Angiogenesis has been recognised as a precursor of fibrosis in several pathologic conditions. Its participation has been demonstrated in schistosomiasis, both during periovular granuloma formation and in the genesis of schistosomal periportal fibrosis. Paradoxically, proliferation of new blood vessels, accompanied by production of vascular-endothelial growth factor, appeared prominent during fibrosis regression months after curative treatment of schistosomiasis. Thus, angiogenesis in schistosomiasis seems to have a two-way mode of action, participating both in fibrogenesis and in fibrosis degradation. Morphological observations presented here are in keeping with the possibility that, in the first case, angiogenesis allows pericytes to come in great numbers to the site of lesions and be detached from capillary walls and transformed into myofibroblasts, which are important extra-cellular matrix forming cells. During post-curative fibrosis regression, actin-containing pericytes appeared at various foci of tissue remodelling, especially at sites of repair of vascular lesions. The molecular and cell factors involved in both situations seem to be important subjects in need of further investigations and the schistosomiasis model certainly will be of great avail in this regard.

Hepatosplenic schistosomiasis was the first human disease in which the possibility of extensive long standing hepatic fibrosis being degraded and removed has been demonstrated. When such changes occurred, the main signs of portal hypertension (splenomegaly, esophageal varices) progressively disappeared, implying that a profound vascular remodeling was concomitantly occurring. Hepatic vascular alterations associated with advanced schistosomiasis have already been investigated. Obstruction of the intrahepatic portal vein branches, plus marked angiogenesis and compensatory hyperplasia and hypertrophy of the arterial tree are the main changes present. However, there are no data revealing how these vascular changes behave during the process of fibrosis regression. Here the mouse model of pipestem fibrosis was used in an investigation about these vascular alterations during the course of the infection, and also after treatment and cure of the disease. Animals representing the two polar hepatic forms of the infection were included: (1) "isolated granulomas" characterized by isolated periovular granulomas sparsely distributed throughout the hepatica parenchyma; and (2) 'pipestem fibrosis' with periovular granulomas and fibrosis being concentrated within portal spaces, before and after treatment, were studied by means of histological and vascular injection-corrosion techniques. Instances of widespread portal vein obstruction of several types were commonly found in the livers of the untreated animals. These obstructive lesions were soon repaired, and completely disappeared four months following specific treatment of schistosomiasis. Treatment was accomplished by the simultaneous administration of praziquantel and oxamniquine. The most impressive results were revealed by the technique of injection of colored masses into the portal system, followed by corrosion in strong acid. The vascular lesions of non-treated pipestem fibrosis were represented in the plastic casts by considerable diminution of the fine peripheral portal vein radicles, plus dilatation of periportal collaterals. Four months after treatment, this last picture appeared replaced by tufts of newly interwoven vessels formed along the main portal vein branches, disclosing a strong angiomatoid reparative change. Understanding about the cellular elements at play during fibro-vascular repairing changes of hepatic schistosomiais represents a matter of considerable scientific and conceptual importance. At present time one may only speculate about the participation of some type of natural stem-cell capable of restoring the diseased liver back to normal once the cause of the disorder has been eliminated.