Vascular growth responses to chronic arterial occlusion are unaffected by myeloid specific focal adhesion kinase (FAK) deletion.

Arteriogenesis, or the lumenal expansion of pre-existing arterioles in the presence of an upstream occlusion, is a fundamental vascular growth response. Though alterations in shear stress stimulate arteriogenesis, the migration of monocytes into the perivascular space surrounding collateral arteries and their differentiation into macrophages is critical for this vascular growth response to occur. Focal adhesion kinase's (FAK) role in regulating cell migration has recently been expanded to primary macrophages.

Computational Network Model Prediction of Hemodynamic Alterations Due to Arteriolar Rarefaction and Estimation of Skeletal Muscle Perfusion in Peripheral Arterial Disease.

Objective: To estimate the relative influence of input pressure and arteriole rarefaction on gastrocnemius muscle perfusion in patients with PAD after exercise and/or percutaneous interventions.

Methods: A computational network model of the gastrocnemius muscle microcirculation was adapted to reflect rarefaction based on arteriolar density measurements from PAD patients, with and without exercise. A normalized input pressure was applied at the feeder artery to simulate both reduced and restored ABI in the PAD condition.

Laser speckle flowmetry method for measuring spatial and temporal hemodynamic alterations throughout large microvascular networks.

Objectives: 1) To develop and validate laser speckle flowmetry (LSF) as a quantitative tool for individual microvessel hemodynamics in large networks. 2) To use LSF to determine if structural differences in the dorsal skinfold microcirculation (DSFWC) of C57BL/6 and BALB/c mice impart differential network hemodynamic responses to occlusion.

Methods: We compared LSF velocity measurements with known/measured velocities in vitro using capillary tube tissue phantoms and in vivo using mouse DSFWCs and cremaster muscles.