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The hepatopulmonary syndrome (HPS) consists of a triad of liver dysfunction, increased alveolar-arterial oxygen gradient and intrapulmonary vascular dilations. The mechanisms of impaired arterial oxygenation are still debated but the multiple inert gases elimination technique and more recently contrast echocardiography, greatly facilitated the investigation of such mechanisms. Subsequently the cause of hypoxemia can be attributed to several mechanisms such as ventilation-perfusion mismatch, right-to-left intrapulmonary shunts and alveolar-to-capillary diffusion defect, variously implicated in the severity of the disease. SHP may result from intrapulmonary vascular dilations and angiogenesis but the pathogenesis of such abnormalities is not completely explained. The hypothesis of an imbalance in vasoactive mediators and angiogenic factors has been put forward. Increasing data support the theory that the increase in synthesis and release of nitric oxide (NO) is the key factor modulating vascular tone. If this hypothesis is true, the use of compettive inhibitors of NO synthesis should restore pulmonary vascular tone, reversing the hemodynamic changes and gas exchange impairment of HPS.

Section of the anterior cruciate ligament of the right knee was performed in 20 rabbits which were sacrificed 3 months later. During that time, 10 animals were treated with a proteino-polysaccharide compound. The importance of cartilage destruction was evaluated by measuring the articular surfaces and the surface of the fissured areas using an automatic image analyzer; osteophytes were measured by a volumetric study. The percentage of the fissured areas appears to be without correlation with the osteophytosis, the increase of the water content or the decrease of glycosaminoglycans following the procedure. In animals which were treated, the extent of the fissure is significantly reduced but the biochemical and histometric modifications are not too different from those of the reference group.