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恶性腹水的发病机制:重新审视毛细血管血流动力学的斯塔林定律。

Pathogenesis of malignant ascites: Starling's law of capillary hemodynamics revisited.

作者信息

Tamsma J T, Keizer H J, Meinders A E

机构信息

Department of General Internal Medicine, Leiden University Medical Center, The Netherlands.

出版信息

Ann Oncol. 2001 Oct;12(10):1353-7. doi: 10.1023/a:1012504904713.

DOI:10.1023/a:1012504904713
PMID:11762804
Abstract

Peritonitis carcinomatosa, indicating the presence of malignant cells in the peritoneal cavity, is a well-known complication of malignant disease. As a result, so-called malignant ascites develops. Malignant ascites is a debilitating condition for which no effective anti-tumor therapy is available. Frequent draining may be necessary to relieve pain and discomfort. Most studies regarding malignant ascites focus on diagnosis and treatment. In this paper. we will address the subject from a pathophysiologic perspective, using the characteristics of malignant ascites, Starling's equation of capillary forces, and recent knowledge regarding biologically active peptides produced by tumor cells. Following this approach. apart from decreased lymphatic ascites absorption, increased net capillary fluid-production can be identified as a contributing feature of ascites formation. The increased net filtration is due to an increase of overall capillary membrane-surface, increased capillary permeability and a subsequent increase of intraperitoneal protein concentration leading to increased intraperitoneal oncotic pressure. This sequence might be the result of biologically active peptides produced by tumor cells such as vascular endothelial growth factor and basic fibroblast growth factor. Interference with these mediators may serve as a target in future therapeutic strategies.

摘要

癌性腹膜炎表明腹腔内存在恶性细胞,是恶性疾病的一种常见并发症。因此,会形成所谓的恶性腹水。恶性腹水是一种使人虚弱的病症,目前尚无有效的抗肿瘤治疗方法。可能需要频繁引流以缓解疼痛和不适。大多数关于恶性腹水的研究集中在诊断和治疗方面。在本文中,我们将从病理生理学角度探讨这个问题,利用恶性腹水的特征、毛细血管力的斯塔林方程以及关于肿瘤细胞产生的生物活性肽的最新知识。按照这种方法,除了淋巴性腹水吸收减少外,净毛细血管液体生成增加可被确定为腹水形成的一个促成因素。净滤过增加是由于毛细血管总膜表面积增加、毛细血管通透性增加以及随后腹腔内蛋白质浓度增加导致腹腔内胶体渗透压升高。这个过程可能是肿瘤细胞产生的生物活性肽如血管内皮生长因子和碱性成纤维细胞生长因子的结果。干扰这些介质可能成为未来治疗策略的一个靶点。

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