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大鼠结肠刺激使膀胱传入神经对机械和化学刺激敏感:盆腔器官交叉致敏的传入神经起源

Colonic irritation in the rat sensitizes urinary bladder afferents to mechanical and chemical stimuli: an afferent origin of pelvic organ cross-sensitization.

作者信息

Ustinova Elena E, Fraser Matthew O, Pezzone Michael A

机构信息

Division of Gastroenterology, Hepatology, and Nutrition, Univ. of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA.

出版信息

Am J Physiol Renal Physiol. 2006 Jun;290(6):F1478-87. doi: 10.1152/ajprenal.00395.2005. Epub 2006 Jan 10.

Abstract

Chronic pelvic pain (CPP) disorders frequently overlap. We have demonstrated that acute and chronic colonic irritation can lead to neurogenic cystitis. We hypothesize that acute colonic irritation can sensitize urinary bladder afferents to mechanical and chemical stimuli. Single-unit afferent activity was recorded from fine filaments of the pelvic nerve in urethane-anesthetized Sprague-Dawley female rats before and 1 h after intracolonic administration of trinitrobenzenesulfonic acid (TNBS). Only spontaneously active afferents with receptive fields in the bladder and conduction velocities <2.5 m/s (unmyelinated C-fibers) were studied. Mechanical sensitivity was tested by bladder distension (BD) during saline infusion, whereas chemical sensitivity was tested with intravesical capsaicin, bradykinin, or substance P. Colonic irritation increased the resting firing rate of bladder afferents twofold (1.0 +/- 0.2 vs. 0.49 +/- 0.2 impulses/s, P < 0.05). Moreover, at low-pressure BDs (10-20 mmHg), a greater percentage of afferents exhibited increased activity following TNBS (73 vs. 27%, P < 0.05). Although the magnitude of the afferent response to BD was unchanged at low pressures, the response was greatly enhanced at pressures 30 mmHg and above (2.36 +/- 0.56 vs. 8.55 +/- 0.73 impulses/s, P < 0.05). Responses to capsaicin, bradykinin, and substance P were also significantly enhanced following TNBS, and all responses were blocked by bladder denervation. In rats, colonic irritation sensitizes urinary bladder afferents to noxious mechanical and chemical stimuli. Interruption of the neural input to the bladder minimized this effect, suggesting a local afferent pathway from the colon. Thus, the overlap of CPP disorders may be a consequence of pelvic afferent cross-sensitization.

摘要

慢性盆腔疼痛(CPP)疾病常常相互重叠。我们已经证明,急性和慢性结肠刺激可导致神经源性膀胱炎。我们推测,急性结肠刺激可使膀胱传入神经对机械和化学刺激敏感。在给氨基甲酸乙酯麻醉的Sprague-Dawley雌性大鼠结肠内注射三硝基苯磺酸(TNBS)之前和之后1小时,从盆腔神经的细丝记录单单位传入活动。仅研究在膀胱中有感受野且传导速度<2.5 m/s(无髓鞘C纤维)的自发活动传入神经。在生理盐水输注期间通过膀胱扩张(BD)测试机械敏感性,而用膀胱内辣椒素、缓激肽或P物质测试化学敏感性。结肠刺激使膀胱传入神经的静息放电率增加两倍(1.0±0.2对0.49±0.2脉冲/秒,P<0.05)。此外,在低压BD(10-20 mmHg)时,TNBS后有更大百分比的传入神经表现出活动增加(73%对27%,P<0.05)。虽然在低压下对BD的传入反应幅度未改变,但在30 mmHg及以上压力时反应大大增强(2.36±0.56对8.55±0.73脉冲/秒,P<0.05)。TNBS后对辣椒素、缓激肽和P物质的反应也显著增强,并且所有反应都被膀胱去神经支配所阻断。在大鼠中,结肠刺激使膀胱传入神经对有害的机械和化学刺激敏感。中断膀胱的神经输入可使这种效应最小化,提示存在从结肠来的局部传入通路。因此,CPP疾病的重叠可能是盆腔传入神经交叉致敏的结果。

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