Publications (7) View all
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Article: Inhibition of bladder overactivity by stimulation of feline pudendal nerve using transdermal amplitude-modulated signal (TAMS).
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ABSTRACT: • To develop a non-invasive neuromodulation method targeting the pudendal nerve. • Bladder overactivity induced by acetic acid (AA) irritation was partially suppressed by electrical stimulation of the pudendal nerve in α-chloralose anaesthetized cats using a transdermal amplitude-modulated signal (TAMS). • During cystometrography (CMG), intravesical infusion of 0.25% AA significantly decreased the mean (se) bladder capacity to 28.8 (5.9)% of the capacity measured during saline infusion. • The TAMS stimulation inhibited AA-induced bladder overactivity at 5, 7 and 10 Hz, and significantly increased the mean (se) bladder capacity to 61.8 (9.9)%, 51.3 (14.5)%, 53.6 (14.9)%, respectively, of the control capacity during saline infusion, whereas stimulation at 20-40 Hz had no effect. • Under isovolumetric conditions at a bladder volume ranging between 130 to 160% of the bladder capacity measured during AA infusion, TAMS stimulation at all frequencies (5-40 Hz) significantly suppressed the irritation-induced rhythmic bladder contractions, reduced the area under the bladder pressure curve, and decreased the frequency of bladder contractions. However, the amplitude of rhythmic bladder contractions was only significantly decreased at stimulation frequencies of 5-20 Hz. • At bladder volumes above the AA control capacity, TAMS stimulation with frequencies of 20-30 Hz had an excitatory effect, resulting in large amplitude (>25 cmH(2) O) bladder contractions. • TAMS stimulation targeting the cat pudendal nerve can inhibit C-fibre afferent-mediated bladder overactivity. • Thus, clinical research seems warranted to explore the usefulness of this technology for patients with overactive bladder symptoms.BJU International 08/2011; 109(5):782-7. · 2.84 Impact Factor -
Article: Plasticity of urinary bladder reflexes evoked by stimulation of pudendal afferent nerves after chronic spinal cord injury in cats.
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ABSTRACT: Bladder reflexes evoked by stimulation of pudendal afferent nerves (PudA-to-Bladder reflex) were studied in normal and chronic spinal cord injured (SCI) adult cats to examine the reflex plasticity. Physiological activation of pudendal afferent nerves by tactile stimulation of the perigenital skin elicits an inhibitory PudA-to-Bladder reflex in normal cats, but activates an excitatory reflex in chronic SCI cats. However, in both normal and chronic SCI cats electrical stimulation applied to the perigenital skin or directly to the pudendal nerve induces either inhibitory or excitatory PudA-to-Bladder reflexes depending on stimulation frequency. An inhibitory response occurs at 3-10 Hz stimulation, but becomes excitatory at 20-30 Hz. The inhibitory reflex activated by electrical stimulation significantly (P<0.05) increases the bladder capacity to about 180% of control capacity in normal and chronic SCI cats. The excitatory reflex significantly (P<0.05) reduces bladder capacity to about 40% of control capacity in chronic SCI cats, but does not change bladder capacity in normal cats. Electrical stimulation of pudendal afferent nerves during slow bladder filling elicits a large amplitude bladder contraction comparable to the contraction induced by distension alone. A bladder volume about 60% of bladder capacity was required to elicit this excitatory reflex in normal cats; however, in chronic SCI cats a volume less than 20% of bladder capacity was sufficient to unmask an excitatory response. This study revealed the co-existence of both inhibitory and excitatory PudA-to-Bladder reflex pathways in cats before and after chronic SCI. However our data combined with published electrophysiological data strongly indicates that the spinal circuitry for both the excitatory and inhibitory PudA-to-Bladder reflexes undergoes a marked reorganization after SCI.Experimental Neurology 03/2011; 228(1):109-17. · 4.70 Impact Factor -
Article: Suppression of bladder overactivity by activation of somatic afferent nerves in the foot.
