Micturition in rats: a chronic model for study of bladder function and effect of anesthetics

Tl, Yaksh; Durant, Philippe A. C.; Brent, C. R.

doi:10.1152/ajpregu.1986.251.6.r1177

Cited by 93 publications

(103 citation statements)

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“…Similar low voiding efficiencies were reported in other studies (Cheng and de Groat 2004, Cruz and Downie 2005, Peng et al 2006, and presumably resulted from the urethrane anesthesia inhibiting reflex bladder contractions and reducing the contraction pressure during micturition (Yaksh et al 1986).…”

Section: Discussionsupporting

confidence: 87%

Improved bladder emptying in urinary retention by electrical stimulation of pudendal afferents

et al. 2008

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Urinary retention is the inability to empty the bladder completely, and may result from bladder hypocontractility, increases in outlet resistance, or both. Chronic urinary retention can lead to several urological complications and is often refractory to pharmacologic, behavioral, and surgical treatments. We sought to determine whether electrical stimulation of sensory fibers in the pudendal nerve could engage an augmenting reflex and thereby improve bladder emptying in an animal model of urinary retention. We measured the efficiency of bladder emptying with and without concomitant electrical stimulation of pudendal nerve afferents in urethane anesthetized rats. Voiding efficiency (VE=voided volume/initial volume) was reduced from 72±7% to 29±7% following unilateral transection of the sensory branch of the pudendal nerve (UST) and from 70±5% to 18±4% following bilateral transection (BST). Unilateral electrical stimulation of the proximal transected sensory pudendal nerve during distention-evoked voiding contractions significantly improved VE. Low intensity stimulation at frequencies of 1-50 Hz increased VE to 40-51% following UST and to 39-49% following BST, while high intensity stimulation was ineffective at increasing VE. The increase in VE was mediated by increases in the duration of distention-evoked voiding bladder contractions, rather than increases in contraction amplitude. These results are consistent with an essential role for pudendal sensory feedback in efficient bladder emptying, and raise the possibility that electrical activation of pudendal nerve afferents may provide a new approach to restore efficient bladder emptying in persons with urinary retention.

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Section: Discussionsupporting

confidence: 87%

Improved bladder emptying in urinary retention by electrical stimulation of pudendal afferents

et al. 2008

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“…11 However, during the first day after catheter implantation, this irritative change in bladder activity is not evident. 12,13 In this study, we inserted the catheter only a few hours before the CMG assessment to minimize the possibility of bladder irritation.…”

Section: Discussionmentioning

confidence: 99%

Mechanism of action of sacral nerve stimulation using a transdermal amplitude-modulated signal in a spinal cord injury rodent model

Elkelini¹,

Pravdivyi²,

Hassouna³

2012

CUAJ

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Introduction: Sacral neuromodulation (SNM) is an effective treatment modality for several urological problems, including neurogenic bladder. However, the invasiveness of this technique makes it unsuitable for many patients. We present a novel transdermal amplitude-modulated signal (TAMS) that may provide a non-invasive alternative to implantable SNM to treat neurogenic detrusor overactivity (NDO). Methods: In this study, we investigated the mechanism of action of non-invasive SNM using TAMS on our established spinal cord injury (SCI) animal model. We demonstrated that spinally transected rats develop urinary bladder hyper-reflexia after 3 weeks of SCI, indicated by the presence of uninhibited contractions, increased resting pressure, increased threshold pressure and increased maximum voiding pressure. Results: Short-term neurostimulation affected urodynamics parameters by significantly reducing the threshold pressure (p = 0.02). Spinal transection also increased calcitonin gene-related protein (CGRP) concentration in the L6 dorsal root ganglia; whereas, neurostimulation significantly reduced CGRP concentration in L6 (p = 0.03). Conclusion: TAMS caused a reduction in NDO by inhibiting C-fibre activity. IntroductionSacral neuromodulation (SNM) is a relatively new concept for the treatment of various lower urinary tract dysfunctions, yet it has gained wide acceptance especially in managing patients with conditions refractory to conventional methods. The U.S. Food and Drug Administration has approved SNM for three indications: urge incontinence, urge frequency and nonobstructive urinary retention. 1 The mechanism of action of SNM is still unknown. It has been suggested that SNM inhibits bladder afferent activities through its action on somatic afferent pathways and thereby blocks abnormal sensory input to the spinal cord and brain. 2 SNM has become more appealing because of simpler, minimally invasive implant techniques and shorter hospital stay.We present a novel, transdermal amplitude-modulated signal (TAMS) that enables non-invasive stimulation of sacral nerves in a spinal cord injury (SCI) rodent model. The signal uses an amplitude-modulated waveform with a high frequency carrier, modulated by a low frequency envelope. The carrier waveform is designed to be of sufficient frequency to overcome skin and tissue impedance. The pulse envelope contains selective frequency, pulse width, amplitude and waveform shape designed to stimulate specific nerves. The efficacy of TAMS has already been demonstrated in a feline overactive bladder (OAB) model. 3,4 We examined TAMS as a treatment modality for neurogenic detrusor overactivity (NDO) caused by SCI. We also assessed the role of C-fibre inhibition by SNM as a possible mechanism of action. MethodsIn the present study, 28 female Sprague Dawley rats (250 g) were stratified into three groups (4 to 6 rats per group): (1) normal controls (C); (2) spinally transected at T10 (S); and (3) spinally transected and electrically stimulated bilaterally at S1 with TAMS for 2 hou...

