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논문 기본 정보

자료유형
학술저널
저자정보
Chuan Zhang (Department of Biomedical Engineering University of Houston) Xuhong Li (The Third Xiangya Hospital Central South University) Timothy B. Boone (Houston Methodist Research Institute) Yolanda Cruz (Universidad Autonoma de Tlaxcala) Yingchun Zhang (Department of Biomedical Engineering University of Houston) Alvaro Munoz (Regenerative Medicine and Tissue Engineering Program-Urology Houston Methodist Research Institute)
저널정보
대한배뇨장애요실금학회 International Neurourology Journal International Neurourology Journal 제24권 제3호
발행연도
2020.1
수록면
258 - 269 (12page)

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Purpose: This study was conducted to evaluate the hypothesis that an enlarged prostate in old rats may lead to complications associated with voiding dysfunction involving ionotropic P2X2/3-type purinergic receptors Methods: Intact animals were divided into male young (MYR; 8?10 weeks old) and male old (MOR; 20 months old) rats. The animals underwent simultaneous detrusor electromyography (EMG) and suprapubic cystometry (CMG) under urethane anesthesia. Immunofluorescence techniques were used to evaluate prostatic autonomic innervation and P2X3R expression in bladder urothelial cells. The functional role of P2X3R was characterized by intramuscular application of AF-353, a selective P2X2/3R antagonist. Results: The prostate index significantly increased in MOR, suggestive of an enlarged prostate affecting micturition patterns. Significant EMG and CMG differences were found between MYR and MOR. Higher immunoreactivity for P2X2/3R in the urothelial layer and for prostatic neurofilaments was seen in MOR. Systemic inhibition of P2X2/3R had minimal effects on MYR responsiveness, but improved voiding function in MOR with a marked decrease of intravesical pressure and bladder contractile responses. Conclusions: The data support the hypothesis that an enlarged prostate in MOR may contribute to voiding dysfunction involving activation of P2X2/3R, which enhances a prostate-bladder reflex. This reflex may increase bladder afferent transmission and activation of increased prostate innervation, leading to voiding dysfunction.

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