el-Salmy S, Downie J W, Awad S A
J Urol. 1985 Nov;134(5):1011-8. doi: 10.1016/s0022-5347(17)47578-1.
The failure of bethanechol chloride to induce voiding in patients with neurogenic bladder, despite a positive bethanechol test, is being reported more frequently. An experimental model was designed in the cat to study the response of the bladder and urethra to subcutaneous and intraarterial bethanechol after complete and partial sacral decentralization. Complete sacral rhizotomy abolished the micturition reflex. Basal urethral perfusion pressure was not affected by complete sacral rhizotomy and a significant part of this basal urethral pressure remained sympathetically mediated. However, the urethral constriction response to bladder filling was lost in half the cats with complete lesions. Bladder and urethral supersensitivity to bethanechol chloride in cats with complete lesions was characterized by a shift to the left of the i.a. dose-response curve, and by the presence of responses to doses of s.c. bethanechol chloride which are subthreshold in normal cats. The urethra also showed exaggerated constriction responses to i.a. and s.c. bethanechol. After complete lesions a part of the bladder and urethral responses to s.c. bethanechol was adrenergically mediated and exerted through the vesicourethral short neuron system. The rest of the response was due to stimulation of urethral muscarinic receptors. Partial sacral lesions were compatible with a micturition reflex and the urethra retained its reflex response to bladder distension. After partial decentralization the bladder and urethra also showed responses to subthreshold doses of s.c. bethanechol. While the bladder response to s.c. bethanechol did not show a significant adrenergic component in cats with partial lesions, most of the urethral response was sympathetically mediated. In conclusion, complete cauda equina lesions result in an areflexic detrusor with frequent loss of the urethral responsiveness to bladder filling. Urethral supersensitivity to s.c. bethanechol might be responsible for a non-voiding outcome after bethanechol injection in patients with complete cauda equina lesions, despite a positive bethanechol test. Because the detrusor reflex is preserved and the urethra is less supersensitive to bethanechol after partial cauda equina lesions, these may represent a better indication for bethanechol therapy than do complete ones.
尽管氯贝胆碱试验呈阳性,但氯贝胆碱仍无法促使神经源性膀胱患者排尿,这种情况的报道日益增多。我们设计了一个猫实验模型,以研究在完全性和部分性骶神经去传入后,膀胱和尿道对皮下及动脉内注射氯贝胆碱的反应。完全性骶神经根切断术消除了排尿反射。完全性骶神经根切断术未影响基础尿道灌注压,且该基础尿道压力的很大一部分仍由交感神经介导。然而,在半数有完全性损伤的猫中,尿道对膀胱充盈的收缩反应丧失。完全性损伤猫的膀胱和尿道对氯贝胆碱超敏,表现为动脉内给药剂量 - 反应曲线左移,以及对皮下注射氯贝胆碱剂量产生反应,而该剂量在正常猫中是阈下剂量。尿道对动脉内和皮下注射氯贝胆碱也表现出过度收缩反应。完全性损伤后,膀胱和尿道对皮下注射氯贝胆碱的部分反应由肾上腺素能介导,并通过膀胱 - 尿道短神经元系统发挥作用。其余反应是由于尿道毒蕈碱受体受到刺激。部分性骶神经损伤与排尿反射相容,且尿道保留了对膀胱扩张的反射反应。部分去传入后,膀胱和尿道对皮下注射氯贝胆碱的阈下剂量也有反应。虽然部分损伤猫的膀胱对皮下注射氯贝胆碱的反应未显示出明显的肾上腺素能成分,但尿道的大部分反应由交感神经介导。总之,完全性马尾损伤导致逼尿肌无反射,且尿道对膀胱充盈的反应性常丧失。完全性马尾损伤患者注射氯贝胆碱后无排尿结果,尽管氯贝胆碱试验呈阳性,尿道对皮下注射氯贝胆碱超敏可能是其原因。由于部分性马尾损伤后逼尿肌反射保留,且尿道对氯贝胆碱的超敏性较低,与完全性损伤相比,这些损伤可能是氯贝胆碱治疗的更好指征。