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odels. Steiger et al in 1975 infused parenteral amino acids with or without hypertonic dextrose for 10 days in Lewis/ Wistar rats with AC - 33 mammary tumor implants. Increased tumor protein content was observed in animals receiving parenteral amino acids with or without hypertonic dextrose compared to control animals. Aproportional increase in host weight was observed in animals receiving parenteral nutrients with no change in the tumor: host weight ratio. Oram-Smith et al in 1977 studied four parenteral solutions in this same animal/tumor model. These investigators compared parenteral amino acids alone, hypertonic dextrose alone, combined parenteral amino acids and hypertonic dextrose and a control solution of 2.5 % dextrose. Tumor protein synthesis rates were measured using N-glycine infusion techniques and demonstrated increased tumor protein synthesis in. all parenteral nutrient groups compared with the control 2.5 % dextrose animals. Torosian et al demonstrated increased tumor size, increased tumor weight, and increased tumor cell proliferation of AC-33 mammary tumor cells in Lewis/Wistar rats receiving TPN. After only 2 hours of initiating TPN, a significant increase in the percentage of S-phase, or DNA synthesizing, tumor cells were seen. Improved anti - tumor activity to cycle-specific agents (methotrexate, adriamycin) occurred due to this burst' in DNA synthesis following short-term TPN. As predicted by the flow cytometry kinetics, no increase in tumor response was observed in this tumor system to cyclenonspecific chemotherapy (cyclophosphamide). This phenomenon occurred independent of host nutrition status and was due to the substrate-induced proliferative changes in tumor growth kinetics. Further studies demonstrated that this substrate-directed response was primarily due to the amino acid component of TPN.
Isolated animal studies have concluded that no significant stimulation of tumor growth occurs with perenteral nutrition. Kishi et al in 1982 compared TPN with 5% dextrose for 7 days in Wistar rats with Walker-256 carcinosarcoma implants. Although this study concluded that TPN did not accelerate tumor growth, a small number of animals were studied and a greater than two fold increase in tumor weight occurred in animals receiving TPN. King et al in 1985 compared TPN with an oral diet in hepatoma " bearing ACI " N rats. Although TPN did not increase tumor protein content or H-thymidine incorporation in this study, the protein intake of control animals receiving oral diets was 25% greater than that of the experimental group receiving parenteral nutrition. Furthermore, both glucose-based and fat-based TPN increased tumor weight compared with animals receiving oral nutrition.
Tumor metastasis may also be influenced by the administration of TPN. In 1987, a series of studies by Mahaffey et al and Brvant et al reported decreased lung metastases in parenterally fed mice with subcutaneous Lewis lung carcinoma implants. In these studies, decreased pulmonary metastasis occurred with infusion of either TPN or control electrolyte solutions. Them investigators suggested that parenteral fluid load (not nutrient content) correlated with alterations in pulmonary metastasis in this model. They hypothesized that changes in circulating levels of prostaglandins or other soluble factors may have accounted for these differences. Torosian et al in 1991 compared three parenteral nu