Brusa Livia, Petta Filomena, Pisani Antonio, Miano Roberto, Stanzione Paolo, Moschella Vincenzo, Galati Salvatore, Finazzi Agrò Enrico
Department of Neurology, University of Rome Tor Vergata, Rome, Italy.
J Urol. 2006 Jan;175(1):202-6; discussion 206-7. doi: 10.1016/S0022-5347(05)00058-3.
The different roles of D1 and D2 dopamine receptors in LUT behavior have been demonstrated in animal studies. In particular D2 selective agonists and D1 selective antagonists seem to produce a reduction of the bladder capacity in conscious rats. This finding has never been confirmed in human studies. Thus, in this study we investigated the role of D1 and D2 agonists/antagonists on LUT behavior in patients with PD.
A total of 87 patients with mild PD were evaluated. Patients were evaluated with urodynamic studies (cystometry followed by a pressure flow study with perineal floor electromyography) performed in off status and after oral administration of 250 mg of LD. In 70 patients a third urodynamic evaluation was conducted in one of the following conditions: after simultaneous administration of 250 mg oral LD and 60 or 120 mg oral domperidone (D2 peripheral antagonist); after simultaneous administration of 250 mg oral LD and 25, 50 or 150 mg intramuscular L-sulpiride (D2 central and peripheral antagonist). Several urodynamic parameters were evaluated and results obtained in different conditions compared.
LD alone worsened detrusor overactivity: in particular, a reduction of first urinary sensation, involuntary detrusor contraction threshold (reflex volume) and bladder capacity was observed. L-sulpiride (central and peripheral D2 antagonist) coadministration counteracted the worsening in a dose dependent manner. Domperidone (peripheral D2 antagonist) coadministration failed to determine the same counteraction.
According to our results, a central acute D2 stimulation seems to be responsible of a reduction of bladder capacity with worsening of detrusor overactivity in patients with mild PD.
动物研究已证实多巴胺D1和D2受体在膀胱尿道功能中的不同作用。特别是D2选择性激动剂和D1选择性拮抗剂似乎会使清醒大鼠的膀胱容量减小。这一发现从未在人体研究中得到证实。因此，在本研究中，我们调查了D1和D2激动剂/拮抗剂对帕金森病患者膀胱尿道功能的作用。
共评估了87例轻度帕金森病患者。患者在非服药状态下以及口服250 mg左旋多巴后接受尿动力学检查（膀胱测压，随后进行压力流率检查并同步记录盆底肌电图）。70例患者在以下其中一种情况下进行了第三次尿动力学评估：同时口服250 mg左旋多巴和60或120 mg口服多潘立酮（外周D2拮抗剂）后；同时口服250 mg左旋多巴和25、50或150 mg肌肉注射舒必利（中枢和外周D2拮抗剂）后。评估了多个尿动力学参数，并比较了不同情况下获得的结果。
单独使用左旋多巴会使逼尿肌过度活动恶化：特别是，首次排尿感觉、逼尿肌不自主收缩阈值（反射尿量）和膀胱容量均降低。联合使用舒必利（中枢和外周D2拮抗剂）可剂量依赖性地抵消这种恶化。联合使用多潘立酮（外周D2拮抗剂）未能产生同样的抵消作用。
根据我们的结果，中枢急性D2刺激似乎是导致轻度帕金森病患者膀胱容量减小和逼尿肌过度活动恶化的原因。
