Ikeda Makoto, Kawatani Masahito, Maruyama Takayuki, Ishihama Hiroko
Department of Neurophysiology, Akita University School of Medicine, Akita, Japan.
Biomed Res. 2006 Apr;27(2):49-54. doi: 10.2220/biomedres.27.49.
We examined the effects of loxoprofen, a cyclooxygenase inhibitor, and ONO-8711, an EP1-receptor antagonist, on afferent nerve activity during acetic acid (AA, 0.1% v/v)-induced inflammation of the rat urinary bladder. Distension stimulation was performed (vesical pressure of 30 cm H2O) for 2 min. The neuronal discharge was recorded from L6 dorsal root filaments. The discharge was observed just after the beginning of distension and increased gradually thereafter. When the vesical pressure returned to control value, the discharge diminished abruptly. AA infusion increased the total number of spikes to 198 +/- 38.8% of control values. AA infusion also produced asynchronous discharge in 39% of the animals. Loxoprofen administration (1 mg/kg, i.v.) reduced the number of spikes to 40.3 +/- 14.8% of control values. ONO-8711 administration (1 and 3 mg/kg, i.v.) reduced the number of spikes to 81.6 +/- 1.6% and 32.2 +/- 7.4% of control values, respectively. These data indicate that loxoprofen or EP1-receptor antagonist inhibit the inflammation-related neuronal activity. EP1 receptors in the peripheral afferent nerve terminal and/or urothelium may facilitate the primary afferent nerve activity, which elicits the inflammation-induced micturition reflex.
我们研究了环氧化酶抑制剂洛索洛芬和EP1受体拮抗剂ONO-8711对大鼠膀胱在乙酸(AA,0.1% v/v)诱导的炎症过程中传入神经活动的影响。进行扩张刺激(膀胱压力为30 cm H2O)2分钟。从L6背根细丝记录神经元放电。在扩张开始后立即观察到放电,并在此后逐渐增加。当膀胱压力恢复到对照值时,放电突然减少。注入AA使总尖峰数增加到对照值的198 +/- 38.8%。注入AA还在39%的动物中产生了异步放电。静脉注射洛索洛芬(1 mg/kg)使尖峰数减少到对照值的40.3 +/- 14.8%。静脉注射ONO-8711(1和3 mg/kg)分别使尖峰数减少到对照值的81.6 +/- 1.6%和32.2 +/- 7.4%。这些数据表明,洛索洛芬或EP1受体拮抗剂抑制炎症相关的神经元活动。外周传入神经末梢和/或尿路上皮中的EP1受体可能促进初级传入神经活动,从而引发炎症诱导的排尿反射。