Emergent vascular network inhomogeneities and resulting blood flow patterns in a growing tumor.
Tumors acquire sufficient oxygen and nutrient supply by coopting host vessels and neovasculature created via angiogenesis, thereby transforming a highly ordered network into chaotic heterogeneous tumor specific vasculature. Vessel regression inside the tumor leads to large regions of necrotic tissue interspersed with isolated surviving vessels. We extend our recently introduced model to incorporate Fahraeus-Lindqvist- and phase separation effects, refined tissue oxygen level computation and drug flow computations. We find, unexpectedly, that collapse and regression accelerates rather than diminishes the perfusion and that a tracer substance flowing through the remodeled network reaches all parts of the tumor vasculature very well. The reason for decreased drug delivery well known in tumors should therefore be different from collapse and vessel regression. Implications for drug delivery in real tumors are discussed.
Welter
M
M
Theoretische Physik, Universität des Saarlandes, PF 151150, 66041 Saarbrücken, Germany.
Bartha
K
K
Rieger
H
H
D000970:Antineoplastic Agents / Q000097:blood; D001783:Blood Flow Velocity; D001809:Blood Viscosity; D017709:Fractals; D006801:Humans; D008955:Models, Cardiovascular; D009369:Neoplasms / Q000097:blood / Q000098:blood supply*; D009389:Neovascularization, Pathologic / Q000097:blood / Q000473:pathology* / Q000503:physiopathology
D000970:Antineoplastic Agents