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Biomedical subjects

T Ohshiro

Publications and source records attributed to T Ohshiro.

At least 55 records · Page 3Linked to original sources
PubMed1987

Mechanism of the haemostatic effect of ethanolamine oleate in the injection sclerotherapy for oesophageal varices.

Changes in coagulation and fibrinolysis were investigated in 20 patients with oesophageal varices, who underwent endoscopic injection sclerotherapy (EIS) with 5 per cent ethanolamine oleate (EO), by means of serial determination of plasma fibrinopeptide A (FPA) and fibrinopeptide B beta 15-42 (B beta 15-42). One hour after the completion of EIS, the value of FPA was significantly increased to 38.1 +/- 11.1 ng/ml (mean +/- s.e.m.) from a pre-EIS value of 7.1 +/- 1.4 ng/ml (P less than 0.01) and it gradually returned to normal range by 48 h after EIS. A very similar change was observed in the value of B beta 15-42 (P less than 0.01). These observations indicated that EIS provokes transient activation of coagulation and fibrinolysis. In vitro studies, however, revealed that EO inhibits fibrin clot formation because of the Ca2+-chelating ability of its constituent ethanolamine, although oleate or benzyl alcohol exhibited procoagulant activity in FPA formation in vitro. Nevertheless, an external application of EO or oleate over decapsulized kidney of rat resulted in a significant accumulation of 125I-labelled fibrin(ogen). From these results it was suggested that intravascular injection of EO, which exerts an inhibitory effect on coagulation in vitro, activates the local coagulation system. The activation may be accelerated by an acute inflammatory process provoked by oleate, which is supported by such clinical manifestations as mild fever, retrosternal pain leukocytosis and an increase in plasma fibrinogen level which was observed in all during the period.

Adult↗
PubMed1987

Elucidation of calpain dependent phosphorylation of myosin light chain in human platelets.

Newly synthetized calpain inhibitors (CI-I approximately III) were used to prove potential participation of calpain in protein phosphorylation. CIs were about 1,000 times more potent against platelet calpain I than N-ethyl-maleimide (NEM) and an epoxy succinate derivative (E-64). CI-II inhibited 20K (myosin light chain) and 47K phosphorylation of Ca2+-stimulated lysed platelets as well as protein degradation (actin binding protein, P235). Both myosin light chain kinase (MLCK) and C-kinase dependent phosphorylation of 20K were inhibited by CI-II as demonstrated in phosphopeptides mapping. Electropermeabilized platelets (EP) were employed to examine the effects of CI-II on Ca2+ mediated reactions in non-lysed platelets. Phosphorylation of 20K and 47K induced by Ca2+ addition to EP was inhibited by CI-II, though secretory response was not modified. Only MLCK dependent phosphorylation of 20K was observed in Ca2+-activated EP, which was inhibited by CI-II. Collectively, the data indicated that calpain may activate both MLCK and C-kinase to phosphorylate 20K by partial proteolysis.

Acriflavine↗
PubMed1986

Studies on liposome-encapsulated heparin.

In order to prolong the anticoagulant activity of heparin in vivo, attempts were made to encapsulate heparin into liposomes. Liposome-encapsulated heparin (lipo-heparin) prepared was large multilamellar vesicles (0.5-4.0 micron in diameter). The activity of lipo-heparin was 1.6-5.2 X 10(3) U/g lipid with recovery rate ranged between 0.4 to 1.3% and stable in saline at 4 degrees C for at least two weeks. When intravenously administered into rats, the anticoagulant activity of lipo-heparin was significantly prolonged (approximately three times), as compared with that of untreated heparin. Furthermore, the activity of lipo-heparin could be neutralized by protamine sulfate. From these observations, it was concluded that liposome-encapsulation of heparin results in the prolonged anticoagulant effect in vivo and lipo-heparin may be applicable for clinical use, after further studies on side effects of liposomes are completed.

Animals↗
PubMed1986

Analysis of platelet phospholipids by high performance liquid chromatography. II--Studies on hitherto unknown peak of phospholipid of human platelets.

