Effects of anaesthesia on the nitrergic pathway during the micturition reflex in rats.
Effects of anaesthesia on the nitrergic pathway during the micturition reflex in rats.
复制标题
麻醉对大鼠排尿反射过程中氮能通路的影响。
DOI：
10.1111/j.1464-410x.2007.06872.x
复制
发表时间：
2007
影响因子：
4.5
通讯作者：
Yoshimura,Naoki
中科院分区：
文献类型：
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作者：
Masuda,Hitoshi;Ogawa,Teruyuki;Kihara,Kazunori;Chancellor,MichaelB;deGroat,WilliamC;Yoshimura,Naoki
目的探讨麻醉对大鼠排尿反射过程中氮能通路的影响。材料与方法采用等容灌注膀胱测压法（CMG）和尿道灌注压法，观察一氧化氮（NO）合酶抑制剂L-硝基-L-精氨酸甲酯（L-NAME）对清醒或氨基甲酸乙酯麻醉大鼠膀胱和尿道活动的影响。静脉内（i. v.）给予L-NAME，鞘内（i.t.），侧脑室注射或膀胱内注射或预先用树脂毒素（一种强效C纤维传入神经毒素）处理的大鼠。静脉注射CITSL ‐NAME可缩短清醒大鼠的收缩间期（ICI），但增加麻醉大鼠的ICI。L-NAME i.t.注射增加了两种状态下的ICI，并且在用树脂毒素预处理后，这些影响不明显。静脉注射L-NAME可降低清醒时的ICI，但增加i.t.在麻醉的大鼠中。膀胱内注射L-NAME可降低清醒大鼠的ICI，但对麻醉大鼠无影响。静脉注射L-NAME，但不是IT。或静脉注射，CMG期间膀胱收缩增加。在等容条件下，静脉注射L-NAME，但不是IT。或静脉注射，结论这些结果表明，脊髓NO的释放有利于机械感受性C纤维，这种促进作用被掩盖的脊髓上（可能是前脑）和局部抑制作用的NO在清醒大鼠排尿反射。氨基甲酸乙酯似乎抑制脊髓上和局部抑制作用的NO，从而揭示了在脊髓和脑干的易化作用的NO。在排尿期，尿道松弛依赖于外周而不是中枢NO系统。
OBJECTIVETo investigate the effects of anaesthesia on the nitrergic pathway during the micturition reflex in rats.MATERIALS AND METHODSThe effects of NG‐nitro‐l‐arginine methyl ester (L‐NAME), an inhibitor of nitric oxide (NO) synthase, on bladder and urethral activities were evaluated by infusion cystometrography (CMG) and urethral perfusion pressure under isovolumetric conditions in awake or urethane‐anaesthetized rats. L‐NAME was administered intravenously (i.v.), intrathecally (i.t.), intracerebroventriculary (i.c.v.) or intravesically in normal rats or rats pre‐treated with resiniferatoxin, a potent C‐fibre afferent neurotoxin.RESULTSL‐NAME injected i.v. decreased the intercontraction interval (ICI) in the awake but increased it in the anaesthetized rats. L‐NAME injected i.t. increased the ICI in both states and these effects were not apparent after pre‐treatment with resiniferatoxin. L‐NAME injected i.c.v. decreased the ICI in the awake but increased i.t. in the anaesthetized rats. Intravesical L‐NAME decreased the ICI in the awake but not in the anaesthetized rats. L‐NAME administered i.v., but not i.t. or i.c.v., increased bladder contraction during CMG. Under isovolumetric conditions, L‐NAME administered i.v., but not i.t. or i.c.v., reduced the urethral relaxation without changing bladder contraction.CONCLUSIONSThese results indicate that spinal NO release facilitates the mechanoceptive C‐fibres, and this facilitatory effect is masked by supraspinal (possibly forebrain) and local inhibitory effects of NO during the micturition reflex in awake rats. Urethane seems to inhibit the supraspinal and local inhibitory effects of NO, resulting in unmasking the facilitatory effect of NO in the spinal cord and brain stem. During the voiding phase, urethral relaxation depends on the peripheral but not the central NO system.