A Hemodynamic Model of Pelvic Venous Insufficiency-Induced Prostatic Stasis: A Computational, Falsifiable Framework Calibrated Against Independent Experimental Data

Benign prostatic hyperplasia (BPH) and chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) are traditionally viewed through the lens of hormonal dysregulation or occult infection. We examine a complementary, hemodynamic contributor: pelvic venous insufficiency (PVI) leading to chronic prostatic venous stasis. The prostate's valveless venous drainage (Batson's and Santorini's plexuses) creates a hydraulic vulnerability that, when combined with increased intra-abdominal pressure, may produce blood pooling, tissue hypoxia, and fibrosis. We formalize this mechanism with a lumped-parameter Windkessel–fibrosis model and calibrate it directly against the only directly relevant published dataset we could locate: the hydroxyproline time-course of Tsukanov et al. (2021), a rabbit model of chronic pelvic venous congestion, sampled at four timepoints over 180 days. Because the data comprise only four points, we treat every fitted parameter with corresponding caution: we report the fit with its true (low) degrees of freedom, run a practical identifiability analysis that reveals a wide equifinality ridge in (λ, H0)-space and near-total non-identifiability of the remodelling-rate constant kf, and perform global (Sobol) sensitivity and Bayesian (Markov chain Monte Carlo) uncertainty analyses that make this uncertainty explicit rather than concealing it behind a single point estimate. All simulations extending beyond the 180-day observed window (including a therapeutic-timing projection analogous to venotonic therapy) are explicitly and consistently labelled as untested model extrapolations. The central, comparatively robust finding is not a precise numerical prediction but a qualitative therapeutic-timing effect: in the calibrated model, an identical reduction in venous outflow resistance prevents 91% of projected excess collagen accumulation when applied on day 30, but essentially none of it when applied on day 180, after the fibrotic process has already saturated. We present this as a motivating hypothesis together with a falsifiability roadmap that specifies the direct pressure measurements and prospective trials needed to test it, rather than as a validated clinical claim.