下泌尿道主要功能為儲尿與週期性排尿，此功能需膀胱與尿道出口(包含膀胱頸、尿道與外尿道括約肌)兩單位呈現交互協調活動完成。大白鼠會陰神經（pudendal nerve）起源於第六腰椎至第一薦椎脊髓區間，此神經包含一條運動神經支配外尿道括約肌(external urethral sphincter)，以及一條感覺神經分支分佈在尿道周圍或外陰部區域。會陰神經切斷除了癱瘓外尿道括約肌的活動，同時也抑制會陰-膀胱反射(pudendal-bladder reflex)，因此造成尿道阻力下降、排尿效率低落，以及餘尿增加。
此研究主要目的是藉由損傷大白鼠會陰神經方式，建立一個兼具應力性尿失禁(stress urinary incontinence)以及尿液滯留(urine retention)的動物模式，然後利用此動物模式評估血清素藥物以及電刺激方式恢復下泌尿道功能的可行性。本研究主要包含四個實驗分別為，(1)建立慢性會陰神經損傷動物模式，(2)檢視會陰傳入與傳出神經在排尿反射過程中扮演的角色，(3)藥物治療恢復下泌尿道功能，以及(4)藉由電刺激會陰傳入神經方式增進下泌尿道功能。
本研究首先證實大白鼠接受會陰神經切斷六週後，明顯降低漏尿壓力點(leak point pressure)數值，並且產生不正常外尿道括約肌肌電圖(EUS-EMG)和膀胱壓力圖(cystometrograph) ，以上結果顯示神經損傷不只造成尿道阻力下降同時也會造成排尿效率低落，因此會陰神經切斷是一個適合做為應力性尿失禁與尿液滯留研究使用的動物模式。後續實驗則進一步證明，一個有效率的膀胱排尿反射，會陰感覺神經與運動神經兩者皆扮演相當重要的角色；然而會陰傳入(afferents)神經與會陰傳出(efferents)神經相較之下，排尿效率似乎主要由會陰傳入神經主宰。另一方面，以8-OH-DPAT施打於我們所建立的會陰神經損傷動物模式時，明顯改變整個外尿道括約肌肌電圖活動型式，並且增進排尿效率，但卻沒有明顯提升膀胱出口阻力，這可能是由於會陰神經切斷後造成永久的會陰-交感神經反射損傷。最後，本研究結果顯示狀態性(conditional)與連續性(continuous)的會陰傳入神經電刺激施行於急性會陰神經損傷大白鼠，藉由調控電流大小可以達成選擇性控制膀胱儲尿與排尿的目的。
綜合言之，本研究提供我們更深入瞭解大白鼠會陰傳入與傳出神經在排尿反射所扮演的角色，而我們所建立的會陰神經損傷模式，未來則可更進一步應用於各種應力性尿失禁與尿液滯留相關研究。另一方面8-OH-DPAT增進排尿效率但是並沒有明顯提升膀胱出口阻力數值，此結果與臨床上病灶於會陰神經損傷的尿失禁病患，使用duloxetine的藥物時常產生不同的治療效果，有顯著臨床相關意義，然而未來仍需進一步進行電生理的實驗，探討改變血清素藥物的效果的生理機制。此外，電刺激會陰傳入神經成功地選擇性控制膀胱功能，顯示會陰神經電刺激在未來或許可以提供尿液滯留病患以及其他下泌尿道障礙病人一種新的電刺激模式。

The primary functions of the lower urinary tract (LUT) are storage and periodic elimination of urine. These functions require reciprocal coordination of the urinary bladder and the outlet including bladder neck, urethra, and external urethral sphincter (EUS). The pudendal nerve in rat originated from L6-S1 nerve trunk, which contains one motor branch innervated the EUS muscle and one sensory branch innervated sensory receptors of periurethral or genital areas. Transection of pudendal nerves could eliminate the EUS activity and pudendal-bladder reflex, which leads to decrease urethral outlet resistance and voiding efficiency as well as increase residual urine.
The main objectives in this study are to setup a stress urinary incontinence (SUI) and a urine retention models in the rat by pudendal nerve injury, and then we utilize the animal models to evaluate the possibility of using serotonergic agent and electrical stimulation approaches to restore the LUT functions. Four major experiments were conducted in this study: (1) the setup of chronic pudendal nerve injured animal model; (2) examination of roles of pudendal nerve afferents and efferents in micturition reflexes; (3) restoration of LUT functions by pharmacological treatment and (4) improvement of LUT functions by electrical stimulation of pudendal afferents.
Our results initially demonstrated that 6 weeks following pudendal nerve transections, rats exhibit a marked reduction in leak point pressure (LPP) values as well as abnormal EUS-electromyogram (EMG) and cystometrograph (CMG), which indicated the decrease in bladder outlet resistance and inefficient voiding. Thus, our results indicated that pudendal nerve transection(s) is a suitable animal model to study SUI as well as urine retention. Subsequent experiments manifested that the roles of pudendal sensory and motor components both appear to be important for an efficient bladder emptying reflex. However, the voiding efficiency seems to be dominated by pudendal nerve afferents rather than pudendal nerve efferents. On the other hand, 8-OH-DPAT significantly altered the patterns of EUS-EMG activity and improved voiding efficiency in our established pudendal nerve injured rat model but did not elevate the bladder outlet resistance which may be due to the permanent impairment of pudendal-lumbar sympathetic reflex after pudendal nerve transections. Finally, the study showed that both conditional and continuous electrical stimulation of pudendal nerve afferents could selectively control bladder continence and emptying by adjusting the stimulation strengths in acute pudendal nerve injured rats.
In summary, the present study contributes to the understanding of the role of pudendal nerve afferents and efferents in micturition reflexes in the rat. Furthermore, our developed pudendal nerve injured model could further be applied in various studies related to SUI or urine retention. 8-OH-DPAT did not elevate the value of bladder outlet resistance but improved voiding efficiency, which is clinically relevant because subjects with SUI induced by pudendal nerve damage the drugs like duloxetine might have different effects. Thus, further electrophysiological experiments are needed to investigate the physiological mechanisms of the changes in the effect of 5-HT drugs. In addition the electrical stimulation of pudendal nerve afferents was successfully applied to selectively control bladder functions. Our results support that the pudendal nerve stimulation may provide a new stimulation scheme to restore bladder emptying in persons with urinary retention as well as other LUT dysfunctions.

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