The plasminogen-activation system in ovarian tumors

We studied the plasminogen activation system in tumor tissue by measuring the antigen level of the 2 plasminogen activators, tissue-type (t-PA) and urokinase-type (U-PA) and their inhibitors, plasminogen-activator inhibitors type-1 (PAI-1) and type-2 (PAI-2) in the tissue extracts of 43 human benign and malignant ovarian tumors. U-PA levels were significantly higher in malignant than in benign tumors. In addition, U-PA antigen levels were higher in the metastatic tissue of advanced disease (FIGO stage III) than in the primary localized tumor (FIGO stage I/II). Also PAI-1 concentrations tended to be higher in malignant than in benign tumors, but this difference was not statistically significant. In contrast, t-PA levels were lower in metastatic than in non-metastatic tumors, whereas PAI-2 levels were unrelated to the stage of ovarian malignancy. These results were integrated in a plasminogen-activation-dependent malignancy index (U-PA × PAI-1/t-PA). This index distinguished the different groups of benign ovarian tumors, localized and metastatic ovarian carcinomas better than U-PA levels. It could be useful as a prognostic indicator in ovarian cancer © 1993 Wiley-Liss, Inc.     

Mechanism of electrolyte and water transport in the first 2 minutes of hypotonic water resorption

1.2 ml of water or 1.2-2.4 ml of 1/2-isotonic saline were injected into the duodenum of the unanaesthetized rat. Continuous measurements of conductivity and sodium concentration in whole blood, the last by means of ion-selective electrodes, and of protein and electrolyte concentration in a filtrate of portal vein blood were made. Whereas conductivity and sodium or electrolyte concentration dropped promptly and steeply, the drop of protein concentration (Cprot) was registered with a delay of 1.9 min. A quantitative comparison of the conductivity and sodium concentration curves, showing strictly synchronous courses, suggested that no hematocrit changes (these would have influenced conductivity) had taken place during the period of constancy of Cprot. In rats having thirsted for 36 h, Cprot did not fall during a period of 5-8 min in which they drank up to 5.5 ml of water, despite a great drop of electrolyte concentration. It is concluded that at the beginning of water absorption all the fluid absorbed is transported via the lymph ducts. A gradient of negative pressure from the interstitial tissues to the lymphatic system in the non-absorbing gut is proposed, an additional electrolyte secretory process being taken into consideration.     

Functional abnormalities of experimental autogenous vein graft neoendothelium.

When a vein is grafted into the arterial circulation, the endothelium of the graft is damaged. Regeneration of an intact neoendothelium occurs, but the functional properties of this surface have not been clarified. In this study, the functional integrity of the neoendothelium of veins grafted into the carotid artery of the rabbit was assessed through the use of acetylcholine and histamine to stimulate the production of the important endothelium-derived relaxing factor (EDRF). Control veins, precontracted with norepinephrine [10(-5) M], relaxed after exposure to acetylcholine [( 10(-7) M], 42.4% +/- 6.4%, p = 0.008) and histamine [( 10(-6) M], 30.6% +/- 4.3%, p = 0.03). This relaxation response was abolished after mechanical removal of the endothelium. By contrast, neither acetylcholine nor histamine caused an endothelium-dependent relaxation in the vein grafts, even though scanning electron microscopy demonstrated the presence of a morphologically intact endothelium. However, addition of stabilized EDRF purified from cultured endothelial cells induced relaxation of the vein grafts (35.8% +/- 3.6%, p = 0.002). These data indicate that vein graft endothelium is unable to produce EDRF in response to exposure to acetylcholine or histamine. The inability to produce this potent smooth muscle cell relaxing factor and anti-aggregatory substance may be a predisposition to vein graft failure.     

Traumatic rupture of extracardiac valved conduit: unusual late complication producing outflow tract obstruction

A 22-year-old woman died suddenly 15 years after successful repair of truncus arteriosus with a valved Dacron conduit. At autopsy there was complete obstruction of the right ventricular outflow tract by a large organizing thrombus between the outer aspect of the conduit and the adherent pericardial tissue. This rare late complication may have resulted from an unrecognized deceleration injury occurring at the time of a serious automobile accident 5 months before death.