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U Bagge

Publications and source records attributed to U Bagge.

80 records · Page 5Linked to original sources
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Differences in lodgement of tumour cells in muscle and liver.

Differences in the lodgement of circulating tumour cells in various organs are considered an important factor in metastatic organ selection. The present vital microscopic studies show that the pattern of intravascular arrest of tumour cells in muscle after intra-arterial injection is similar to that observed earlier, in the liver, after intraportal injection. However, parallel isotope studies on the lodgement process (at 5 min and 3 h after injection) showed that the tumour cells trapped in the muscle microvasculature were destroyed at a higher rate than in the liver. Tumour cells kept in test tubes, and thus not being subjected to the shearing forces of the circulation, had a higher survival rate than cells trapped in the muscle. The results indicate that stronger retardation forces acting on the tumour cells in muscle (arterial dissemination) than in the liver (venous dissemination) may be one mechanism behind the increased tumour cell destruction in muscle.

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A comparison between morphological, rheological and lodgement properties of rat fibrosarcoma cells harvested from solid tumours and cultures.

Vital microscopic studies on tumour cell lodgement in the rat liver have suggested that tumour cells from culture (CTCs) and from solid tumour (STCs) have different rheological properties. In the present study CTCs and STCs from a rat fibrosarcoma were compared in respect to their morphology, rheology and lodgement properties. The ultrastructural examination showed that the CTCs had a larger mean diameter (14.9 microns) than the STCs (11.2 microns). Both cell types had a very irregular nucleus. Surface irregularities provide the CTCs and STCs with a 'membrane excess', i.e. a larger plasmalemma than required to enclose the cells as smooth spheres, amounting to 46.8% and 60.9%, respectively. These values indicate that both CTCs and STCs can be substantially deformed with preservation of the volume and area. The CTCs were stiffer than the STCs when deformed at constant pressure in 6.5 microns glass pipettes, the nucleus appearing to be a significant hindrance to CTC deformation. Five minutes after intraportal injection of radiolabelled CTCs and STCs a much higher percentage of CTCs (82%) than of STCs (20%) remained lodged in the rat liver. The results indicate that the propagation in culture of fibrosarcoma cells alters the morphology and rheology of the cells such that CTCs are not suited for studies in vivo where the spontaneous intravascular dissemination and organ lodgement of tumour cells is simulated.

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The role of calcium channels and serotonin (5-HT2) receptors for tumour cell lodgement in the liver.

The effect of blockade of calcium channels and/or 5-HT receptors on the hepatic lodgement of intraportally injected fibrosarcoma cells was studied in rats. The calcium channel blocker verapamil and the 5-HT2 antagonist ketanserin each had a significant lodgement reducing effect. The pure 5-HT2 antagonist R 56413 was most effective and dose-dependent in its tumour cell lodgement reducing effect. At the highest dose tested (2.5 mg/kg body weight) R 56413 was as effective as thrombocytopenia, indicating that 5-HT is the most important platelet-released product that influences tumour cell lodgement.

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The tracheal mucosa microvasculature and microcirculation. Intravital microscopic observations in rabbits and a histologic study in man.

A method for the intravital microscopic study of the tracheal mucosal microcirculation in the rabbit is described. A low tracheostomy is performed for ventilation, while a hole cut in the ventral portion of the trachea cranial to the tracheostomy is used for observations. The trachea is immobilized by a fixation device. Microscopic observations are made with a Leitz stereo microscope. The microvasculature of the rabbit tracheal mucosa is characterized by centripetally arranged arterioles which subdivide into a fairly sparse capillary network at the mucosal surface. The capillaries drain into venular networks at different levels of the mucosa and collect finally into circumferentially arranged veins which run mainly between the cartilages. For comparative purposes the microvasculature of the human tracheal mucosa has been analysed in clarified (Spalteholz) preparations. This investigation shows that the microvascular architecture is principally the same in the human and rabbit tracheal mucosa. There is, however, a much denser capillary network in the human tracheal mucosa.

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Tumor blood supply and tumor localization by adoptively transferred IL-2 activated natural killer cells.

