Spinal cord injury (SCI) often results in progressive bladder dysfunction, which varies in severity according to the level and completeness of the original injury. A combination of bladder storage and emptying functions are affected by SCI, which in turn can result in significant morbidity due to recurrent urinary tract infections, pyelonephritis, sepsis, and renal failure in extreme cases. The neurologic injury affects both the ability of the detrusor muscle to contract as a coordinated unit and the interplay between the detrusor muscle and sphincteric mechanism.

Little is known about the smooth muscle cell (SMC) response to the central denervation of SCI. For example, what phenotypic changes occur in smooth muscle cells as a result of denervation? Are the typical patterns of SMC contractile protein gene expression altered with SCI injury, and if so, at what point are they altered? What is the pattern and time course of extracellular matrix deposition following SCI? Are the collagen isoform changes seen similar to those seen with bladder outlet obstruction? Finally, does the mode of bladder drainage effect any of the changes in smooth muscle expression, detrusor function, or collagen deposition?

While it is possible that the absence of neurological stimulation alone inexorably alters smooth muscle function over time, regardless of the manner in which the urine is stored and emptied, perhaps the manner of bladder drainage (reflex voiding, intermittent catheterization, sphincter ablation, urinary diversion) can affect smooth muscle function. This distinction is important, not only to better understand the complex relationship between the detrusor smooth muscle cell and the single neuron which innervates each one, but also practically to determine what factors best preserve function. Preserving normal function and avoiding altered collagen deposition should result in improved continence, controlled intravesical pressures, and less upper tract-related morbidity.

Our initial studies, investigating detrusor smooth muscle cells phenotypic alterations at one, three, and six weeks following a complete transection at spinal cord level T8, uncovered unique changes in smooth muscle cell gene expression patterns which may underlie aberrant bladder function.

Research interest

Principal Investigator: Gary E. Lemack, M.D.: 214-648-7190

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