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Biomedical subjects

M Shimazaki

Publications and source records attributed to M Shimazaki.

At least 73 records · Page 4Linked to original sources
PubMed1985

Experimental pulmonary fibrosis induced by trisodium citrate and acid-citrate-dextrose.

A single intrapulmonary injection of 3.8% trisodium citrate and acid-citrate-dextrose (ACD) into rabbits results in extensive degeneration and necrosis of alveolar pneumocytes, including the type II pneumocyte, and of bronchiolar or bronchial epithelial cells. Subsequently, the alveoli and alveolar ducts collapse, and the septa and ductal walls adhere to each other, accompanied by the proliferation of interstitial fibroblasts. These fibroblasts produce fibrous connective tissue which is followed by pulmonary fibrosis in 1 week. Epithelial regeneration, especially that resulting from the proliferation of immature type II pneumocytes, occurs around the periphery of the fibrous lesions. The synthesis and release of large amounts of surfactant materials by the proliferated type II pneumocytes may induce the surfactant materials to reopen the air spaces of the collapsed and adhesive alveoli. By 4 weeks those fibrous areas in the pathological lungs become smaller and/or appear normal. These results suggest that this is a useful experimental animal model for pulmonary fibrosis, and that epithelial cells, especially type II pneumocytes, are associated with both the induction of and the recovery from the disorder; in the early stage, interference by reepithelization resulting from type II pneumocyte proliferation may elicit the proliferation of fibroblasts, and in later stages, reepithelization and surfactant synthesis by newly proliferated type II pneumocytes may permit the reopening of collapsed and adhesive air spaces.

Animals↗
PubMed1983

Morphological studies on proliferation and desquamation of the alveolar lining epithelium in carrageenan-induced experimental pneumonia.

An experimental model of carrageenan-induced pneumonia in rabbits was used to study the proliferation and desquamation of alveolar lining epithelium, light and electron microscopically. Observation at 5 hr after intrapulmonary injection of 0.5% lambda carrageenan solution revealed epithelial cell (predominantly type 1 pneumocyte) injury, exposing the basement membrane of the alveolar wall, and that at 40 hr demonstrated an appearance of many large pneumocytes among the alveolar lining epithelium as a reparative reaction. This proliferative response of immature type 2 pneumocytes reached to the maximum in 60 and 72 hr followed by an intense desquamative response of the excessive alveolar epithelium in 5 and 6 days. The sloughed off epithelial cells were demonstrated as cell sheets or as clusters of epithelial cells. Inflammatory infiltrates in alveolar and interstitial spaces consisted of neutrophils and monocytes (or macrophages) at early stages, and mononuclear cells or macrophages at latter stages. Observation in 2nd and 3rd week showed accumulation of macrophages with many osmiophilic lamellar bodies in the alveolar spaces. The alveolar wall lining epithelium was still cuboidal or elliptical in shape in some alveoli and membranous in the others. Thickened alveolar septa at this stage were also noted. Thus this animal model appears to be a valuable tool for further understanding of the events leading to proliferation and desquamation of the alveolar lining epithelium.

Animals↗
PubMed1980

Effects of a new adenosine deaminase inhibitor, isocoformycin, on toxicity, antitumor activity and tissue distribution of formycin A and 9-beta-D-arabinofuranosyladenine.

Single intraperitoneal and intravenous injections of isocoformycin at 1,200 mg/kg did not cause the death of mice. Isocoformycin which inhibited adenosine deaminase enhanced significantly the toxicity of formycin A and ara-A at various combination ratios. Isocoformycin potentiated antitumor activity of formycin A and ara-A against L1210 leukemia. Formycin A and ara-A disappeared rapidly from the blood and tissues and could not be found in any tissues even 0.5 hour after a single intraperitoneal injection. However, when used in combination with isocoformycin both were detected in the blood and tissues, especially at high concentration in liver and kidney. These indicate that the deamination of formycin A and ara-A is blocked by isocoformycin in vivo.

Adenosine Deaminase Inhibitors↗