Kempinas W D, Suarez J D, Roberts N L, Strader L F, Ferrell J, Goldman J M, Narotsky M G, Perreault S D, Evenson D P, Ricker D D, Klinefelter G R
Departamento de Morfologia, Instituto de Biociências - UNESP, Botucatu, SP, Brazil.
Biol Reprod. 1998 Oct;59(4):897-904. doi: 10.1095/biolreprod59.4.897.
Guanethidine, a chemical that selectively blocks sympathetic noradrenergic neurons, was used to investigate the role of sympathetic innervation in the fertility of rat epididymal sperm, using both natural mating and in utero insemination protocols. This animal model correlates, at least in part, with spinal cord injury (SCI) in men. Adult male rats were treated daily by i.p. injections, for 21 or 42 days, with 0 or 6.25 mg/kg guanethidine. To compare the effects of guanethidine-induced sympathectomy with those following surgically induced sympathectomy, the inferior mesenteric ganglion and the proximal hypogastric nerves were removed in another group of rats. Both chemically and surgically induced sympathectomy increased the weight of the epididymis and seminal vesicles/coagulating glands as well as the number and the transit time of cauda epididymal sperm. Neither serum testosterone levels nor LH was affected by treatment with guanethidine. Using natural mating, no litters were produced by guanethidine-treated rats. Chemically denervated rats failed to produce copulatory plugs or ejaculate into the uterus. However, distal cauda epididymal sperm from chemically or surgically denervated rats displayed normal fertilization ability (80%) using in utero inseminations. In addition, the sperm of denervated rats did not show abnormal sperm chromatin structure using an assay that detects DNA damage. We conclude that sympathectomy delays the transit of sperm through the cauda epididymidis and produces ejaculatory dysfunction but does not compromise sperm quality in the distal cauda epididymidis. Moreover, these data provide compelling evidence that there is no association between the prolonged transit time of sperm within the epididymis, i.e., pre-ejaculatory sperm aging, and the fertility of those sperm, which has important implications for artificial insemination using sperm from men with SCI.
胍乙啶是一种能选择性阻断交感去甲肾上腺素能神经元的化学物质，本研究使用自然交配和子宫内授精方案，探讨交感神经支配在大鼠附睾精子生育能力中的作用。该动物模型至少部分与男性脊髓损伤（SCI）相关。成年雄性大鼠每天经腹腔注射0或6.25mg/kg胍乙啶，持续21或42天。为比较胍乙啶诱导的交感神经切除术与手术诱导的交感神经切除术后的效果，另一组大鼠切除了肠系膜下神经节和近端腹下神经。化学和手术诱导的交感神经切除术均增加了附睾、精囊/凝固腺的重量以及附睾尾精子的数量和转运时间。胍乙啶治疗对血清睾酮水平和促黄体生成素均无影响。使用自然交配时，胍乙啶处理的大鼠未产仔。化学去神经支配的大鼠未能产生交配栓或射精到子宫内。然而，使用子宫内授精时，化学或手术去神经支配大鼠的附睾尾远端精子显示出正常的受精能力（80%）。此外，使用检测DNA损伤的试验，去神经支配大鼠的精子未显示异常的精子染色质结构。我们得出结论，交感神经切除术会延迟精子通过附睾尾的转运并导致射精功能障碍，但不会损害附睾尾远端精子的质量。此外，这些数据提供了令人信服的证据，即精子在附睾内的转运时间延长，即射精前精子老化，与这些精子的生育能力之间没有关联，这对使用脊髓损伤男性的精子进行人工授精具有重要意义。