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“…One or 2 weeks after intrathecal injection of vehicle or NGF, cystometry in conscious rats was performed according to previously published methods (Yaksh et al, 1986). Under halothane anesthesia, a catheter (PE 50) was inserted via a midline abdominal incision into the bladder through the bladder dome, and the abdomen was closed by sutures.…”

Section: Experiments 1: Bladder Activity and Ngf Level In Drgs After Nmentioning

confidence: 99%

Bladder Overactivity and Hyperexcitability of Bladder Afferent Neurons after Intrathecal Delivery of Nerve Growth Factor in Rats

Yoshimura¹,

Bennett²,

Hayashi³

et al. 2006

J. Neurosci.

154

170

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Nerve growth factor (NGF) has been proposed as an important mediator inducing bladder overactivity under pathological conditions such as spinal cord injury, bladder outlet obstruction, or cystitis. We therefore examined the effects of chronic NGF treatment on bladder activity and the properties of bladder afferent neurons. In adult female rats, NGF (2.5 g/l) was infused continuously into the intrathecal space at the L6 -S1 level of spinal cord for 1 or 2 weeks using osmotic pumps (0.5 l/h). Bladder afferent neurons were labeled with axonal transport of Fast Blue injected into the bladder wall. After intrathecal injection of NGF, cystometrograms under an awake condition showed bladder overactivity revealed by time-dependent reductions in intercontraction intervals and voided volume. ELISA analyses showed significant increases in NGF levels in L6 -S1 dorsal root ganglia of NGF-treated rats. In patch-clamp recordings, dissociated bladder afferent neurons exhibiting tetrodotoxin (TTX)-resistant action potentials from NGF-treated animals were larger in diameter and had significantly lower thresholds for spike activation compared with sham rats. In addition, the number of TTX-resistant action potentials during 600 ms depolarizing pulses was significantly increased time dependently after 1 or 2 weeks of NGF application. The density of slowly inactivating A-type K ϩ currents was decreased by 52% in bladder afferent neurons with TTX-resistant spikes after 2 week NGF treatment. These results indicate that increased NGF levels in bladder afferent pathways and NGF-induced reduction in A-type K ϩ current density could contribute to the emergence of bladder overactivity as well as somal hypertrophy and hyperexcitability of bladder afferent neurons.

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Micturition in rats: a chronic model for study of bladder function and effect of anesthetics

Cited by 93 publications

References 0 publications

Improved bladder emptying in urinary retention by electrical stimulation of pudendal afferents

Improved bladder emptying in urinary retention by electrical stimulation of pudendal afferents

Mechanism of action of sacral nerve stimulation using a transdermal amplitude-modulated signal in a spinal cord injury rodent model

Bladder Overactivity and Hyperexcitability of Bladder Afferent Neurons after Intrathecal Delivery of Nerve Growth Factor in Rats

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