With our proposed method to analyze platelet phospholipids, utilizing a normal phase high performance liquid chromatography (HPLC), it was able to quantify the amount of major platelet phospholipids (Thromb. Res. 36, 335-344, 1984). A prominent peak of unknown nature (PX) was identified close to the peak of phosphatidylcholine in the HPLC analysis of platelet phospholipids, and the attempts were made to elucidate the nature of PX. By applying several additional authentic phospholipids and those treated by acids on both the HPLC and thin layer chromatography, it was concluded that the major component of PX is 1-lyso phosphatidylethanolamine plasmalogen (PEP), artificially degraded from PEP by the acidic HPLC solvent system. No further degradation of 1-lyso PEP was observed and the absorbance of possibly co-migrated 2-lyso PE in activated platelets was negligible because it was devoid of C-2 double bonds sensitive to the absorbance used in the assay. Therefore, the relative amount of PEP may be detected based on the number of double bonds in platelet PEP. The amount of PEP thus measured was significantly decreased in thrombin-stimulated platelets, suggesting a possible participation of PEP in stimulus-linked platelet reaction.

Blood Platelets↗
PubMed1986

Interrelationship between secretion, protein phosphorylation and intracellular Ca2+ concentration in platelets stimulated by thrombin or thromboxane A2 analogue.

The interrelationship between ATP-secretion, protein phosphorylation and intracellular Ca2+ concentration ([Ca2+]i) was studied in both 32P and quin 2 loaded human platelets stimulated by thrombin or thromboxane A2 analogue (STA2). In platelets stimulated by thrombin, the degree of 47,000 dalton polypeptides (P47) phosphorylation was observed in completely dose-related manner, regardless of the amount of [Ca2+]i. In the same condition, the degree of myosin light chain (P20) phosphorylation, however, was well correlated with ATP secretion and [Ca2+]i, when platelets were stimulated by lower dose of thrombin. The similar results were obtained in platelets stimulated by STA2. These findings suggested that P20, but not P47, phosphorylation in activated platelets is mediated by a rise of [Ca2+]i and is well correlated with the secretory reaction. It was unlikely that P47 phosphorylation plays any role in promoting platelet activation.

Adenosine Triphosphate↗
PubMed1986

Chromogenic assay of endotoxin in platelet poor or rich plasma.

In order to determine which sample preparation, platelet rich plasma (PRP) or platelet poor plasma (PPP), is more suitable for clinical endotoxin assay, we investigated the binding of endotoxins to platelets by comparing the amount of endotoxin in PRP with that in PPP, using a newly developed colorimetric assay with chromogenic substrate (Boc-Leu-Gly-Arg-pNA). When purified endotoxins were added to human whole blood, the amount of endotoxin recovered in PPP was significantly lower than that in PRP for all endotoxins tested except that from E. coli 0111:B4 and their ability to bind to platelets was varied depending on the species of bacteria from which they were purified. However, the amount of endotoxin in PRP obtained from surgical patients (n = 50) was almost same as that in PPP with a correlation coefficient r = 0.95, indicating that natural endotoxins circulating in human blood may not bind to platelets and that PPP can be used for endotoxin assay as well as PRP.

Binding Sites↗
PubMed1986

The CO2 laser as an ideal microsurgical tool.

The CO2 laser was used as a multipurpose microsurgical tool. It effectively evacuated cysts, vaporized tumors, coagulated fine blood vessels, abraded and flattened scars and rough tissue, and separated the epidermis from the dermis. Focused and defocused modes were applied to various lesions ranging from cysts to freckles. CO2 laser microsurgery differs from previous methods in that extremely fine and controlled therapy can be conducted with minimal damage to surrounding tissues and organs. Theories, techniques, and several case reports are described.

Acne Vulgaris↗
PubMed1986

Imaging platelet deposition on Dacron bifurcation grafts in man: quantification by a dual-tracer method using 111In-labeled platelets and 99mTc-labeled human serum albumin.

