues when these undergo acute post-traumatic inflammation are considered increasingly complex trophic functional systems for using oxygen. The nervous or immediate functional system presents ischemia-revascularization and edema, which favor nutrition by diffusion through injured tissue. In this phase of the inflammatory response, while the progression of the interstitial edema produces progressive distancing of the epithelial cells from the capillaries, it simultaneously enhances lymphatic circulation, which assumes an unusually important role. During immune system function, tissue nutrition is carried out by leukocytes through symbiosis with bacteria. Improper use of oxygen persists in this immune phase. Activated phagocytes would require anaerobic glycolysis as the main source of ATP for their functions. During this immune phase, lymphatic circulation still plays a major role. The dilatation of lymphatics may be mediated by cytokines, leuokotrienes, and prostaglandins produced at the trauma site by activated resident and infiltrating cells. Finally, the endocrine functional system facilitates the arrival of oxygen, transported by red blood cells and capillaries. Their trophic potential permits the tissue specialization required for tissue repair to take place. However, if complications occur during the evolution of acute inflammation, the tissues could go back to using more primitive trophic mechanisms. In summary, the ability of the interstitial tissue to express increasingly complex nutritional systems in relation to oxygen use could reflect the importance of this space as a battleground for inflammation and, as a result, for evolution.

Topics: Animals; Endocrine Glands; Humans; Immune System; Inflammation; Life; Models, Immunological; Nervous System Physiological Phenomena

With increased life expectancy worldwide, there is an urgent need for improving preventive measures that delay the development of age-related degenerative diseases. Here, we report evidence from mouse and human studies that this goal can be achieved by maintaining optimal hydration throughout life. We demonstrate that restricting the amount of drinking water shortens mouse lifespan with no major warning signs up to 14 months of life, followed by sharp deterioration. Mechanistically, water restriction yields stable metabolism remodeling toward metabolic water production with greater food intake and energy expenditure, an elevation of markers of inflammation and coagulation, accelerated decline of neuromuscular coordination, renal glomerular injury, and the development of cardiac fibrosis. In humans, analysis of data from the Atherosclerosis Risk in Communities (ARIC) study revealed that hydration level, assessed at middle age by serum sodium concentration, is associated with markers of coagulation and inflammation and predicts the development of many age-related degenerative diseases 24 years later. The analysis estimates that improving hydration throughout life may greatly decrease the prevalence of degenerative diseases, with the most profound effect on dementia, heart failure (HF), and chronic lung disease (CLD), translating to the development of these diseases in 3 million fewer people in the United States alone.

Topics: Acute Kidney Injury; Aging; Animals; Atherosclerosis; Biomarkers; Chronic Disease; Dehydration; Dementia; Fibrosis; Heart Failure; Humans; Inflammation; Life; Lung Diseases; Male; Mice; Neurodegenerative Diseases; Organism Hydration Status; Regression Analysis; Risk Factors; Sodium; Water-Electrolyte Balance

Topics: Humans; Inflammation; Life; Neoplasms