Background: An investigation of the effect of laparoscopy and CO2 pneumoperitoneum on the pattern of tumour implantation and growth in the peritoneal cavity was carried out. Methods: A suspension of viable adenocarcinoma cells was introduced into the left upper quadrant of the peritoneal cavity of 36 syngeneic immune‐competent rats at laparotomy, laparoscopy with CO2 insufflation, and gasless laparoscopy (12 rats in each group). Six days later the peritoneal cavity and surgical wounds were examined for macroscopic evidence of implanted tumour. The abdominal cavity was divided into sectors and macroscopic tumour implantation was determined for each sector and wound. This was confirmed by histological examination. Results: While tumour implantation occurred in the vicinity of the tumour suspension introduction site in the laparotomy and gasless laparoscopy groups, implantation occurred throughout the peritoneal cavity, including areas remote to the introduction site, in the laparoscopy with CO2 insufflation group. Tumour growth was more likely in the port wounds of rats undergoing laparoscopy with insufflation than without. Conclusions: In this model, CO2 insufflation during laparoscopy resulted in widespread tumour dissemination and implantation, when compared to laparotomy and gasless laparoscopy, supporting the postulate that wound metastasis and tumour spread may be more likely following laparoscopic cancer surgery in humans when CO2 insufflation is used.

No abstract

Carbon dioxide insufflation results in tumor dissemination during laparoscopy, leading to port site metastasis. Gasless laparoscopy may prevent this problem.

SummaryThe metabolic response of the tumour-bearing host to methotrexate (MTX) therapy was investigated with particular attention to effects resulting from MTX-induced anorexia. Biochemical changes in female Dark Agouti rats bearing mammary adenocarcinomas and treated with MTX (0.5 mg/kg. 2 i.m. injections, 24 h apart) were compared with untreated (CON) tumour-bearing rats, and tumour-bearing rats pair-fed (PF) to the MTX group. MTX treatment halted progression ofthe tumour (tumour 6% of bodyweight) while the tumour burden doubled in the CON and PF groups.A number of biochemical and haematological changes were specific to MTX treatment and did not result from decreased food intake. MTX treatment was associated with significantly decreased plasma calcium, bilirubin. alkaline phosphatase, aspartate aminotransferase and the total white cell count. Decreases in plasma albumin and total protein concentrations were observed in both MTX and PF rats. Other parameters commonly used to assess renal and liver function were not significantly affected by MTX.MTX reversed the hypoglycaemia, hyperketonaemia and hypertriglyceridaemia induced by tumourbearing. In contrast, PF rats had an even more pronounced hypoglycaemia and hyperketonaemia than the CON rats. Measurement of glucose uptake in vivo with 2-deoxy[U-'''C]-glucose showed that MTX treatment halved the glucose requirement ofthe tumour (8.2% of bodyweight compared to 12.2% in the control). It is concluded that the potentially adverse effects of MTX treatment on host metabolism are outweighed by the beneficial effects of a reduced metabolic demand resulting from inhibition of tumour progression.

SummaryThe physical and metabolic characteristics of a Dark Agouti ral mammary adenocarcitioma and its effects on host tnctabolism arc described-The tumour was characterized by a lack of glandular diffcrcntiatioti, tetraploidy. a rapid milotic index and a high rale of glycolysis. The adenocarcinoma was readily maintained in tissue culture and could be passaged through the host by inoculating either cell suspensions or tissue explants. In the rat, tumour growth resulted in a loss of adipose tissue at a lumour mass of less than 5% body weight indicating that increased energy expenditure was already present al that stage. In addition the tumour caused anaemia, hypercalcaemia and hypoglycaemia. Hyperketonaemia was also observed in fasted tumour-bearing rats. Methotrexatc arrested tumour growth in vivo. These aspects of the lumour model make it useful for investigations into host-tumour competition and mechanisms of cachexia.