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MODEL RELATING SKELETAL MUSCLE CONTRACTION AND FLUID FLOW IN BONE
C.Caulkins3,
H.Winet1,2,3, J.Bao1
1Orhtopeadic Hospital/UCLA, 2UCLA Dept. Orthopaedic Surgery, 3UCLA Dept.
Biomedical Engineering, USA
It has been demonstrated that forces generated by bone bending alone are not sufficient to produce the fluid shear strain required to activate bone cells. Skeletal muscle contraction coordinated with venous valve function normally prevents blood pooling in the lower extremities. Shortening and widening of the contracting muscle compresses blood vessels outside and within the muscle compartment, generating soliton (solitary pressure wave) which travels down both veins and arteries toward bone capillaries. During exercise heart and skeletal muscle both increase pressure. As a result venous valves are forced shut and intraluminal capillary pressure increases, driving plasma through the porous endothelium by capillary filtration. Extravasating plasma drives interstitial fluid flow over osteocytes in the lacunocanalicular matrix, osteoclasts, and osteoblasts. We are addressing the questions: Is this muscle-driven transport sufficient to cause a shear stress on or streaming potential over bone cells sufficient to activate their receptors?
We are examining effects of transcutaneous electrical muscle stimulation (TENS) on blood flow and capillary filtration in NZW rabbit tibial cortical bone, using optical bone chamber intravital fluorescence microscopy. We hypothesized a relatively large resultant increase in capillary filtration. Extravasation of fluorescein isothiocyanate (70kDa) from the blood stream into surrounding tissue was observed during and following TENS with monophasic pulsatile current square waveforms (2Hz) as applied externally to the gastrocnemius muscle of 4 rabbits for 1 hour, 6 days/week. Flow velocity, angiogenesis and fluorescence intensity was measured. Results indicate changes in velocities of blood flow and capillary filtration following TENS.