Abstract
Spinal cord injury (SCI) disconnects supraspinal micturition centers from the lower urinary tract resulting in immediate and long-term changes in bladder structure and function. While cervical and high thoracic SCI have a greater range of systemic effects, clinical data suggest that those with lower (suprasacral) injuries develop poorer bladder outcomes. Here we assess the impact of SCI level on acute changes in bladder activity. We used two SCI models, T3 and L2 complete transections in male Wistar rats, and compared bladder pressure fluctuations to those of naïve and bladder-denervated animals. By 2 days after L2 transection, but not T3 transection or bladder denervation, small amplitude rhythmic contractions (1 mmHg, 0.06 Hz) were present at low intravesical pressures (<6 mmHg); these were still present 1 month following injury, and at 3 months, bladders from L2 SCI animals were significantly larger than those from T3 SCI or naïve animals. Low-pressure contractions were unaffected by blocking ganglionic signaling or bladder denervation at the time of measurements. L2 (and sham surgery) but not T3 transection preserves supraspinal adrenal control, and by ELISA we show lower plasma adrenal catecholamine concentration in the latter. When an adrenalectomy preceded the L2 transection, the aberrant low-pressure contractions more closely resembled those after T3 transection, indicating that the increased bladder activity after lumbar SCI is mediated by preserved adrenal function. Since ongoing low-pressure contractions may condition the detrusor and exacerbate detrusor-sphincter dyssynergia, moderating bladder catecholamine signaling may be a clinically viable intervention strategy.
Highlights
Voluntary control of the urinary bladder relies on the coordination of autonomic, sensory and somatic nervous systems (Yoshimura and de Groat, 1997)
When we assessed bladder activity at low pressures (
The development of neurogenic bladder hyperactivity that occurs in the weeks following Spinal cord injury (SCI) in the rat is expected and well documented (Kruse et al, 1993; Yoshimura and de Groat, 1997; de Groat and Yoshimura, 2006)
Summary
Voluntary control of the urinary bladder relies on the coordination of autonomic, sensory and somatic nervous systems (Yoshimura and de Groat, 1997). The Adrenogenic Bladder in SCI to the development of detrusor-sphincter-dyssynergia (DSD), where the bladder and sphincter contract together, resulting in high intravesical pressures and inefficient voiding (de Groat and Yoshimura, 2006). Without intervention, these complications can lead to vesicoureteral reflux, urinary tract infections, and upper urinary tract damage, all of which impact health care costs and quality of life for individuals with SCI (Al Taweel and Seyam, 2015). Aberrant NVC patterns after SCI are linked to overactivity in the detrusor muscle and changes to primary afferent signaling, which contribute to bladder dysfunction (Kruse et al, 1993; Cheng et al, 1995)
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