Abstract
Background. Spontaneous collateral growth (arteriogenesis) restores original blood flow only partially because of quick normalization of an initially elevated fluid shear stress. Micro array data from collateral growth in a porcine model with artificially elevated blood flow have increased our knowledge about the molecular mechanisms involved. Material and Methods. Further molecular analysis ...
Abstract
Background. Spontaneous collateral growth (arteriogenesis) restores original blood flow only partially because of quick normalization of an initially elevated fluid shear stress. Micro array data from collateral growth in a porcine model with artificially elevated blood flow have increased our knowledge about the molecular mechanisms involved. Material and Methods. Further molecular analysis requires use of a gene-deficient mouse model. A previously developed method, whereby the fluid shear stress in the peripheral (cerebral) circulation is increased via a cuff anastomosis technique, was transferred to the mouse model. After ligation of the superficial femoral artery (common carotid artery), the peripheral collateral flow was shunted to the femoral vein (jugular vein). To increase cerebral blood flow, we have developed different techniques, including the one-sided arteriovenous fistula (solo shunt model) and a two-sided carotid ligature followed by a one-sided arteriovenous fistula (ligature shunt model). Results. Anastomotic techniques to increase the flow rate and fluid shear stress have been successfully transferred from porcine, rabbit, and rat models to the mouse model. Conclusion. In a gene-deficient mouse model, these new anastomotic techniques allow investigation into the molecular mechanisms involved in collateral growth.
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