The circulatory pattern of IL-2 activated natural killer (A-NK) cells was studied in C57BL/6 mice bearing 10 day-old pulmonary and subcutaneous (s.c.) metastases of the B16 melanoma in order to evaluate the roles of the concentration of A-NK cells in the blood and of tumor blood flow on accumulation of A-NK cells in tumors. Kinetic studies of the presence of A-NK cells in peripheral blood after adoptive transfer revealed that these cells rapidly disappear from the blood. Via intravital microscopy of animals with exposed lung tissue, we have shown that the vast majority of transferred A-NK cells become efficiently arrested within the lung microcirculation at their first encounter with this organ, thereby explaining the fast disappearance of the cells from the bloodstream. Despite the low number of A-NK cells circulating in the blood, systemically injected A-NK cells (20 million per mouse) localized significantly (70-80 million cells/g) into most pulmonary metastases within 8-16 hours. In contrast, very few A-NK cells (< 0.2 million cells/g) were found in the s.c. metastases. Based on measurements of tumor blood flow (showing a classic inverse relationship between tumor size and tumor blood flow) and the blood concentration of A-NK cells, we estimated the highest intratumoral density of A-NK cells that theoretically can be generated by A-NK cells transported to the tumor by way of the blood. In s.c. tumors, the observed density of A-NK cells was at all times lower (10-50 fold) than the estimated density, indicating that only a few percent of the A-NK cells arriving at these tumors become retained in them. In contrast, the observed density of A-NK cells in pulmonary metastases was at all times higher (2-3 fold) than the estimated density. This finding indicates that A-NK cells might not reach the pulmonary metastases solely by way of the blood stream. In conclusion, i.v. injected A-NK cells become immediately entrapped in the lungs and, consequently, circulate poorly. While lung metastases become significantly infiltrated by i.v. injected A-NK cells, metastases in organs down-stream from the lungs become poorly infiltrated. We hypothesize that only a part of the A-NK cells found in lung metastases 8-16 hours following injection reach these metastases by way of the blood-vascular system. They might also migrate into the metastases from the surrounding normal lung tissue.

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The effect of hypoperfusion on the capillary distribution of leukocytes in cross-striated muscle.

In order to analyse whether microvascular redistribution of the leukocytes has any influence on the development of leukocyte capillary plugging at low flow states, the arteriole to capillary distribution of leukocytes was studied with vital microscopy in the rat cremaster muscle at normal perfusion pressure and after blood pressure reduction by 50% through aortic clamping. The reduction of the blood pressure led to a redistribution of the leukocytes, characterized by a shift of the leukocyte flux from capillaries at the downstream end of the arterioles towards more proximal branches in 8 of 19 networks studied, but flow cessation due to permanent leukocyte plugging was observed in only 2 of 94 capillaries observed. The arterioles of the 8 networks showing redistribution of the leukocytes had a significantly larger diameter than the rest of the arterioles. A possible explanation to the redistribution of leukocytes in 8 of the networks might be that their wider arterioles allowed a peripheral displacement and a skimming off of the leukocytes upon pressure reduction. The results from this investigation do not indicate that redistribution of leukocytes in the capillary networks of muscle should be significantly involved in the development of permanent leukocyte capillary plugging at low flow states.

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PubMedDate not supplied

An evaluation of resting arterial ischemia models in the rat hind limb.

Techniques for using the rat hind limb as a model of pure arterial ischemia at rest have not been well defined. Because the rat has no profunda femoral artery, numerous collateral pathways exist to the hind limb, and femoral artery ligation is not an effective method of inducing arterial ischemia. After several anatomic studies, a two stage operation to produce arterial ischemia in the left hind limb was devised. The first stage involved surgical interruption of collateral and re-entrant vessels, and the second stage involved femoral artery ligation. Using Xenon 133 clearance as an estimate of blood flow, reduction in flow to 14, 24, and 37% of the simultaneously measured value in the right hind limb was obtained at 2 hours, 2 days, and 5 days post ligation. Oxygen extraction in the left hind limb doubled both at 2 hours and at 2 days post ligation. Histological evaluation of the anterior compartment musculature after 5 days demonstrated loss of nuclei, degenerating contractile elements, edema, and inflammatory infiltrate. Evaluation of rats that had undergone isolated femoral artery ligation showed a 66% reduction in flow 2 hours after ligation, but no reduction in flow at 5 days, no increase in oxygen extraction, and only nuclear changes on histological exam at five days.

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