Department of Surgery, University of California, Los Angeles, CA 90095, USA.
J Pediatr Surg. 2010 Dec;45(12):2408-11. doi: 10.1016/j.jpedsurg.2010.08.045.
BACKGROUND/PURPOSE: The anorectal spasticity in Hirschsprung disease may be caused by the absence of enteric ganglia and/or the presence of hypertrophic nerves. Anorectal manometry of chemically denervated rectums was compared with that of congenital aganglionic rectums that also possessed hypertrophic nerves.
Aganglionic and ganglionic littermates were produced from breeding heterozygous lethal-spotted mice. Benzalkonium chloride was endorectally injected into ganglionic rectums to ablate the neural elements. Anorectal manometry was performed before the injection and on day 14 postinjection. The anorectal resting pressure was calculated based on the manometric tracing. Rectums were retrieved on day 14 for histologic evaluations.
Benzalkonium chloride injection successfully ablated the rectal ganglia. Although ganglionic littermates exhibited regular slow waves on anorectal manometry, aganglionic lethal-spotted mice showed irregular waves. Similar to lethal spotted mice, benzalkonium chloride-treated mice exhibited significantly higher anorectal resting pressure than that of ganglionic mice. The slow waves were absent in benzalkonium chloride-treated mice.
Benzalkonium chloride treatment produced aganglionic rectums that had higher resting pressure similar to the congenital aganglionic rectums. This suggests that hypertrophic nerves in congenital aganglionosis are not necessary to produce the anorectal spasticity.
背景/目的:先天性巨结肠症的肛门直肠痉挛可能是由于肠神经节缺失和/或神经纤维肥大引起的。本研究比较了化学去神经的直肠与具有肥大神经的先天性无神经节直肠的肛门直肠测压。
通过杂交培育杂合子致死斑点(lethal-spotted)小鼠,产生无神经节和神经节同窝仔鼠。用苯扎氯铵(benzalkonium chloride)经肛门直肠内注射到神经节直肠,以消除神经成分。在注射前和注射后第 14 天进行肛门直肠测压。根据压力描记图计算肛门直肠静息压。在第 14 天取直肠组织进行组织学评估。
苯扎氯铵注射成功地消除了直肠神经节。尽管神经节同窝仔鼠的肛门直肠测压显示出规则的慢波,但无神经节的致死斑点小鼠表现出不规则的波。与致死斑点小鼠相似,用苯扎氯铵处理的小鼠的肛门直肠静息压明显高于神经节小鼠。在苯扎氯铵处理的小鼠中,慢波消失。
苯扎氯铵处理产生了无神经节的直肠,其静息压与先天性无神经节的直肠相似。这表明先天性无神经节病中肥大神经并不是产生肛门直肠痉挛所必需的。