Kumsar Şükrü, Keskin Ulya, Akay Alaaddin, Bilgilisoy Uğur Taylan, Erdem Ş Remzi, Peşkircioğlu Ç Levent, Özkardeş Hakan
Urology Department, Sakarya Training and Research Hospital, Sakarya, Turkey.
Neuromodulation. 2015 Jan;18(1):67-74; discussion 74-5. doi: 10.1111/ner.12189. Epub 2014 Jun 10.
Sacral neuromodulation has been considered as an effective treatment option for various types of chronic voiding dysfunction, but the mechanism of action has not been well understood. The aim of this study was to evaluate the effect of chronic sacral neuromodulation on isolated bladder functions in a rat model of spinal cord injury.
Female Sprague-Dawley rats (250-300 g; N = 20) were assigned to four groups as follows: 1) control group (N = 6); 2) spinal cord transection group (SCT; N = 5); 3) spinal cord transection + sacral neuromodulation group (SCT + SNM; N = 5); 4) sham (spinal cord transection + electrode wire implantation without sacral neuromodulation; N = 4). The rats in the SCT, SCT + SNM, and sham groups were anesthetized with ketamine (60 mg/kg, i.p.) and xylazine (7 mg/kg, i.p.). The spinal cord was completely transected at T8-T9 level in SCT and SCT + SNM groups. Electrode wires were implanted into S3 dorsal foramina in both sham and SNM groups, but only the SNM group was subjected to electrical stimulation for four hours a day for three weeks. Twenty-one days later, the rats were sacrificed via anesthetic overdose, and isolated longitudinal bladder strip preparations were placed in organ baths for the investigation of their isometric responses to pharmacological agents.
In isometric contraction experiments, SCT was found to increase the contraction responses of the bladder strips to muscarinic stimulation, and SNM could not prevent this increase. In isometric relaxation experiments, SCT caused a decrease in β-adrenergic relaxation responses, and SNM augmented the bladder's β-adrenergic relaxation responses. Nitric oxide did not affect the relaxation responses.
In our rat model of SCT, SNM seemed to alter adrenergic receptor function in the urinary bladder. Further studies are required to clarify the mechanism of these alterations at the level of bladder receptors following sacral neuromodulation.
骶神经调节已被视为治疗各种类型慢性排尿功能障碍的一种有效选择，但作用机制尚未完全明确。本研究的目的是评估慢性骶神经调节对脊髓损伤大鼠模型中离体膀胱功能的影响。
将雌性斯普拉格-道利大鼠（250 - 300克；N = 20）分为以下四组：1）对照组（N = 6）；2）脊髓横断组（SCT；N = 5）；3）脊髓横断 + 骶神经调节组（SCT + SNM；N = 5）；4）假手术组（脊髓横断 + 植入电极丝但未进行骶神经调节；N = 4）。SCT组、SCT + SNM组和假手术组的大鼠用氯胺酮（60毫克/千克，腹腔注射）和赛拉嗪（7毫克/千克，腹腔注射）麻醉。SCT组和SCT + SNM组在T8 - T9水平完全横断脊髓。假手术组和SNM组均将电极丝植入S3背侧椎间孔，但只有SNM组每天接受4小时电刺激，持续3周。21天后，通过过量麻醉处死大鼠，将离体的膀胱纵行肌条标本置于器官浴槽中，研究其对药理学试剂的等长反应。
在等长收缩实验中，发现SCT可增加膀胱条对毒蕈碱刺激的收缩反应，而SNM无法阻止这种增加。在等长舒张实验中，SCT导致β - 肾上腺素能舒张反应降低，而SNM增强了膀胱的β - 肾上腺素能舒张反应。一氧化氮不影响舒张反应。
在我们的SCT大鼠模型中，SNM似乎改变了膀胱中的肾上腺素能受体功能。需要进一步研究以阐明骶神经调节后膀胱受体水平这些改变的机制。
