Abstract

Purpose In an animal model of urethral obstruction glycogen deposition in the bladder muscle was found to be a marker for previous increased voiding pressure and decreased compliance [de Jong et al. Neurourol Urodynam 2008; 27: 454-60]. Here we measured if also in the human bladder glycogen deposition marks adaptation to increased pressure in the filling phase by comparing two groups: normal leak-point pressure + normal compliance (Vesico Ureteral Reflux) and high leak-point pressure + low compliance (MyeloMeningoCele). Material and Methods Rest material was obtained from patients undergoing a ureter reimplantation (VUR group, n = 8) or an augmentation (MMC group, n = 16). Glycogen deposition was scored from 0 to 3 on periodate acid Schiffs (PAS) stained sections. Bladder function was assessed with video urodynamics yielding: CAPacity (ml), COMpliance (from 0,good, to 2, bad), INStability (0,absent, to 2, severe), Leak Point Pressure (cm water). Significance of difference was tested with a student t-test. Results Group PAS Cap COM INS LPP VVR group 1.6 ± 0.3 217 ± 47 0.29 ± 0.17 0.13 ± 0.13 17 ± 3 MMC group 2.5 ± 0.12 83 ± 11 1.19 ± 0.15 0.8 ± 0.23 64 ± 5 p -value Discussion In Guinea pigs glycogen deposition in the bladder muscle marks adaptation to prolonged periods of increased bladder pressure. This marker function has now been confirmed for the human bladder. As glycogen is deposited in response to ischemia this suggests the increased pressure is linked with ischemic conditions. Next to extrinsic conditions like an obstruction downstream this intrinsic bladder condition might be involved in the continuing loss of bladder function that, often unexplained, occurs in patients with structural/functional obstruction. This opens new venues for monitoring bladder function (bladder wall blood supply and saturation) and new angles of treatment (maintaining proper bladderwall saturation).

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