Guan Kao-Ping, Yuan Zheng-Wei, Wang Wei-Lin, Gao Fei, Su Peng-Jun
Department of Pediatric Surgery, Shengjing Hospital of China Medical University, Shenyang 110004, China.
Zhonghua Yi Xue Za Zhi. 2007 Jan 9;87(2):131-3.
To quantitatively observe the sensory neurons innervating the levator ani muscle and explore the cause of poor post-operative anorectal function in patients with anorectal malformation (ARM).
Combining the microsurgery and microinjection techniques, we investigated the deficiency of sensory neurons of the spinal cord in fetal rats with anorectal malformation by injecting the retrograde tracer fluorogold (FG) into the muscle levator ani. Sixty 11 days pregnant female rats were fed with ethylenethiourea (ETU) so as to cause ARM in the fetuses. When the female rats were 20 days pregnant they underwent hysterectomy and the male fetal rats were taken out. Fluorogold (FG), a tracer, was injected into their levator ani muscles. Then the fetal rats were put back into the uteri. Twenty-four hours later hysterectomy was performed for the second time to take out and kill the live fetuses that had undergone FG injection. Their lumbo-sacral spinal cords were taken out, fixed and made into serial longitudinal sections. Digital camera system and fluorescent microscopy were used to observe the FG-labeled sensory neurons. Fifteen normal female rats were used as controls.
The FG-labeled sensory neurons innervating levator ani muscle were located mainly in the posterior root ganglia of the 5 th segment of lumber and the 1 st sacral cord. The number of FG-labeled sensory neurons in the normal control fetuses, fetuses without defect of the ETU-fed female rats, fetuses with low type imperforate anus, and fetuses with high type imperforate anus were 11 804 +/- 2362, 10 429 +/- 708, 2886 +/- 705, and 1026 +/- 425 respectively, the latter 2 number being significantly fewer than that in the fetuses without defects (P < 0.05) and that in the normal controls (P < 0.05).
Defective sensory neurons innervating the levator ani muscle co-exists with the alimentary tract anomaly in rat fetuses with ARM. The defective development of sensory neurons is an important factor likely to contribute to poor post-operative anorectal function despite surgical correction of the ARM.
定量观察支配肛提肌的感觉神经元,探讨肛门直肠畸形(ARM)患者术后肛门直肠功能不良的原因。
结合显微手术和显微注射技术,通过将逆行示踪剂荧光金(FG)注入肛提肌,研究肛门直肠畸形胎鼠脊髓感觉神经元的缺陷情况。60只怀孕11天的雌性大鼠喂食乙硫脲(ETU),以使胎儿发生ARM。当雌性大鼠怀孕20天时,进行子宫切除术并取出雄性胎鼠。将示踪剂荧光金(FG)注入其肛提肌。然后将胎鼠放回子宫。24小时后再次进行子宫切除术,取出并杀死接受过FG注射的活胎鼠。取出其腰骶脊髓,固定并制成连续纵切片。使用数码相机系统和荧光显微镜观察FG标记的感觉神经元。15只正常雌性大鼠作为对照。
支配肛提肌的FG标记感觉神经元主要位于腰5节段和骶1脊髓的后根神经节。正常对照胎鼠、未受ETU喂养的雌性大鼠所生无缺陷胎鼠、低位肛门闭锁胎鼠和高位肛门闭锁胎鼠中FG标记感觉神经元的数量分别为11 804±2362、10 429±708、2886±705和1026±425,后两者数量明显少于无缺陷胎鼠(P<0.05)和正常对照胎鼠(P<0.05)。
ARM胎鼠中支配肛提肌的感觉神经元缺陷与消化道异常并存。感觉神经元的发育缺陷是一个重要因素,可能导致尽管对ARM进行了手术矫正,但术后肛门直肠功能仍不良。