Qin Chao, Malykhina Anna P, Akbarali Hamid I, Foreman Robert D
Department of Physiology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma 73190, USA.
Gastroenterology. 2005 Dec;129(6):1967-78. doi: 10.1053/j.gastro.2005.09.013.
BACKGROUND & AIMS: Clinical studies show that patients with irritable bowel syndrome and colonic diseases frequently experience sensory and motor dysfunctions of the urinary bladder. The aim of this study was to investigate the spinal neuronal mechanisms responsible for potential cross talk between these visceral organs.
Colonic inflammation was induced by dextran sulfate sodium (5%) in drinking water for 7-12 days (n = 12); another group of rats without dextran sulfate sodium (n = 12) was used as control. Extracellular potentials of single L6 to S2 spinal neurons were recorded in pentobarbital-anesthetized and paralyzed rats with dextran sulfate sodium-induced colitis or normal colon. Urinary bladder distention (0.5-2.0 mL; 20 seconds) was produced with saline inflation, and colorectal distention was induced by inflation of an air balloon (80 mm Hg; 20 seconds).
A total of 58 of 153 (38%) and 55 of 152 (36%) spinal neurons responded to urinary bladder distention in dextran sulfate sodium-treated and control animals, respectively. The mean background activity of neurons excited by urinary bladder distention in rats with dextran sulfate sodium-induced colitis was significantly higher than in the control group. The threshold volume for excitatory responses to urinary bladder distention in rats with inflamed colon (0.024 +/- 0.09 mL; n = 30) was significantly lower than for control rats (0.062 +/- 0.016 mL; n = 31; P < .05). The stimulus-response curves of excitatory responses to graded urinary bladder distention were significantly increased for both viscerovisceral (urinary bladder distention and colorectal distention) convergent neurons and urinary bladder distention-receptive neurons in rats with colitis compared with control animals.
Acute colitis sensitized lumbosacral spinal neurons receiving input from the urinary bladder. Thus, spinal neuronal hyperexcitability may be involved in central cross-organ sensitization of visceral nociception between the colon and urinary bladder.
临床研究表明,肠易激综合征和结肠疾病患者经常出现膀胱感觉和运动功能障碍。本研究的目的是探讨这些内脏器官之间潜在相互作用的脊髓神经元机制。
通过在饮用水中加入5%的葡聚糖硫酸钠诱导结肠炎症7 - 12天(n = 12);另一组未加入葡聚糖硫酸钠的大鼠(n = 12)作为对照。在戊巴比妥麻醉并麻痹的葡聚糖硫酸钠诱导结肠炎或正常结肠大鼠中记录单个L6至S2脊髓神经元的细胞外电位。用生理盐水充盈产生膀胱扩张(0.5 - 2.0 mL;20秒),通过气囊充气诱导结肠扩张(80 mmHg;20秒)。
在葡聚糖硫酸钠处理的动物和对照动物中,分别有153个中的58个(38%)和152个中的55个(36%)脊髓神经元对膀胱扩张有反应。葡聚糖硫酸钠诱导结肠炎大鼠中由膀胱扩张激发的神经元的平均背景活动显著高于对照组。结肠发炎大鼠对膀胱扩张的兴奋性反应的阈值体积(0.024 ± 0.09 mL;n = 30)显著低于对照大鼠(0.062 ± 0.016 mL;n = 31;P < 0.05)。与对照动物相比,结肠炎大鼠中内脏 - 内脏(膀胱扩张和结肠扩张)汇聚神经元和膀胱扩张感受神经元对分级膀胱扩张的兴奋性反应的刺激 - 反应曲线显著增加。
急性结肠炎使接受膀胱输入的腰骶脊髓神经元敏感化。因此,脊髓神经元的过度兴奋可能参与结肠和膀胱之间内脏痛觉的中枢跨器官敏感化。