Ching-Chung Liang1,2, Yi-Hao Lin1,2, Ho-Ling Liu3, Tsong-Hai Lee2,4. 1. Division of Urogynecology, Department of Obstetrics and Gynecology, Chang Gung Memorial Hospital, Linkou Medical Center, Taoyuan, Taiwan. 2. College of Medicine, Chang Gung University, Taoyuan, Taiwan. 3. Department of Medical Imaging and Radiological Sciences, and Healthy Aging Research Center, Chang Gung University College of Medicine, Taoyuan, Taiwan. 4. Stroke Section, Department of Neurology and Stroke Center, Chang Gung Memorial Hospital Linkou Medical Center, Taoyuan, Taiwan.
Abstract
AIMS: The role of forebrain in controlling micturition has been studied extensively using rat model with ischemic injury; however, the influence of cerebral hypoperfusion on voiding function remains unclear. The study was conducted to evaluate the bladder dysfunction and the temporal expression of bladder nerve growth factor (NGF) after cerebral hypoperfusion induced by bilateral common carotid artery occlusion (BCCAO). MATERIALS AND METHODS: Forty female rats were subjected to either BCCAO or sham operation. Cerebral T2-weighted magnetic resonance images (MRI) and diffusion and perfusion change were studied to characterize the extent of the ischemic injury in the cortex and hippocampus. On 1, 7, and 28 days after BCCAO, the bladder dysfunction was assessed by cystometric studies, and the expressions of NGF in bladder muscle and urothelium were measured by immunohistochemistry and real-time polymerase chain reaction. RESULTS: In the MRI study, cerebral blood flow in the cortex and hippocampus was significantly decreased from 1 day and subsequently returned to sham-operated level at 28 days after BCCAO. Compared with the sham-operated group, significant reduction in voided volume and intercontraction interval was found from 1 to 28 days after cerebral hypoperfusion. The NGF immunoreactivity and mRNA in the bladder muscle and urothelium were transiently increased at 1 day, and declined significantly at 28 days after BCCAO. CONCLUSIONS: Our results indicate that bladder dysfunction may be caused by cerebral hypoperfusion and is less likely related to bladder NGF expression.
AIMS: The role of forebrain in controlling micturition has been studied extensively using rat model with ischemic injury; however, the influence of cerebral hypoperfusion on voiding function remains unclear. The study was conducted to evaluate the bladder dysfunction and the temporal expression of bladder nerve growth factor (NGF) after cerebral hypoperfusion induced by bilateral common carotid artery occlusion (BCCAO). MATERIALS AND METHODS: Forty female rats were subjected to either BCCAO or sham operation. Cerebral T2-weighted magnetic resonance images (MRI) and diffusion and perfusion change were studied to characterize the extent of the ischemic injury in the cortex and hippocampus. On 1, 7, and 28 days after BCCAO, the bladder dysfunction was assessed by cystometric studies, and the expressions of NGF in bladder muscle and urothelium were measured by immunohistochemistry and real-time polymerase chain reaction. RESULTS: In the MRI study, cerebral blood flow in the cortex and hippocampus was significantly decreased from 1 day and subsequently returned to sham-operated level at 28 days after BCCAO. Compared with the sham-operated group, significant reduction in voided volume and intercontraction interval was found from 1 to 28 days after cerebral hypoperfusion. The NGF immunoreactivity and mRNA in the bladder muscle and urothelium were transiently increased at 1 day, and declined significantly at 28 days after BCCAO. CONCLUSIONS: Our results indicate that bladder dysfunction may be caused by cerebral hypoperfusion and is less likely related to bladder NGF expression.
Authors: Ching-Chung Liang; S W Steven Shaw; Yung-Hsin Huang; Yi-Hao Lin; Tsong-Hai Lee Journal: Stem Cells Transl Med Date: 2017-01-03 Impact factor: 6.940