RES function and tumour take and tumour growth in the liver and in the kidney—An experimental study in rats

Holmberg, Stig B.; Hafström, Larsolof; Kjellberg, Gunilla

doi:10.1016/0277-5379(87)90054-x

Cited by 6 publications

(3 citation statements)

References 14 publications

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“…Dynamic liver Nanocoll scintigraphy was used to measure non-parenchymal Kupffer cell clearance function (12)(13)(14)18). Dynamic liver IODIDA scintigraphy was used to measure parenchymal hepatocyte clearance function (9, l l , 15).…”

Section: Dynamic Liver Scintigraphymentioning

confidence: 99%

“…Assessment of Kupffer cell phagocytic function with dynamic liver scintigraphy in experimental procedures has been performed to study improved immunologic host function in sepsis and cancer (1 3). Improved Kupffer cell phagocytic function was then correlated to improved host defence function (18). Nanocoll with 50 nm diameter has been found suitable for studies of Kupffer cell-macrophage phagocytic function (14).…”

Section: Allogenic Transplantationmentioning

confidence: 99%

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Hepatocyte and Kupffer cell function after liver transplantation in the rat –in vivo evaluation with dynamic scintigraphy

Svensson

Friman

Jacobsson

et al. 1995

Liver

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In vivo physiological measurements of hepatocyte and Kupffer cell function after liver transplantation are desirable. Orthotopic liver transplantation was performed in 54 rats. Hepatocyte and Kupffer cell function were measured with dynamic liver scintigraphy. Hepatic clearance of 99mTc‐Nanocoll (%/min), an albumin colloid phagocytosed by the Kupffer cells, was used to evaluate Kupffer cell function. Hepatic clearance of 99mTc‐IODIDA (%/min), an imino‐diacetic‐acid taken up and secreted by the hepatocytes, was used to evaluate the hepatocyte function. Hepatic clearance in control rats was 27±2 %/min for Nanocoll and 30±3 %/min for IODIDA. After syngenic liver transplantation, without rejection, there was a rise in Nanocoll clearance (34±2 %/min p<0.01) after 3 weeks, but no change in IODIDA clearance (32±3 %/min N.S.). After syngenic liver transplantation with preservation time prolonged to 16 h, there were no changes in IODIDA or Nanocoll clearance 1 day after transplantation. Both IODIDA (11±2 %/min) and Nanocoll clearance (22±2 %/min) were decreased (p<0.001) during rejection after allogenic transplantation. An in vivo method of measuring the hepatocyte and Kupffer cell function in the transplanted liver is described. Kupffer cell function was increased after syngenic liver transplantation. Kupffer cell and hepatocyte function were decreased during rejection. Dynamic liver scintigraphy seems a suitable procedure for examining liver injury after liver transplantation in the experimental setting.

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Section: Dynamic Liver Scintigraphymentioning

confidence: 99%

Section: Allogenic Transplantationmentioning

confidence: 99%

Hepatocyte and Kupffer cell function after liver transplantation in the rat –in vivo evaluation with dynamic scintigraphy

Svensson

Friman

Jacobsson

et al. 1995

Liver

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“…The relationship between RES function and tumor take and growth in the rat has been investigated using zymosan as a Kupffer cell-stimulant, and methylpalmitatc as a Kupffer cell depressant [45]. Using nitrosoguanidine-induced adenocarcinoma tumor cells injected directly into the liver or a kidney to induce experimental metastatic growths, treatment with zymosan for 3 days before tumor cell challenge resulted in significant reductions in liver tumor take and tumor volume when compared to control treated animals.…”

Section: Modulation Of Kupffer Cell Activity and Metastasis In The Livermentioning

confidence: 99%

Kupffer cells and liver metastasis

Phillips

1989

Cancer Metast Rev

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Kupffer cells, tissue-fixed macrophages located in the sinusoids of the liver, represent the highest concentration of mononuclear phagocytes in the body. Their ability to act as scavengers of particulate material in the blood has given rise to speculation that they play a role in controlling hepatic metastases derived from blood-borne tumor cells. Circumstantial evidence for such a role has been obtained from animal studies where Kupffer cell function has been compromised or inhibited, and from anecdotal clinical observations. Current evidence suggests that Kupffer cells are capable of nonspecifically eliminating some circulating tumor cells from the circulation via phagocytosis. This surveillance mechanism would appear to be limited in capacity, and subject to a number of external factors. Recent studies have demonstrated that Kupffer cells can be activated to a tumoricidal state via the administration of biological response modifiers such as gamma interferon or muramyl peptides. The localization of liposomes within Kupffer cells after systemic administration has provided a considerable stimulus for the efficient targeting of macrophage-activating compounds to these cells. Such therapeutic intervention, while capable of inducing Kupffer cell tumoricidal activity in situ and inhibiting tumor growth, is limited with respect to the location of the tumor cells (sinusoidal versus parenchymal) and to the size of the metastatic nodule. Therapeutic intervention using liposomes containing macrophage-activating agents may only be of benefit in patients with minimal tumor load who are at risk for hepatic metastases, rather than those patients who already have clinically detectable liver tumors.

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