Vernon M W, Wilson E A
Fertil Steril. 1985 Nov;44(5):684-94.
As a model to examine the pathophysiologic attributes of endometriosis, attempts were made to surgically induce the disease in the rat by autotransplanting endometrial or uterine tissue to the peritoneum. Rats (n = 46) were randomly assigned to one of four surgical techniques: (1) four uterine squares sutured to the peritoneal cavity; (2) uterine luminal lavages instilled into the peritoneal cavity; (3) endometrial scrapings flushed into the peritoneal cavity; and (4) sham-operated controls. Rats were examined at various days after surgery for the presence of endometrial implants. The autotransplantation of uterine squares to the peritoneal cavity was the only treatment that yielded healthy endometriotic implants. These implants grew into ellipsoidal cystic structures that were composed of both endometrial glands and stroma and were found to contain prostaglandin F (202 ng/mg) at concentrations similar to those measured in uterine tissue (205 ng/mg). To examine the effect of surgically induced endometriosis upon fecundity, rats (n = 40) were autotransplanted with uterine squares or were sham operated and mated. The presence of ectopic endometrial tissue reduced the number of pups at term by 48% and the number of day 14 embryos by 28% (P less than 0.05). Peritoneal adhesions were greater in rats with induced endometriosis than in sham-operated controls (P less than 0.05); however, in rats with induced endometriosis, no differences were noted in the severity of adhesions between pregnant and nonpregnant rats. Endometriotic implants underwent complete regression in the day 14 pregnant rat but had doubled in size in the nonpregnant rat. At term, the endometriotic implants were larger than in the day 14 pregnant rat (P less than 0.05) and similar to their original size. The successful growth and development of surgically transplanted endometrial tissue in the rat offers a research model that can be used to study those aspects of endometriosis that cannot be adequately investigated in women.
作为一种研究子宫内膜异位症病理生理特征的模型，人们尝试通过将子宫内膜或子宫组织自体移植到大鼠腹膜来手术诱导该疾病。46只大鼠被随机分配到四种手术技术之一：（1）将四个子宫方块缝合到腹腔；（2）将子宫腔灌洗液注入腹腔；（3）将子宫内膜刮屑冲洗到腹腔；（4）假手术对照组。在手术后的不同天数检查大鼠是否存在子宫内膜植入物。将子宫方块自体移植到腹腔是唯一产生健康子宫内膜异位植入物的治疗方法。这些植入物生长为椭圆形囊性结构，由子宫内膜腺体和基质组成，发现其中前列腺素F的浓度（202 ng/mg）与子宫组织中测得的浓度（205 ng/mg）相似。为了研究手术诱导的子宫内膜异位症对生育力的影响，40只大鼠接受子宫方块自体移植或假手术并进行交配。异位子宫内膜组织的存在使足月幼崽数量减少了48%，第14天胚胎数量减少了28%（P<0.05）。诱导性子宫内膜异位症大鼠的腹膜粘连比假手术对照组更严重（P<0.05）；然而，在诱导性子宫内膜异位症大鼠中，怀孕和未怀孕大鼠之间的粘连严重程度没有差异。子宫内膜异位植入物在怀孕第14天的大鼠中完全消退，但在未怀孕大鼠中大小增加了一倍。足月时，子宫内膜异位植入物比怀孕第14天的大鼠更大（P<0.05），且与原始大小相似。手术移植的子宫内膜组织在大鼠体内的成功生长和发育提供了一个研究模型，可用于研究在女性中无法充分研究的子宫内膜异位症的那些方面。
