Masaharu Tsuchiya

An electron microscopic study of hepatocellular injury due to activated hepatic macrophagesin vitro

Activated hepatic macrophages (Mp) were shown to injure hepatocytes (Hc)in vitro by producing active oxygen radicals. In this study, cocultured Hc and hepatic Mp were observed using scanning electron microscopy in order to investigate the mechanism of hepatocellular injury by Mp. Activated hepatic Mp appeared to be irregular in shape with long pseudopodia, as opposed to inactivated Mp, which were oval in shape with a small number of short cytoplasmic processes. The former frequently touched the surfaces of the Hc, most of which were injured. The addition of an antioxidant into the medium seemed to block contact of the hepatic Mp and the Hc, and protected the Hc. These observations indicate that activated hepatic Mp may cause hepatocellular injuryin vivo in various liver diseases.

Granulocyte-mediated oxidative stress on microvascular endothelial cells demonstrated by digital-imaging photonic intensified microscopy. Effects of PAF, leukotriene B4 and FMLP.

Oxyradicaldependent chemiluminescence from granulocytes was visualized in rat mesenteric microvascular beds treated with platelet-activating factor (PAF), leukotriene B4 (LTB4) and bacterial chemotactic peptide (FMLP) by means of digital imaging photonic intensified microscopy. The topical application of PAF-acether (100 nM) caused remarkable granulocyte adherence on venular endothelial walls and the subsequent activation of a luminol-dependent photonic burst. Chemilumigenic sites clearly corresponded to the spatial distribution of sticking cells in post-capillary venules. LTB4 and FMLP, however, did not induce any significant photonic burst at concentrations which caused adherent changes between endothelial cells and granulocytes.These findings suggest that PAF may play a role in granulocyte-mediated oxidative stress on venular endothelial cells during acute inflammatory processes, and also provide the first evidence of an intravital oxidative burst of granulocytes in microcirculatory disturbances.

Protein-losing Enteropathy Including Intestinal Lymphangiectasia and Ménétrier’s Disease

Protein-losing gastroenteropathy, characterized by an excessive loss of plasma protein into the gastrointestinal lumen, is caused by a wide variety of gastrointestional disorders, which may be classified into three categories:1 The first category includes disorders that cause an obstruction of intestinal lymphatics. Direct leakage of intestinal lymph into the intestinal lumen is thought to be the mechanism of protein loss. Primary intestinal lymphangiectasia is a typical example of this group.2,3 Secondary intestinal lymphangiectasia may occur in certain cardiac diseases such as constrictive pericarditis4 and congestive heart failure, lymphoma, Whipple’s disease, Crohn’s disease,5 intestinal tuberculosis, and retroperitoneal fibrosis.6

Aminergic and Peptidergic Innervation of the Gastric Mucosa—Its Possible Relevance to Ulcerogenesis

A number of studies on the relationship between autonomic nervous abnormalities and gastric ulcer formation were performed since the pioneering reports of Cushing1 and Bergamann.2 However, further investigation of this pathognomonic relationship from a different angle or using a newly developed technique is still warranted in order to clarify the mechanism of gastric ulceration.