A dual tracer technique using 111In-labeled platelets and 99mTc-labeled human serum albumin was applied to evaluate the thrombogenicity of Dacron bifurcation arterial grafts. The level of platelet accumulation over the whole of the graft was estimated from the ratio of 111In-platelet radioactivity deposited on the vascular wall to these radioactivity circulating in the blood pool, i.e., the platelet-accumulation index (PAI). Furthermore, the PAI value was calculated for each pixel in digitized images and the PAI distribution image (PAI image) was reconstructed. Eighteen patients with DeBakey knitted Dacron bifurcation grafts and 11 normal volunteers were studied. Of the 18 patients, 11 had no graft occlusion (group I) and the remaining 7 (group II) had occlusion. The mean PAI value (+/- SD) over the whole of the graft in group I was 32.6% +/- 33.7% as compared to -8.8% +/- 4.5% in the control group (P less than 0.01). In group I, the PAI value over the entire graft decreased with the age of the graft (r = -0.763; P less than 0.01). In contrast, in group II, platelet accumulation did not diminish with time and persisted beyond the time of which platelet accumulation was no longer found in group I. Moreover, analysis of the PAI images revealed enhanced platelet accumulation on the proximal part of the graft to be more frequent in group II than in group I (6/7 vs 0/11; chi 2c = 10.55; P less than 0.005). The method used for platelet imaging in the present study may be useful in the study of platelet reactions on Dacron arterial prostheses.

Aged↗
PubMed1986

Possible participation of calpain in myosin light chain phosphorylation of human platelets.

We previously demonstrated that myosin light chain kinase (MLCK) of gizzard is proteolyzed by platelet calpain. It has been also reported that partially cleaved MLCK may phosphorylate myosin light chain (20K) in the absence of calmodulin. Therefore, a possible participation of calpain in 20K phosphorylation was studied in human platelets, utilizing various inhibitors. An epoxy succinate derivative (E-64) or N-ethylmaleimide (NEM), used as calpain antagonist, inhibited 20K phosphorylation of Ca2+-stimulated lysed platelets. A synergistic effect between these calpain antagonists and calmodulin antagonist W-7 was observed. Also, the similar results were obtained in 20K phosphorylation of intact platelets. From these observations, it was suggested that 20K phosphorylation in platelets is mediated by two separate pathways, namely calmodulin and calpain dependent pathways, provided that calpain activity is specifically inhibited by the antagonists used.

Blood Platelets↗
PubMed1985

Fluorescent Ca2+-indicator quin 2 as an intracellular Ca2+ antagonist in platelet reaction.

Preincubation of fluorescent Ca2+-indicator quin 2 resulted in inhibition on platelet aggregation and secretion in the absence of extracellular Ca2+. And the mechanism of the inhibition was studied. The inhibition by quin 2 of thrombin stimulated aggregation and ATP secretion of human platelets was dose and incubation time dependent and the inhibition was overcome by an addition of CaCl2 to the suspending buffer. Combination of quin 2 and Ca2+-blockers exerted the complete inhibition of the reaction in the presence of extracellular Ca2+. The inhibitory effect was observed when the intracellular concentration of quin 2 exceeds 3 mM, regardless of the initial dose or the preincubation time. The cellular content of ATP was not reduced by loading platelets with quin 2 in the concentration which exerted an inhibitory effect on the platelet reaction. From these observations, it was postulated that the inhibition is due to chelation of intracellular Ca2+ by quin 2 and the application of this agent as an intracellular Ca2+ antagonist was proposed. Also, we discussed the limitations in the use of quin 2 system as an intracellular Ca2+ indicator.

Adenosine Triphosphate↗
PubMed1985

Hemostatic defects in experimental obstructive jaundice.

To elucidate the etiology of hemostatic abnormalities in cases of obstructive jaundice, we occluded the bile duct of rats for one week and found that the moderately jaundiced rats exhibited a marked reduction in the value of Hepaplastin test and Thrombotest with minimum histological changes in liver. All other coagulation and fibrinolysis profiles were within normal limits. These findings exclude the occurrence of a hypercoagulable state or hypofibrinolytic state in the jaundiced rats due to bile duct occlusion. Similar results were obtained in rats with tube choledochostomy. The abnormalities were almost completely prevented by the daily parenteral administration of vitamin K. These observations suggest that malabsorption of vitamin K may be the sole etiologic factor producing hemostatic defects in case of uncomplicated obstructive jaundice.

Animals↗