Change in Bladder Contractility Associated With Bladder Overactivity in Rats With Cerebral Infarction

Yokoyama, Osamu; Komatsu, Kazuto; Ishiura, Yoshiyuki; Nakamura, Yasuo; Morikawa, Kouji; Namiki, Mikio

doi:10.1016/s0022-5347(01)63987-9

Cited by 39 publications

(18 citation statements)

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“…Aging-dependent changes occur in many tissues, including the bladder, peripheral nerve, spinal cord, and brain. Recently, bladder function has been examined using aged rats [13] , cerebral infracted rats [1,3,4] , spinal cord injury rats [14] , bladder outlet obstruction [15] , Parkinson's disease model [16] , Alzheimer's disease model [2] , and chemical bladder irritation model [17] . However, there have been no previous investigations regarding the effects of brain aging without destructive lesions under physiological conditions.…”

Section: Discussionmentioning

confidence: 99%

“…The role of the forebrain in controlling micturition has been studied extensively using rats with cerebral infarction (CI), decerebrated rats, and drug-induced models [1,2] . In the CI model, damage to the neural circuitry in the forebrain can produce hyperactivity of the bladder [1,3,4] . Bladder capacity in CI rats was markedly reduced, indicating bladder hyperactivity, which has been attributed to the interruption of inhibitory pathways from the forebrain to the pontine micturition center [3,4] .…”

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confidence: 99%

“…In the CI model, damage to the neural circuitry in the forebrain can produce hyperactivity of the bladder [1,3,4] . Bladder capacity in CI rats was markedly reduced, indicating bladder hyperactivity, which has been attributed to the interruption of inhibitory pathways from the forebrain to the pontine micturition center [3,4] . However, the observations that bladder capacity in CI rats was lower than that in sham-operated (SO) decerebrated rats, and that decerebration increased bladder capacity in CI rats, indicating that CI induces tonic facilitatory input to brainstem/spinal pathways controlling voiding [1] .…”

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Mild Brain Ischemia Produces Bladder Hyperactivity without Brain Damage in Rats

Yotsuyanagi

Narimoto

Namiki³

2006

Urol Int

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Introduction: The influence of brain ischemia without cerebral infarction on voiding function is unknown. To investigate the effects of a reduction in cerebral blood flow on voiding function, the influence of chronic cerebral hypoperfusion (CH) on bladder activity was examined in rats. Materials and Methods: CH was induced in each of 11 female Sprague-Dawley rats by anastomosis between the right external jugular vein and the right common carotid artery with partial obstruction of the left common carotid artery. Twelve intact animals comprised a control group. Voided volume per micturition was assessed in a metabolic cage for 24 h on weeks 2, 4, and 8. Eight weeks after the operation, the rats were tested in a hippocampus-related learning paradigm, the Morris water maze. Bladder activity was monitored in 13 rats with continuous infusion cystometrography (CMG) at 2 weeks. After evaluation, the rats’ brains were stained by perfusion with 2% 2,3,5-triphenyltetrazolium chloride (TTC). Results: Voided volume per micturition was significantly reduced and voiding frequency was significantly increased in CH rats 2 weeks after CH as compared to the control group (p < 0.05). Bladder capacity on CMG of CH rats was significantly reduced 14 days after CH as compared to the controls (p < 0.05). Although TTC staining of the CH rat brain did not show cerebral infarction, CH induced impairment of water maze learning. Conclusions: These results indicate that mild forebrain ischemia without infarction results in the development of bladder hyperactivity and impairment of memory. Mild brain ischemia with aging may induce bladder overactivity in humans. Further studies of the nervous system related to bladder hyperactivity using this animal model may lead to pharmacological therapy or prevention of bladder overactivity in the aging individual with an unidentified origin of voiding dysfunction.