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ABSTRACT: To investigate the possibility of suppressing bladder overactivity by electrical activation of somatic afferent nerves in the foot. Cats with an intact spinal cord were studied under α-chloralose anaesthesia. Bladder pressure was recorded via a urethral catheter. Foot stimulation was applied via surface pad electrodes attached to the skin of the front or hind foot. Reflex micturition was inhibited by electrical stimulation of the hind foot at either low (5 Hz) or high (20 Hz) frequencies, but stimulation of the front foot was ineffective. The mean (sem) bladder capacity during a saline infusion cystometrogram (CMG) was significantly (P < 0.05) increased to 153.2 (18.2)% and 136.9 (14.3)% of the control bladder capacity by stimulation at frequencies of 5 Hz and 20 Hz, respectively. Intravesical infusion of 0.25% acetic acid (AA) induced bladder overactivity and reduced bladder capacity to 20.3 (8.9)% of the control capacity measured during saline infusion. Foot stimulation inhibited the AA-induced bladder overactivity recorded under isovolumetric conditions, and significantly (P < 0.05) increased bladder capacity during AA infusion. However, it only restored the small bladder capacity caused by AA irritation to 40-50% of the control bladder capacity measured during saline infusion. The effect of foot stimulation did not persist after termination of stimulation during repeated CMG tests. This study shows the potential of noninvasive transcutaneous electrical stimulation of somatic nerves in the foot to inhibit reflex bladder activity and treat overactive bladder symptoms.BJU International 01/2011; 107(2):303-9. · 2.84 Impact Factor -
Article: Influence of naloxone on inhibitory pudendal-to-bladder reflex in cats.
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ABSTRACT: To determine the involvement of opioid receptors in the inhibitory pudendal-to-bladder reflex, the effect of naloxone (0.01-1 mg/kg, i.v.), an opioid receptor antagonist, on the inhibition of bladder activity evoked by pudendal nerve stimulation was investigated in alpha-chloralose anesthetized cats. The inhibition of reflex isovolumetric bladder contractions induced by pudendal nerve stimulation (5-10 Hz) at intensity threshold (T) for producing complete inhibition was significantly suppressed by naloxone at a high dose (0.3 mg/kg). However, the inhibition elicited at higher intensities (1.5-3 T) was not changed. Naloxone (1 mg/kg) did not alter the frequency dependence of the inhibitory effect of pudendal stimulation. During cystometrograms (CMGs) pudendal nerve stimulation significantly increased bladder capacity to 155.1+/-24.5% and 163.4+/-10% of the control at stimulation intensities of 1 T and 1.5-3 T, respectively. After administration of naloxone (1 mg/kg), the bladder capacity during pudendal nerve stimulation at inhibition threshold (1 T) was not significantly different from control, but it was significantly increased at higher intensities (1.5-3 T). Naloxone alone markedly reduced bladder capacity to 43+/-11.1% of the control, and pudendal stimulation completely reversed this facilitatory effect. This study revealed that activation of opioid receptors contributes to or facilitates the inhibitory pudendal-to-bladder reflex. The reduction in bladder capacity after naloxone treatment also indicates that endogenous opioid peptides mediate a tonic inhibition of micturition. Understanding the neurotransmitter mechanisms involved in the inhibitory pudendal-to-bladder reflex could promote the development of new treatments for bladder overactivity and incontinence.Experimental Neurology 04/2010; 224(1):282-91. · 4.70 Impact Factor -
Article: The Role of Slow Potassium Current in Nerve Conduction Block Induced by High-Frequency Biphasic Electrical Current
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ABSTRACT: The role of slow potassium current in nerve conduction block induced by high-frequency biphasic electrical current was analyzed using a lumped circuit model of a myelinated axon based on the schwarz-reid-bostock model. The results indicate that nerve conduction block at stimulation frequencies above 4 kHz is due to constant activation of both fast and slow potassium channels, but the block at stimulation frequencies below 4 kHz could be due to either anodal or cathodal dc block depending on the time of the action potiential arriving at the block electrode. When stimulation frequency was above 4 kHz, the slow potassium current was about 3.5 to 6.5 times greater than the fast potassium current at blocking threshold, indicating that the slow potassium current played a more dominant role than the fast potassium current. The blocking location moved from the node under the blocking electrode to a nearby node as the stimulation intensity increased. This simulation study reveals that in mammalian myelinated axons, the slow potassium current probably plays a critical role in the nerve conduction block induced by high-frequency biphasic electrical current.IEEE Transactions on Biomedical Engineering 02/2009; · 2.28 Impact Factor
