Lymphatic obstruction in carcinomatous ascites.
Lymphatic obstruction in carcinomatous ascites.
复制标题
癌性腹水淋巴阻塞。
作者：
G. Feldman
用5倍于10-6的可移植卵巢癌细胞腹腔接种C3H小鼠，不可避免地引起大量腹水的积聚。组织学和药物治疗研究表明，腹膜淋巴引流阻塞是该模型中癌性腹水形成的关键因素。在腹水形成的早期阶段，强烈的炎症反应会阻塞连接腹膜腔和膈下淋巴丛的导管。这种由腹膜腔内肿瘤细胞引起的炎症反应可以通过大剂量全身皮质类固醇治疗来抑制。经这种治疗的动物腹水积聚明显迟缓。肿瘤细胞不能进入引流腹腔的淋巴毛细血管，直到腹水大量积聚。肝素或华法林钠的全身抗凝不能阻止肿瘤细胞在这些淋巴毛细血管内的沉积，也不能改变腹水积聚的模式。多种因素提示，腹水的过量产生不可能是小鼠癌性腹水的致病因素。
The i.p. inoculation of C3H mice with 5 times 10-6 cells of a transplantable ovarian carcinoma invariably evokes accumulation of large amounts of ascitic fluid. Histological and pharmacotherapeutic studies indicate that obstruction to peritoneal lymphatic drainage is a key factor in the formation of carcinomatous ascites in this model. In the early stages of ascites formation, an intense inflammatory reaction appears to occlude the condusts that connect the peritoneal cavity to the subdiaphragmatic lymphatic plexus. This inflammatory reaction, elicited by the presence of tumor cells within the peritoneal cavity, can be inhibited with high-dose systemic corticosteroid therapy. Ascitic fluid accumulation in animals so treated is markedly retarded. Tumor cells do not gain access to lymphatic capillaries draining the peritoneal cavity until ascitic fluid accumulation is massive. Systemic anticoagulation with heparin or sodium warfarin does not prevent lodgment of tumor cells within these lymphatic capillaries, nor does it alter the pattern of ascitic fluid accumulation. Various considerations suggest that excess production of ascitic fluid is not a likely pathogenetic factor in murine carcinomatous ascites.