PubMed · 6821314
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S Forconi, M Guerrini, D Pieragalli, A Acciavatti. 1981. [Hematic viscosimetry. Methodologic approach].. https://pubmed.ncbi.nlm.nih.gov/6821314/
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An increasing body of experimental data supports the important, etiologic role of advanced glycosylation end products (AGEs) in the development of the renal and vascular complications of diabetes. Advanced glycosylation end products arise from glucose-derived Amadori products and act to increase vascular permeability, enhance protein and lipoprotein deposition, inactivate nitric oxide, and promote matrix protein synthesis and glomerular sclerosis. Loss of normal renal function increases the level of circulating plasma AGEs and contributes markedly to their ultimate tissue toxicity. Aminoguanidine, a recently developed pharmacologic inhibitor of advanced glycosylation, is presently undergoing phase II/III clinical trials in diabetic nephropathy and may offer a specific therapeutic modality for diminishing the formation and toxicity of AGEs.
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The primary function of the circulatory system is to transport oxygen, nutrients, and waste products. Hemodynamics of the vessels are governed by a variety of physical properties and laws that explain blood flow through the vascular system. Blood flow is affected by pressure differences, radius of the vessel, length, and viscosity (Poiseuille's Law). Flow is directly proportional to the difference in pressure and inversely proportional to resistance. Any disturbance in blood flow in the arterial and venous system disrupts the delivery of oxygen and nutrients and the elimination of waste products. Disturbances of blood flow can be due to compression of the blood vessel (edema, hematoma, compartment syndrome), structural changes within the vessel (atherosclerosis), vasospasm (Raynaud's syndrome), vasodilatation (sepsis, distributive problems), or blood clot (thrombus or embolus). Decrease in perfusion will promote compensatory mechanisms such as vasodilatation, development of collateral vessels, and anaerobic metabolism. If compensatory mechanisms are unable to meet the oxygen demand by the tissues, ischemia develops, and eventually, tissue death occurs.