Ultrastructural observations on inflammatory angiogenesis in gastric carcinomas with massive neutrophil infiltration.

Neutrophils are traditionally thought of as terminal effectors of inflammatory reaction, but experimental studies suggest that they play a direct role in the inflammatory angiogenesis of tumors. Thus, further evidence in humans is required regarding the mechanisms by which neutrophils induce tumor angiogenesis. In this study, 4 cases of human gastric carcinomas with massive neutrophil infiltration were studied by light and electron microscopy, focusing on the inflammatory angiogenesis in the tumor stroma. At light microscopy, the tumors were advanced gastric carcinomas in which various degrees of tubular differentiation were present. Under an electron microscope, pericytes exhibited two major differentiated states with distinct ultrastructural features: a contractile phenotype and a synthetic phenotype. The contractile phenotype was characterized by abundant microfilaments. Synthetic pericytes contained abundant rough endoplasmic reticulum, lipid bodies, and numerous membrane-bound vesicles. These ultrastructural findings extend concept of contractile/synthetic phenotype modulation, originally described in smooth muscle cells, to tumor microvascular pericytes. Tumor microvasculature was also characterized by abortive or slit-like lumina, endothelial cell mitoses, and replicating basement membranes. These qualitative and observational transmission electron microscopy findings provide additional morphological evidence of active inflammatory angiogenesis in gastric carcinomas with massive neutrophil infiltration.

Microvascular changes in human gastric carcinomas with coagulative necrosis: an ultrastructural study.

Ultrastructural findings in three cases of gastric carcinoma with coagulative necrosis are reviewed with special emphasis on microvascular changes. Intratumoral microvasculature revealed more or less stabilized vessels. Some were characterized by a close association between pericytes and endothelial cells, whereas others showed laminated basement membrane, with a loose association between pericytes and endothelial cells. Some mural cells exhibited ultrastructural signs of regressive changes, including lipofuscin granules, swollen mitochondria, and cytoplasmic lucency. These findings are discussed in relationship to a number of recent studies of the microvascular injury caused by hypoxia and reoxygenation, in humans and animals.