pressure. This increase in osmotic pressure leads to cellular injury. In the nerves, sorbitol affects ion pumps, causes injury to Schwaan cells and interferes with nerve conduction. Red blood cells are stiffened and then become more difficult to circulate throughout the body at the microvascular level. Aldose reductase inhibitors such as epalrestat and ranirestat may help delay the onset of complications that are linked to the polyol pathway.5(p758) Protein Kinase C (PKC) is an enzyme that is activated by increased glucose levels inappropriately. Outcomes of this activation have lead to increased thickening of vascular structures, increased production of extracellular cytokines, increased permeability and increased contractility. observations may contribute to both the micro and macrovascular complications of diabetes.5(p758-759) Nonenzymiatic glycoslyation is the non-covalent binding of gluose to proteins, lipids, and nucleic acids without the assistance of enzymes. In a chronic hyperglycemic state, glucose binds to collagen, vasculature, interstitial tissues and red blood cells thus becoming more permanent. The product of this process is known as advanced glycoslyation end product (AGE) and it’s receptor (RAGE). Both AGE and RAGE have several characteristics that cause tissue injury. These products can lead to the trapping and cross-linking of proteins such as albumin, low density lipoprotein, immunoglobulin and complement. This results in an increased thickening and permeability in blood vessels and nerves. They can also bind to cellular receptors that then release growth factors and cytokines. Increases in growth factors and cytokines result in cell proliferation in glomueruli, smooth muscle of blood vessels and exhibits a fibrous effect on collagen production. Additionally, AGE and RAGE can inactivate nitric oxide and hence a loss of vasodilatation and decreased endothelium function. AGE and RAGE have been linked to the induction of inflammation and destructive oxidative stress. The final detrimental component of
pressure. This increase in osmotic pressure leads to cellular injury. In the nerves, sorbitol affects ion pumps, causes injury to Schwaan cells and interferes with nerve conduction. Red blood cells are stiffened and then become more difficult to circulate throughout the body at the microvascular level. Aldose reductase inhibitors such as epalrestat and ranirestat may help delay the onset of complications that are linked to the polyol pathway.5(p758) Protein Kinase C (PKC) is an enzyme that is activated by increased glucose levels inappropriately. Outcomes of this activation have lead to increased thickening of vascular structures, increased production of extracellular cytokines, increased permeability and increased contractility. observations may contribute to both the micro and macrovascular complications of diabetes.5(p758-759) Nonenzymiatic glycoslyation is the non-covalent binding of gluose to proteins, lipids, and nucleic acids without the assistance of enzymes. In a chronic hyperglycemic state, glucose binds to collagen, vasculature, interstitial tissues and red blood cells thus becoming more permanent. The product of this process is known as advanced glycoslyation end product (AGE) and it’s receptor (RAGE). Both AGE and RAGE have several characteristics that cause tissue injury. These products can lead to the trapping and cross-linking of proteins such as albumin, low density lipoprotein, immunoglobulin and complement. This results in an increased thickening and permeability in blood vessels and nerves. They can also bind to cellular receptors that then release growth factors and cytokines. Increases in growth factors and cytokines result in cell proliferation in glomueruli, smooth muscle of blood vessels and exhibits a fibrous effect on collagen production. Additionally, AGE and RAGE can inactivate nitric oxide and hence a loss of vasodilatation and decreased endothelium function. AGE and RAGE have been linked to the induction of inflammation and destructive oxidative stress. The final detrimental component of
Continuous-Subcutaneous-Insulin-Infusion-Pumps-in-the-Perioperative-Period.docx