Wegner H E, Knispel H H
Department of Urology, Universitätsklinikum Steglitz, Freie Universität Berlin, Germany.
Urology. 1993 Oct;42(4):409-11. doi: 10.1016/0090-4295(93)90371-g.
Recent experimental work has demonstrated that nitric oxide (NO) is the neurotransmitter responsible for cavernous smooth muscle relaxation. We studied the effect of a direct NO-donor, linsidomine chlorhydrate (SIN-1), in 30 patients with venous leakage confirmed by dynamic pharmacocavernosography and pharmacocavernosometry that was refractory to prostaglandin E1 (PGE1) under the assumption that the more physiologic approach might give better results. In all 30 patients, response to SIN-1 was no better, and in 22 cases it was less than the response to PGE1. No systemic or local side effects of SIN-1 were observed. SIN-1 is not superior to PGE1 in the treatment of erectile dysfunction caused by venous leakage, and failure of NO-mediated smooth muscle relaxation does not play a part in the entity, "venous leakage."
近期的实验研究表明，一氧化氮（NO）是导致海绵体平滑肌松弛的神经递质。我们对30例经动态海绵体药物造影和药物海绵体测压确诊为静脉漏且对前列腺素E1（PGE1）治疗无效的患者，研究了直接NO供体盐酸林西多明（SIN - 1）的疗效，我们的假设是采用更符合生理机制的方法可能会取得更好的效果。在所有30例患者中，SIN - 1的疗效并不优于PGE1，22例患者对SIN - 1的反应比PGE1差。未观察到SIN - 1有全身或局部副作用。在治疗由静脉漏引起的勃起功能障碍方面，SIN - 1并不优于PGE1，且NO介导的平滑肌松弛功能障碍在“静脉漏”这一病症中不起作用。
