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Mohit Khera

Publications and source records attributed to Mohit Khera.

4 recordsLinked to original sources
PubMed2005

In vivo effects of botulinum toxin A on visceral sensory function in chronic spinal cord-injured rats.

OBJECTIVES: To analyze the in vivo effects of botulinum toxin type A (BTX-A) on visceral sensory function in chronic spinal cord-injured (SCI) rats. METHODS: One group of rats underwent spinal cord transection at the T8-T9 level (SCI) and the other group was left untreated. In 21 days, baseline open cystometrography (CMG) was performed. The rats were then treated intravesically with either 1 mL of 1% protamine sulfate (PS) to increase urothelial permeability or saline, followed by either 1 mL of BTX-A (20 U) or saline. CMG was repeated 48 hours after instillation, and any changes in the bladder contraction frequency and amplitude were evaluated. RESULTS: After the instillation of PS and BTX-A or BTX-A alone, the bladder contraction frequency was significantly decreased in the SCI rats compared with the control rats (P < 0.05); no change was seen in the contraction amplitude. When normal rats were given intravesical PS and/or BTX-A, or SCI animals were treated with PS alone, neither the frequency nor the amplitude of the contractions was affected. Also, no significant differences were found in the bladder contraction frequency or amplitude of contractions in any animal treated with instillation of saline alone. CONCLUSIONS: Intravesical BTX-A inhibits bladder sensory mechanisms by reducing the frequency of bladder contractions in an SCI rat model. Furthermore, our results suggest that intravesically applied BTX-A does not penetrate to the smooth muscle layer even after PS disruption of the bladder urothelium. These findings may have important clinical applications in treating overactive bladders after SCI.

Animals↗
PubMed2004

Botulinum toxin A inhibits ATP release from bladder urothelium after chronic spinal cord injury.

The effects of mechanoreceptor stimulation and subsequent ATP release in spinal cord injured and normal bladders was examined to demonstrate if spinal cord injury (SCI) modulates the basal or evoked release of ATP from bladder urothelium and whether intravesical botulinum toxin A (BTX-A) administration inhibits urothelial ATP release, a measure of sensory nerve activation. A Ussing chamber was used to isolate and separately measure resting and mechanoreceptor evoked (e.g. hypoosmotic stimulation) ATP release from urothelial and serosal sides of the bladder. Following spinal cord injury, resting urothelial release of ATP was ninefold higher than that of normal rats. Botulinum toxin A instillation did not significantly affect the resting release of ATP after spinal cord injury. Evoked ATP release following hypoosmotic stimulation was significantly higher in chronic spinal cord injured compared to normal rat bladders. However, botulinum toxin A treatment markedly reduced ATP release in spinal cord injured bladders by 53% suggesting that ATP release by mechanoreceptor stimulation, as opposed to basal release, occurs by exocytotic mechanisms. In contrast, there was no significant difference in basal or evoked ATP release from bladder serosa following spinal cord injury. Moreover, intravesical instillation of botulinum toxin A did not affect ATP release from the serosal side after spinal cord injury, suggesting that its effects were confined to the urothelial side of the bladder preparation. In summary: (1) increased release of ATP from the urothelium of spinal cord injured bladders may contribute to the development of bladder hyperactivity and, (2) mechanoreceptor stimulated vesicular ATP release, as opposed to basal non-vesicular release of ATP, is significantly inhibited in spinal cord injured bladders by intravesical instillation of botulinum toxin A. These results may have important relevance in our understanding of the mechanisms underlying plasticity of bladder afferent pathways following SCI.

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