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W J Vankan

Publications and source records attributed to W J Vankan.

4 recordsLinked to original sources

Spatial interaction between tissue pressure and skeletal muscle perfusion during contraction.

The vascular waterfall theory attributes decreased muscle perfusion during contraction to increased intramuscular pressure (P(IM)) and concomitant increase in venous resistance. Although P(IM) is distributed during contractions, this theory does not account for heterogeneity. This study hypothesises that pressure heterogeneity could affect the interaction between P(IM) rise and perfusion. Regional tissue perfusion during submaximum (100kPa) tetanic contraction is studied, using a finite element model of perfused contracting skeletal muscle. Capillary flow in muscles with one proximal artery and vein (SIM(1)) and with an additional distal artery and vein (SIM(2)) is compared. Blood flow and pressures at rest and P(IM) during contraction ( approximately 25kPa maximally) are similar between simulations, but capillary flow and venous pressure differ. In SIM(2), venous pressure and capillary flow correspond to P(IM) distribution, whereas capillary flow in SIM(1) is less than 10% of flow in SIM(2), in the muscle half without draining vein. This difference is caused by a high central P(IM), followed by central venous pressure rise, in agreement with the waterfall theory. The high central pressure (SIM(1)), obstructs outflow from the distal veins. Distal venous pressure rises until central blood pressure is reached, although local P(IM) is low. Adding a distal vein (SIM(2)) restores the perfusion. It is concluded that regional effects contribute to the interaction between P(IM) and perfusion during contraction. Unlike stated by the vascular waterfall theory, venous pressure may locally exceed P(IM). Although this can be explained by the principles of this theory, the theory does not include this phenomenon as such.

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Mechanical blood-tissue interaction in contracting muscles: a model study.

A finite element (FE) model of blood perfused biological tissue has been developed. Blood perfusion is described by fluid flow through a series of 5 intercommunicating vascular compartments that are embedded in the tissue. Each compartment is characterized by a blood flow permeability tensor, blood volume fraction and vessel compliance. Local non-linear relationships between intra-extra vascular pressure difference and blood volume fraction, and between blood volume fraction and the permeability tensor, are included in the FE model. To test the implementation of these non-linear relations, FE results of blood perfusion in a piece of tissue that is subject to increased intramuscular pressure, are compared to results that are calculated with a lumped parameter (LP) model of blood perfusion. FE simulation of blood flow through a contracting rat calf muscle is performed. The FE model used in this simulation contains a transversely isotropic, non-linearly elastic description of deforming muscle tissue, in which local contraction stress is prescribed as a function of time. FE results of muscle tension, total arterial inflow and total venous outflow of the muscle during contraction, correspond to experimental results of an isometrically and tetanically contracting rat calf muscle.

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Finite-element simulation of blood perfusion in muscle tissue during compression and sustained contraction.

Mechanical interaction between tissue stress and blood perfusion in skeletal muscles plays an important role in blood flow impediment during sustained contraction. The exact mechanism of this interaction is not clear, and experimental investigation of this mechanism is difficult. We developed a finite-element model of the mechanical behavior of blood-perfused muscle tissue, which accounts for mechanical blood-tissue interaction in maximally vasodilated vasculature. Verification of the model was performed by comparing finite-element results of blood pressure and flow with experimental measurements in a muscle that is subject to well-controlled mechanical loading conditions. In addition, we performed simulations of blood perfusion during tetanic, isometric contraction and maximal vasodilation in a simplified, two-dimensional finite-element model of a rat calf muscle. A vascular waterfall in the venous compartment was identified as the main cause for blood flow impediment both in the experiment and in the finite-element simulations. The validated finite-element model offers possibilities for detailed analysis of blood perfusion in three-dimensional muscle models under complicated loading conditions.

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A 3-D finite element model of blood perfused rat gastrocnemius medialis muscle.

A finite element description of blood perfusion has been developed, and is applied to skeletal muscles. Three-dimensional distributions of blood pressures and flows in deforming muscles are calculated. The muscle tissue is considered as a fluid-saturated porous solid. The blood is modeled as a series of five intercommunicating compartmental fluids, representing arterial, arteriolar, capillary, venular and venous blood, that reside in the pores (blood vessels) of the muscle tissue. The blood vessels are modeled as distensible tubes, embedded in the muscle tissue. A 3-D finite element mesh has been mapped on a reconstructed geometry of a gastrocnemius medialis muscle of the rat. Blood perfused linear elastic muscle material behaviour has been assigned to this mesh. A simulation of blood perfusion, resulting from a constant arterio-venous pressure difference, through the reconstructed muscle has been performed. Calculated blood pressure and flow distributions were within physiological range.

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