Control of Urinary Drainage and Voiding

Abstract

Urine differs greatly in ion and solute composition from plasma and contains harmful and noxious substances that must be stored for hours and then eliminated when it is socially convenient to do so. The urinary tract that handles this output is composed of a series of pressurizable muscular compartments separated by sphincteric structures. With neural input, these structures coordinate the delivery, collection, and, ultimately, expulsion of urine. Despite large osmotic and chemical gradients in this waste fluid, the bladder maintains a highly impermeable surface in the face of a physically demanding biomechanical environment, which mandates recurring cycles of surface area expansion and increased wall tension during filling, followed by rapid wall compression during voiding. Afferent neuronal inflow from mucosa and submucosa communicates sensory information about bladder fullness, and voiding is initiated consciously through coordinated central and spinal efferent outflow to the detrusor, trigonal internal sphincter, and external urethral sphincter after periods of relative quiescence. Provocative new findings suggest that in some cases, lower urinary tract symptoms, such as incontinence, urgency, frequency, overactivity, and pain may be viewed as a consequence of urothelial defects (either urothelial barrier breakdown or inappropriate signaling from urothelial cells to underlying sensory afferents and potentially interstitial cells). This review describes the physiologic and anatomic mechanisms by which urine is moved from the kidney to the bladder, stored, and then released. Relevant clinical examples of urinary tract dysfunction are also discussed.

Single layer cystotomy closure of excised porcine bladders with barbed versus smooth suture material

“…When bladder compliance reaches its limit, intravesicular pressure rises abruptly. Previous studies have shown intraluminal bladder pressures in humans can reach 50‐60 cm H 2 O (37‐44 mm Hg) during . In this study, only 5 samples leaked at pressures greater than 40 mm Hg; thus, most specimens did not withstand pressures required for normal voiding.…”

“…Indeed, the bladder wall normally restructures as it fills in live animals. As tension increases, the epithelium and connective tissue are stretched and the smooth muscle cells undergo histologic restructuring to accommodate urine and maintain low pressures . In this study, the fluid infusion rate was much faster than the rate of normal urine production, preventing any assessment of the bladder's response to normal fluid expansion rates.…”

“…In this ex vivo study, cystotomy incisions closed with unidirectional barbed suture leaked at pressures similar to those closed with conventional smooth sutures and knot tying. Intravesicular pressure is usually low (4‐7.3 mm Hg) and the bladder wall restructures as it expands to accommodate an increase in urine volume . Since no sample leaked at pressures <19 mm Hg, both suture types resulted in watertight closures during the compliance phase of bladder filling.…”

“…In this study, the fluid infusion rate was much faster than the rate of normal urine production, preventing any assessment of the bladder's response to normal fluid expansion rates. As the urinary bladder fills more slowly in vivo, fibrin formation or a gradual restructuring may contribute to preventing leakage during voiding …”

Attenuation of Cystitis and Pain Sensation in Mice Lacking Fatty Acid Amide Hydrolase

“…While urothelium has historically been viewed as a simple barrier separating the bladder wall from urine, increasing evidence also suggests that the urothelial cells play a critical role in physiological and pathophysiological processes in the bladder (Daly et al, 2011; Birder and Andersson, 2013; Hill, 2014; Keay et al, 2014; Gonzalez et al, 2014). Specifically, urothelial cells have the capacity to secrete a variety of signaling molecules such as PGE 2 , NGF, nitric oxide, and cytokines in response to various stimuli (Malley and Vizzard, 2002; Wang et al, 2008; Birder and Andersson, 2013; Hill, 2014; Keay et al, 2014; Gonzalez et al, 2014). Conceivably, chemical mediators derived from urothelial cells could significantly influence bladder function and pain sensation during bladder inflammation.…”