Hanyu S, Iwanaga T, Kano K, Sato S
Department of Urology, Niigata University School of Medicine, Japan.
Urol Int. 1987;42(6):401-12. doi: 10.1159/000282004.
A pressure-flow study of the corpus cavernosum penis in the dog was performed during the flaccid, tumescent, erect and rigid stages. Perfusion was selectively made into the penile deep artery. The erect stage was induced with the local administration of papaverine hydrochloride, and the rigid stage by electrostimulation of the ischiocavernous muscle during the erect stage. Concurrently, vascular casts of the penis at each stage of erection were observed under a scanning electron microscope for the anatomical analysis of the mechanisms controlling cavernous pressure. In the pressure-flow study, it was demonstrated that a combination of decreased arterial resistance and restricted venous outflow was essential to both cause and maintain the erect state. The rigid stage was generated by contraction of the ischiocavernous muscle tightly compressing the crus penis. In the rigid stage, the cavernous pressure was elevated as high as five times the perfusion pressure; nevertheless, no backflow from the cavernous sinus to the deep artery was recognized. By use of the casts, it was confirmed that venous outflow restriction in the erect and rigid stages was due to compression of the postcavernous venules and penetrating veins in the tunica albuginea. The deep artery was occluded in the tunica albuginea in the casts made during the rigid stage, suggesting that the backflow from the corpus cavernosum penis to the deep artery was prevented by this occlusion. Therefore, in the rigid stage, the arterial and venous occlusion isolated the cavernous sinus from the systemic circulation; this mechanism seems to account for the maintenance of the extremely high cavernous pressure.
在犬阴茎海绵体的松弛、肿胀、勃起和坚硬阶段进行了压力-血流研究。选择性地向阴茎深动脉进行灌注。通过局部给予盐酸罂粟碱诱导勃起阶段，在勃起阶段通过电刺激坐骨海绵体肌诱导坚硬阶段。同时，在扫描电子显微镜下观察阴茎勃起各阶段的血管铸型，以对控制海绵体压力的机制进行解剖学分析。在压力-血流研究中，结果表明，动脉阻力降低和静脉流出受限相结合对于引起和维持勃起状态至关重要。坚硬阶段是由坐骨海绵体肌收缩紧密压迫阴茎脚产生的。在坚硬阶段，海绵体压力升高至灌注压力的五倍之高；然而，未发现从海绵窦向深动脉的逆流。通过使用铸型，证实勃起和坚硬阶段的静脉流出受限是由于白膜内海绵体后小静脉和穿通静脉受压所致。在坚硬阶段制作的铸型中，深动脉在白膜内被阻塞，这表明这种阻塞阻止了阴茎海绵体向深动脉的逆流。因此，在坚硬阶段，动脉和静脉阻塞使海绵窦与体循环隔离；这种机制似乎解释了极高海绵体压力的维持。