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Section: Discussionmentioning

confidence: 99%

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Mild Brain Ischemia Produces Bladder Hyperactivity without Brain Damage in Rats

Yotsuyanagi

Narimoto

Namiki³

2006

Urol Int

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“…12 Briefly, rats were anesthetized with 2% isoflurane and the right carotid bifurcation was exposed through a midline incision in the neck. The common carotid artery was occluded and the branches of the external carotid artery were dissected and divided.…”

Section: Methodsmentioning

confidence: 99%

Effects of Duloxetine on Urethral Continence Reflex and Bladder Activity in Rats with Cerebral Infarction

et al. 2015

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Purpose: We investigated the effect of duloxetine, a norepinephrine and serotonin reuptake inhibitor, on the sneeze induced continence reflex and on bladder function in rats with cerebral infarction. Materials and Methods: Using urethane anesthesia the effect of duloxetine (1 mg/kg intravenously) on the amplitude of urethral responses during sneezing as well as urethral baseline pressure at the mid urethra was evaluated in normal female adult rats and cerebral infarction rats. Tilt leak point pressure was also measured. In normal and cerebral infarction rats continuous cystometry was evaluated before and after duloxetine injection. Results: Incerebralinfarctionratsurethralbaselinepressurewas43%lowerthan in normal rats but the amplitude of urethral responses during sneezing did not differ in the 2 groups. Duloxetine increased the amplitude of urethral responses during sneezing and urethral baseline pressure by 31% and 21%, respectively, in normal rats but did not affect either in cerebral infarction rats. Also, in cerebral infarction rats leak point pressure was 29% lower compared with normal rats. Duloxetine increased leak point pressure in normal rats but not in cerebral infarction rats. Cerebral infarction reduced intercontraction intervals without affecting the amplitude of bladder contractions compared with normal rats. Duloxetine prolonged intercontraction intervals in cerebral infarction rats but not in normal rats. Conclusions: These results suggest that cerebral infarction induces not only bladder overactivity but also stress urinary incontinence, which may account for mixed incontinence in patients with cerebral infarction. After cerebral infarction duloxetine reduced bladder overactivity but failed to enhance active urethral closure mechanisms during sneezing, suggesting that disorganization of the brain network after cerebral infarction might influence the effect of duloxetine on lower urinary tract function.

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“…Bladder capacity is signi cantly reduced just after MCA occlusion, and remains consistently at less than half that of sham operated (SO) rats for 24 hours after MCA occlusion. The differences in bladder capacity continue for as long as four months after MCA occlusion (6).…”

Section: Advances In Animal Models Of Overactive Bladdermentioning

confidence: 97%

Overactive Bladder - Experimental Aspects

Yokoyama

Komatsu

Ishiura

et al. 2002

Scandinavian Journal of Urology and Nephrology

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Scand J Urol Nephrol Suppl 210: 59-64, 2002 Supra-pontine lesions resulting from neurological disorders such as vascular disease, Parkinson's disease, or Alzheimer type senile dementia lead to an increase in bladder activity. This is due in part to the removal at the cortical inhibitory control of the micturition center in the brain stem -i.e. the pontine micturition center (PMC) -and in part to facilitation of excitatory control. These inhibitory or excitatory controls consist of several neurotransmitter systems, including glutamate, dopamine, gaminobutyric acid (GABA), and acetylcholine. Bladder overactivity caused by cerebral infarction is mediated by upregulation of N-methyl-D-aspartate (NMDA) glutamatergic and D2 dopaminergic excitatory mechanisms, and by downregulation of NMDA glutamatergic and M1 muscarinic inhibitory mechanisms in the brain. Bladder overactivity associated with Parkinson's disease is reportedly induced by a loss of input to the D1 dopaminergic receptor. Furthermore, bladder overactivity caused by Alzheimer type dementia is thought to be mediated by downregulation of M1 muscarinic inhibitory mechanisms. Development of bladder overactivity following cerebral infarction is mediated by activation of the NMDA receptor and accompanied by an increase in c-fos, zif268 and COX-2 mRNA expression in the dorsal pontine tegmentum.

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Change in Bladder Contractility Associated With Bladder Overactivity in Rats With Cerebral Infarction

Abstract: This animal model will be useful for chronic studies on the mechanism of detrusor hyperactivity (DH).

Cited by 39 publications

References 19 publications

Mild Brain Ischemia Produces Bladder Hyperactivity without Brain Damage in Rats

Mild Brain Ischemia Produces Bladder Hyperactivity without Brain Damage in Rats

Effects of Duloxetine on Urethral Continence Reflex and Bladder Activity in Rats with Cerebral Infarction

Overactive Bladder - Experimental Aspects

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