摘要
The efficacy and safety of intraperitoneal administration of vincristine sulphate was determined in mice bearing Ehrlich ascitic carcinoma. The tumor bearing animals were administered with 0.5 mg/kg body weight (b.wt) of freshly prepared vincristine sulphate intraperitoneally on day 6 after tumor transplantation followed by drug administration once daily 5 days a week consecutively. The observations regarding the survival, alteration in the volume of peritoneal fluid, increase in life span and pathological changes in the liver, kidney, gastrointestinal tract and bone tissues were made. The vincristine sulphate treatment reduced the malignant cell population significantly and there were no significant changes in the histological picture of liver, kidney, bone, except the intestine, where atropy of villi demonstrating nests and cords of uniform small round cells were observed. Our experimental data suggests that intraperitoneal administration of vincristine is beneficial in malignant peritoneal effusion.
Subject(s)
Animals , Antineoplastic Agents, Phytogenic/administration & dosage , Ascitic Fluid/drug therapy , Carcinoma, Ehrlich Tumor/complications , Cell Survival/drug effects , Digestive System/pathology , Female , Gastrointestinal Transit/drug effects , Injections, Intraperitoneal , Kidney/pathology , Liver/pathology , Mice , Rats , Rats, Wistar , Survival Analysis , Vincristine/administration & dosage摘要
It is claimed that diuretics can change the pattern of ascitic fluid analysis in heart failure, but, it has remained a controversial issue. To test the hypothesis that in heart failure diuretics change the transudative pattern of ascites to exudative. In a prospective study, 50 patients [32 male, 18 female] with a mean age of 49 years [range, 26-67 years], and ascites secondary to heart failure were randomly allocated to two therapeutic groups. Group I: 30 patients received furosemide and group II: 20 patients received triamtrene H for two weeks. Abdominal paracentesis was performed before, and one and two weeks after diuretic therapy. The difference in ascitic fluid total protein [AFTP] and cell count was not significant at baseline between the two groups. In patients on furosemide, the change in AFTP compared to the baseline was significant [p<0.001 and p<0.001, respectively] one and two weeks after therapy. In patients on triamtrene H, the change in AFTP one and two weeks after therapy compared to the baseline was significant [p<0.01 and p<0.001, respectively]; ascitic fluid met exudative criteria in three patients [15%]. In group I patients, the difference in ascitic fluid cell count, one and two weeks after therapy was statistically significant [p<0.001 and p<0.001 respectively] compared to the baseline. In group II, the difference in ascitic fluid cell count one and two weeks after therapy compared to the baseline was not significant. In group I: 23 patients [76.6%] showed a significant change in their ascitic fluid pattern while in group II: 3 patients [15%] showed ascitic fluid changes toward the exudative pattern [p<0.05]. In patients with heart failure, furosemide changes transudative ascitic to exudative; the change is more significant in the amount of protein than in the cell count, and occurs at the end of the first week of therapy and continues thereafter