Tatsuo Shimamoto

Estrogen and hyperaggregability of platelets measured by the screen filtration pressure (SFP) method in Takayasu's disease.

Platelet aggregability in 10 females (32.2 ± 3.1 years) with Takayasu’s disease and 16 healthy males (31.7 ± 2.7 years) and 14 females (28.6 ± 2.8 years) was measured by the screen filtration pressure

Effects of Adrenaline and Noradrenaline on Euglobulin Lysis Time and Effects of Adrenergic Receptor Blocking Agents on Shortening of Lysis Time by Adrenaline

Adrenaline in an intravenous dose of 0.1 µg per kg induced a significant shortening of the euglobulinlysis time in 8 healthy subjects. On the other hand, the euglobulin lysis time was not hastened by intravenous injections of the same dose of 1-noradrenaline in 8 healthy subjects. The shortening of the euglobulin lysis time induced by 0.1 µg per kg of adrenaline was blocked by the pretreatment with 300 mg of nethalide in 8 healthy subjects but not blocked by the pretreatment with 30 mg of phenoxybenzamine in 5 healthy subjects.

Treatment of Experimental and Human Atherosclerosis with Bradykinin-Antagonist, Pyridinolcarbamate: A Preliminary Report

At the beginning of this century there were three incurable lesions having dead spaces with an accumulation of dead subtances: gummatous in syphilis, caseous in tuberculosis, and atheromatous in atherosclerosis. The discovery of modern chemotherapeutic agents has enabled cures for the first two, but the problem of atherosclerosis remains to be solved.

Platelet aggregation by platelet-clumping substance

Abstract The platelet-clumping substance isolated from rabbit plasma by the authors aggregated washed rabbit platelets, while ADP did not. The presence of AMP or adenosine did not inhibit the appearance of platelet aggregation induced by the clumping substance. Pretreatment of phosphoenol-pyruvate and pyruvate kinase on unwashed platelets did not affect the platelet aggregation by the clumping substance. It clumped human platelets and also shrimp thrombocytes. Electron microscopic findings showed that platelets to which the clumping substance was added aggregated in their original form as falt disc shapes with few pseudopods. While fusion of membrane was present, microtubules were observed in its regular form. These results showed the existence of a platelet-clumping substance in blood that is different from ADP, collagen, thrombin, adrenaline etc. and may play an important role in hemostasis and thrombogenesis.

A CASE OF SARCOIDOSIS WITH A MANIFESTATION OF MENINGITIS AND POLYRADICULONEURITIS

髓膜炎および多発神経根炎症状を呈したサルコイドージス(サ症)の1例を報告するとともに,本邦神経サ症例を文献で検討し,本例が極めて希な症例であることを示した.症例は36才,女性.約5カ月間微熱が持続していたが,昭和53年4月16日から頭痛,悪心,傾眠傾向, 20日から全身の不定の疼痛,下肢にはじまる上行性の運動麻痺が出現, 27日には起立不能となり, 5月11日に当科に入院した.入院時,発熱(37.2°C)の他は理学的所見,一般検査に特別な異常なく,神経学的には,髄膜刺激症状,右第VII, IX, X脳神経障害,両側第VIII脳神経障害,四肢でび漫性の筋萎縮を伴う対称性の筋力低下,腱反射低下を認めた.髄液は初圧70mmH2O,細胞数9/mm3,蛋白187ng/dl,グロブリン反応陽性,糖39mg/ml,筋電図では神経原性変化,腓骨神経伝導速度低下の所見を得た.画側肺門リンパ節腫脹,耳下腺および斜角筋リンパ節生検でサ肉芽腫を証明,細胞免疫低下等の所見から,神経サ症と診断した. prednisoloneme経口投与により,著明改善し10月25日杖歩行で退院.文献的には, 1978年までに本邦で86例の神経サ症の報告があり,うち中枢神経障害は25例(29.1%),脳神経障害は61例(70.9%),脊髄神経障害は10例(11.6%)に認められた.しかし,臨床的に明確な髄膜炎症状または多発神経根炎症状を呈した症例の報告は極めて少なく,本症例の臨床像は希なものと考え報告した.

A role of extracorporeal circuit in the post-perfusion thrombocytopenia: A scanning electronmicroscopic observation

Thrombocytopenia is one of the adverse effects of extracorporeal circulation (ECC) but the mechanism of which has not been fully understood. Blood-gas interface, mechanical agitation, rough surface of extracorporeal circuit and sequestration in the liver have been considered to be a cuase of platelet loss. Extracorporeal circuit which provides large artificial surface for contact of blood has been blamed as the site of platelet destruction during oxygenation. However, the part of the oxygenator responsible for platelet loss has not been located. This study was designed to identify the sites of extracorporeal circuit responsible for platelet loss during ECC with scanning electron microscopy (SEM) of the post-perfusion circuit. The accumulation of platelet aggregates was most pronounced at the defoaming net and blood filter where a sudden changes in velocity of blood flow take place. The aggregates were considered to be formed locally at these sites. However, there were no accumulation and/or adherence of platelet aggregates of significant degree at the other parts of the circuit, namely venous and arterial tubings, venous colum and arterial reservoir. Platelets seem to be removed from the circulation during each passage by defoaming net and blood filter. However the other parts of the circuit seem to be less blamed for the platelet loss. It was not possible to conclude whether the formation and trapping of platelet microaggregates at the defoaming net and blood filter or the destruction by oxygen bubbles is mainly responsible for the plateletloss during ECC.