Investigation on mucosa-derived substance that enhances spontaneous contractions of the urinary bladder in the rat with bladder outlet obstruction

我们检测了在膀胱出口梗阻（BOO）大鼠中，粘膜源性物质可以增强膀胱自发收缩（SCs）。BOO大鼠膀胱条中的SCs与体外粘膜释放的前列腺素（PG） E2的量有关；BOO大鼠体内粘膜释放的PGE2的量增加；体内被认为是膀胱壁上SCs的代用物的非排尿收缩（NVC）与粘膜源性PGE2有关。增强SCs的粘膜源性物质可能是PGE2。我们还发现，支配下尿路的完整神经系统的存在和膀胱壁环氧化酶-2表达的上调与BOO诱导的粘膜PGE2释放量的增加有关。

We examined what the mucosa-derived substance that can act to enhance spontaneous contractions (SCs) of the urinary bladder is in the rat with bladder outlet obstruction (BOO).The SCs in bladder strips from BOO rats were associated with the amount of prostaglandin (PG) E2 released from the mucosa in vitro: The amount of PGE2 released from the mucosa was increased in BOO rats in vivo: The non-voiding contraction (NVC) that was regarded as a surrogate of SCs in the bladder wall in vivo was associated with mucosa-derived PGE2. The mucosa-derived substance to enhance SCs may be PGE2. We also found out that the presence of the intact nervous system innervating lower urinary tract and the up-regulation of the expression of cyclooxygenase-2 in the bladder wall were associated with the increased amount of PGE2 released from the mucosa induced by BOO.