J.Jpn. Surg. Soc.. 80(2): 147-163, 1979
Original article
SCANNING ELECTRON MICROSCOPIC STUDIES ON THE EXPERIMENTAL PERITONEAL DISSEMINATION OF THE RATS IMPLANTED WITH THE ASCITES HEPATOMA CELLS AH 100B
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Department of Surgery, (Director: Prof. S. Koga) and Department of Anatomy (Director: Prof. K. Tanaka), Tottori University School of Medicine, Yonago, Japan Hirofumi Kudo |
1) On 1st and 2nd days after AH100B cells were injected, a few tumor cells were found by SEM adhering to the peritoneal surface of the greater omentum and the liver, though no change could be macroscopically recognized on either surfaces. On the 3rd day after injection, adhering tumor cells vigorously proliferated and formed the stratified tumor cell mass on both peritoneal surfaces. The microvilli of the mesothelial layer surrounding the tumor cell mass were slightly damaged, but other parts of the mesothelial layer did not change.
2) From the 3rd to the 6th day after injection, both peritoneal surfaces looked normal macroscopically. The number and the size of the tumor cell mass, however, increased microscopically. At that time the surface of the mesothelial layers turned uneven. The microbilli of the mesothelial layer surrounding the tumor cell mass were considerably damaged, but other parts of the mesothelial surface were still normal. That is to say that the mesothelial layer might have strong resistance to the tumor cell infiltration.
3) On the 6th day, the hardening and infiltration of the tumor cell mass was macroscopically recognized on both peritoneal surfaces. The tumor cell mass which had respectively increased in size fused together through the microscopic observation. Then the tumor cells rapidly infiltrated into the connective tissue beneath the mesothelium. Mesothelial cells surrounding the tumor cell mass turned into spindle like shape and the attraction between the cells was broken. Other parts of the mesothelial cells which had no relation to the tumor cell mass changed to a spindle like shape and those arrangements also went out of order. Successively the gaps between these mesothelial cells spread themselves and some parts of the cells exfoliated from the peritoneal surfaces.
4) The dissemination process mentioned above did not show much difference between the peritoneal surfaces of the greater omentum whose microvilli density was rough and the peritoneal surface of the liver whose microbilli density was heavy. That is to say that there was almost no relation between microvilli density of the mesothelial cells and the peritoneal dissemination mechanism.
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