Experimental and Clinical Study on The Inhibition of The Accumulation of Carcinomatous Ascites

Abstract

It is well known that carcinomatous ascites, which is often seen at the end-stage of the patients with malignant tumor, is difficult to treat. Satisfactory treatment to reduce carcinomatous ascites has not been found and its mechanism is still controversial. Experimental study was made to clarify its mechanism by using “Ehrlich ascites carcinoma cells.” Some experiments and clinical study were also carried out to inhibit the accumulation of carcinomatous ascites. The following results were obtained.
1. Carcinomatous ascites developed not only by the occulsion of lymphatic vessels of diaphragm but by the accumulation of vascular permeability of the peritoneal membrane. The latter mechanism seems to be strongly participated in the accumulation of carcinomatous ascites.
2. Cathepsin D acid protease and one of lysosomal hydrolase was closely related to the accelaration of vascular permeability.
3. Systemic administr ation of hydrocortisone did not effect on the absorption of particles over 0.5p in diameter through the lymphatic absorption pathway of the diaphragm.
4. Hydrocortisone, pepstatin, Aprotinine and FOY-305 seemed to be related to the inhibition of the accumulation of ascites, since hydrocortisone inhibited the release of cathepsin D and pepstatin decreased the activity of cathepsin D. On the other hand, Aprotinine and FOY-305 inhibited the kinin-system which was induced by cathepsin D.
5. Reinfusion of the sterilized, cell free and concentrated ascitic fl uid of patient with cancer into the vein of same host was quite effective to decrease the ascites. The combination of adjuvant chemotherapy with steroids, Aprotinine and OK-432 was more effective than single therapy.