Current Knowledge and Novel Frontiers in Lower Urinary Tract Dysfunction after Spinal Cord Injury: Basic Research Perspectives.
Current Knowledge and Novel Frontiers in Lower Urinary Tract Dysfunction after Spinal Cord Injury: Basic Research Perspectives.
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脊髓损伤后尿路功能障碍的当前知识和新型边界：基础研究观点。
DOI：
10.4103/uros.uros_31_22
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发表时间：
2022-07
影响因子：
0.5
通讯作者：
Yoshimura N
中科院分区：
文献类型：
--
作者：
Wada N;Karnup S;Kadekawa K;Shimizu N;Kwon J;Shimizu T;Gotoh D;Kakizaki H;de Groat WC;Yoshimura N
本文就脊髓损伤后下尿路功能障碍(LUTD)的基础研究进展作一综述。在脊髓损伤动物模型中，我们特别关注控制下尿路(LUT)功能的神经生理学机制和脊髓损伤引起的排尿控制的改变。LUT有两个主要功能，即储存和排尿，这两个功能由复杂的神经控制系统调节。这个神经系统协调LUT中两个功能单元的活动：膀胱和出口，包括膀胱颈、尿路和盆底横纹肌。在储存阶段，出口关闭，膀胱静止，以维持较低的膀胱内压力和可控性；在排尿阶段，出口放松，膀胱收缩，以促进尿液的有效释放。脊髓损伤损害了排尿的自主控制以及协调膀胱和括约肌功能的正常反射通路。脊髓损伤后，膀胱最初是无反射的，但随后由于脊髓排尿反射通路的出现而变得反射亢进。然而，膀胱排空效率不高，因为膀胱和尿道括约肌之间失去了协调性。在脊髓损伤动物模型中，沉默的C纤维膀胱传入的过度兴奋性是神经源性LUTD的主要病理生理基础，尤其是逼尿肌过度活动。反射可塑性与神经肽、神经营养因子或传入神经元的化学受体的性质变化有关。不仅C纤维，Aδ纤维也参与了脊髓损伤后逼尿肌括约肌协同障碍等神经源性LUTD的发生。利用疾病模型进行的动物研究有助于我们发现脊髓损伤引起的下尿路下尿路不同的致病因素，并为新的治疗寻找潜在的靶点。
This review article aims to summarize the recent advancement in basic research on lower urinary tract dysfunction (LUTD) following spinal cord injury (SCI) above the sacral level. We particularly focused on the neurophysiologic mechanisms controlling the lower urinary tract (LUT) function and the SCI-induced changes in micturition control in animal models of SCI. The LUT has two main functions, the storage and voiding of urine, that are regulated by a complex neural control system. This neural system coordinates the activity of two functional units in the LUT: the urinary bladder and an outlet including bladder neck, urethra, and striated muscles of the pelvic floor. During the storage phase, the outlet is closed and the bladder is quiescent to maintain a low intravesical pressure and continence, and during the voiding phase, the outlet relaxes and the bladder contracts to promote efficient release of urine. SCI impairs voluntary control of voiding as well as the normal reflex pathways that coordinate bladder and sphincter function. Following SCI, the bladder is initially areflexic but then becomes hyperreflexic due to the emergence of a spinal micturition reflex pathway. However, the bladder does not empty efficiently because coordination between the bladder and urethral sphincter is lost. In animal models of SCI, hyperexcitability of silent C-fiber bladder afferents is a major pathophysiological basis of neurogenic LUTD, especially detrusor overactivity. Reflex plasticity is associated with changes in the properties of neuropeptides, neurotrophic factors, or chemical receptors of afferent neurons. Not only C-fiber but also Aδ-fiber could be involved in the emergence of neurogenic LUTD such as detrusor sphincter dyssynergia following SCI. Animal research using disease models helps us to detect the different contributing factors for LUTD due to SCI and to find potential targets for new treatments.
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影响因子：
--
作者：
CHENG, CL;MA, CP;DEGROAT, WC
通讯作者：
DEGROAT, WC
DOI：
10.1152/ajpregu.1999.277.3.r786
发表时间：
1999-09-01
影响因子：
2.8
作者：
Cheng, CL;Liu, JC;De Groat, WC
通讯作者：
De Groat, WC
影响因子：
2.9
作者：
CHENG, CL;MA, CP;DEGROAT, WC
通讯作者：
DEGROAT, WC
DOI：
10.1016/0165-1838(90)90105-r
发表时间：
1990-07-01
期刊：
JOURNAL OF THE AUTONOMIC NERVOUS SYSTEM
影响因子：
--
作者：
DEGROAT, WC;KAWATANI, M;ROPPOLO, JR
通讯作者：
ROPPOLO, JR
影响因子：
6.6
作者：
BENNETT, BC;KRUSE, MN;DEGROAT, WC
通讯作者：
DEGROAT, WC