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S Higasa

Publications and source records attributed to S Higasa.

6 recordsLinked to original sources

Serum macrophage colony-stimulating factor (M-CSF) level is elevated in patients with old cerebral infarction related to vascular damage.

We measured the serum levels of macrophage colony-stimulating factor (M-CSF) in 37 patients with an old cerebral infarction who had been surmised to have a damaged vessel wall and who had been in a stable condition for over three months after stroke onset, and those of 41 healthy control subjects. The M-CSF levels in the patients were significantly higher (P < 0.01) than those of the controls at 1320.4 +/- 410.6 unit/ml and 853.9 +/- 180.3 unit/ml, respectively. The plasma levels of von Willebrand factor (vWF) antigen (P < 0.01) and thrombomodulin (TM) (P < 0.05), as well as those of thrombin-antithrombin III (TAT) complex (P < 0.05), prothrombin fragment 1+2 (F1+2) (P < 0.02), D-dimer products of crosslinked fibrin degradation products (D-dimer) (P < 0.01), and plasmin-antiplasmin (PAP) complex (P < 0.05) in the patients were also significantly higher than those in the controls. Significant positive correlations (P < 0.01) were found between these parameters and the M-CSF level, but there was no significant correlation between the M-CSF level and the white blood cell count, serum lipids, or blood pressure. Based on these results, we suggest that an increased M-CSF level indicates vascular damage or a thrombotic state in patients with an old cerebral infarction.

Aged

[Inhibitory effect of isosorbide dinitrate on whole blood aggregation].

Isosorbide dinitrate (ISDN) has an inhibitory effect on platelet aggregation through the generation of nitric oxide (NO). We examined the effect of ISDN on whole blood aggregation using an impedance aggregometer. Blood samples were obtained from 16 patients with acute myocardial infarction and 4 patients with angina pectoris before and after an intravenous administration of ISDN during coronary arteriography. Whole blood obtained from normal healthy donors was used for an in vitro study. Whole blood aggregation after administration of ISDN was significantly inhibited compared to that before administration (36.1 +/- 8.3 vs 43.7 +/- 8.4 omega, p < 0.001), and cyclic guanine monophosphate (c-GMP) concentration increased (5.56 +/- 2.0 vs 5.14 +/- 1.86 p mol/ml, p < 0.05). The inhibitory effect of ISDN was also observed in the in vitro study, in which the effective concentration of ISDN corresponded to the blood level of ISDN (> or = 10(-7) mol) in the clinical setting. The inhibitory effect of ISDN was diminished by the addition of methylene blue or NG-monomethyl-L-arginine monoacetate in the exo vivo and in vitro studies. The concentration of c-GMP was increased by the addition of ISDN to platelets and white blood cell suspended plasma compared to the control (1.93 +/- 0.50 vs 1.77 +/- 0.42 p mol/ml, p < 0.05), but there was no significant difference when ISDN was added to platelet-rich plasma. These results suggest that ISDN inhibits whole blood aggregation through NO generation and white blood cells are important in the mechanism of ISDN action.

Angina Pectoris

Enhancing effect of platelets on staphylokinase-mediated clot lysis and plasminogen activation.

The effects of platelets on clot lysis and plasminogen activation by staphylokinase (SAK) were investigated. At concentrations ranging from 2 x 10(-7) to 1 x 10(-5)g/ml of SAK, the lysis time of platelet-rich plasma clots (PRP-clots) was shorter than that of platelet-poor plasma clots (PPP-clots). This reduction of clot lysis time was observed in a dose-dependent manner on platelet count in PRP. The activation rate of plasminogen by SAK measured by the amidolytic method using S-2251 was enhanced by the addition of washed platelets. These enhancing effects of platelets on clot lysis and plasminogen activation were not altered by pretreatment of platelets with indomethacin and theophylline, but were diminished by platelet disruption. Thus, we concluded that platelets enhance fibrinolytic activity of SAK, and this effect is not due to the release reaction or intracellular contents of platelets, but to the existence of platelet surface in the intact shape as a catalytic site for fibrinolysis.

Blood Platelets

[Factor IX].

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Factor IX