Knuppe Molecular Urology Laboratory, Department of Urology, University of California, San Francisco, USA.
BJU Int. 2011 Dec;108(11):1866-72. doi: 10.1111/j.1464-410X.2011.10162.x. Epub 2011 Sep 2.
What's known on the subject? and what does the study add? Increased cavernous smooth muscle content has been repeatedly observed in rat models of hyperlipidaemia - associated erectile dysfunction. This study shows that the increased smooth muscle content is due to hyperplasia.
• To investigate the structural changes, including possible smooth muscle hyperplasia, in the penis of a hyperlipidaemia-associated erectile dysfunction (ED) animal model.
• Hyperlipidaemia was induced in rats through a high-fat diet. • Penile tissues of normal and hyperlipidaemic rats were stained with Alexa-488-conjugated phalloidin and/or with antibodies against rat endothelial cell antigen, neuronal nitric oxide synthase (nNOS), and collagen type IV (Col-IV) before image and statistical analyses were carried out. • The main outcome measures were the smooth muscle, endothelial, Col-IV and nNOS content of the corpus cavernosum.
• Phalloidin intensely stained all smooth muscle in the penis, revealing the circular and longitudinal components of cavernous smooth muscle (CSM). • The CSM content was significantly higher in the hyperlipidaemic than in the normal rats (P < 0.05). • Cell numbers in both circular and longitudinal CSM were significantly higher in the hyperlipidaemic than in the normal rats (P < 0.05). • Cavernous endothelial content was significantly lower in hyperlipidaemic than in normal rats (P < 0.05). • nNOS-positive nerves within the dorsal nerves, around the dorsal arteries, and in the corpora cavernosa were all significantly lower in the hyperlipidaemic than in the normal rats (P < 0.05).
• Hyperlipidaemia is associated with reduced nNOS-positive nerves, reduced endothelium, and increased CSM in the penis. • The increased CSM is attributable to hyperplasia. • These structural changes may explain why hyperlipidaemic men are more likely to develop ED.
•研究高脂血症相关勃起功能障碍(ED)动物模型阴茎的结构变化,包括可能的平滑肌增生。
•通过高脂肪饮食诱导大鼠高脂血症。•正常和高脂血症大鼠的阴茎组织用 Alexa-488 缀合的鬼笔环肽和/或针对大鼠内皮细胞抗原、神经元型一氧化氮合酶(nNOS)和胶原 IV(Col-IV)的抗体染色,然后进行图像和统计分析。•主要观察指标为海绵体平滑肌、内皮细胞、Col-IV 和 nNOS 含量。
•鬼笔环肽强烈染色阴茎中的所有平滑肌,显示出海绵体平滑肌(CSM)的环形和纵向成分。•高脂血症大鼠的 CSM 含量明显高于正常大鼠(P<0.05)。•高脂血症大鼠的环形和纵向 CSM 细胞数均明显高于正常大鼠(P<0.05)。•高脂血症大鼠的海绵体内皮细胞含量明显低于正常大鼠(P<0.05)。•背神经、背动脉周围和海绵体中的 nNOS 阳性神经在高脂血症大鼠中明显低于正常大鼠(P<0.05)。
•高脂血症与阴茎中 nNOS 阳性神经减少、内皮减少和 CSM 增加有关。•增加的 CSM 归因于增生。•这些结构变化可能解释为什么高脂血症男性更容易发生 ED。