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Biomedical subjects

A Suehiro

Publications and source records attributed to A Suehiro.

At least 37 records · Page 2Linked to original sources
PubMed1997

[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↗
PubMed1997

[Effect of thrombolytic agents on platelets and blood coagulation system].

The effect of tissue-type plasminogen activator (tPA) on platelet aggregation and blood coagulation was investigated. Collagen-induced platelet aggregation in washed platelet suspension was significantly inhibited by the addition of tPA, but the effect was limited when platelet rich plasma was used instead of washed platelets because of the presence of alpha 2-antiplasmin in plasma. The diluted prothrombin time was significantly shortened by the addition of tPA to normal plasma, and although the levels of molecular markers of thrombin formation were increased compared to that of normal controls, the increase was diminished when factor VII-deficient plasma was used, suggesting that tPA enhances factor VII. The activated factor VII concentration was significantly increased by the addition of plasmin to factor VII solution. These findings suggest that tPA enhances the coagulation system by factor VII activation through the generation of plasmin in normal plasma. This enhancing effect of tPA on coagulation system may be partly related to vascular reocclusion after thrombolytic therapy.

Blood Coagulation↗
PubMed1995

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↗
PubMed1995

Effects of perfluorocarbon exchange transfusion on reducing myocardial infarct size in a primate model of ischemia-reperfusion injury: a prospective, randomized study.

BACKGROUND: This study was undertaken to test the hypothesis that perfluorocarbons were able to reduce myocardial infarct size in a baboon model of ischemia-reperfusion injury. Exchange transfusion of perfluorocarbons has been shown to reduce myocardial infarct size in the dog, who, unlike the baboon, has an extensive collateral circulation. METHODS: After 15 minutes of occlusion of the left anterior descending coronary artery, 14 baboons were bled to attain a hematocrit of 24% to 26% and were simultaneously transfused, six with Fluosol-DA 20% emulsion and eight with FC-43 emulsion. After 2 hours of ligation, the coronary arteries were reperfused. Baboons were killed 24 hours after ligation, and the hearts were excised. Microvascular dye was infused into the coronary artery to delineate its perfusion bed. Ratios of the mean volume of infarct to the mean volume of perfusion bed were calculated and compared by use of planimetry. A similar protocol was followed in two other groups of baboons except that lactated Ringer's solution was infused into six of them, whereas eight had no exchange transfusions. RESULTS: The ratios of the mean volume of infarct to the mean volume of perfusion bed of the four groups were as follows: Fluosol-DA, 38.1% +/- 7.5%; FC-43, 37.7% +/- 8.3%; lactated Ringer's, 46.9% +/- 10.5%; controls, 65.6% +/- 6.9%. Statistical significance was reached when comparing both perfluorocarbon-treated groups with the controls (p < 0.05 for both groups) but not significant when comparing them with the Ringer's lactate-treated group. CONCLUSIONS: Results suggest that the beneficial effects of exchange transfusion with the perfluorocarbons may be primarily due to hemodilution.

Animals↗
PubMed1995

Heterogeneous expression of glycoprotein Ib, IX and V in platelets from two patients with Bernard-Soulier syndrome caused by different genetic abnormalities.

Bernard-Soulier syndrome (BSS) is a rare inherited bleeding disorder, which is caused by deficiency or decrease of the platelet GPIb/IX/V complex. Analysis of two patients with BSS by flow cytometry of the blood revealed different expression patterns of the components of the GPIb/IX/V complex. In case 1, GPIX was completely absent but residual amounts of GPIb alpha and GPV were detectable; in case 2, GPIb alpha was completely absent. We amplified the coding regions of GPIb alpha, GPIb beta, GPV, and GPIX from the patients' genomic DNA with the polymerase chain reaction (PCR) and sequenced the PCR products. in case 1, we identified a point mutation in the GPIX coding region that changes the codon for tryptophan-126 (TGG) to a nonsense codon (TGA). In case 2, we found a deletion of nucleotide within seven adenine repeats at the position of 1932 to 1938 in the coding region of GPIb alpha, which causes a frame shift that results in 58 altered amino acids and a premature stop codon. These genetic changes alter the transmembrane domain of GPIX or GPIb alpha and, therefore, would prevent proper insertion of the proteins in the plasma membrane. Thus, abnormality of a single component protein (GPIX or GPIb alpha) alters the assembly of the GPIb/IX/V complex and causes heterogeneous surface expression of GPIb alpha, GPV and GPIX.

Adult↗
PubMed1994

Does intravenous glutamine prevent bacterial translocation in hemorrhagic shock?

Bacterial translocation across the gut wall may be associated with insult to the latter. In this situation, intestinal flora can enter the blood stream and lymph nodes and be transported to other organs. Glutamine is a nonessential amino acid not presently included in total parenteral nutrition (TPN) preparations. The use of glutamine-enriched TPN in the rat has resulted in a significant reduction in bacterial translocation. This study attempted to evaluate the role of glutamine in preventing bacterial translocation following hemorrhagic shock in a rat model. Forty Sprague-Dawley rats were equally divided into two groups. The controls were given TPN solution, while the treated group had glutamine instead of the standard alanine present in TPN. Hemorrhagic shock was induced in both groups and blood cultures were performed. Glutamine-treated rats did not show a significant difference in survival suggesting that it is of no particular value in severe hemorrhagic shock in rats.

Alanine↗
PubMed1994

Detection of hydroxyl free radicals in the reperfused primate heart.

Early reperfusion of an ischemic region can result in significant salvage of the area at risk. We show the presence of hydroxyl free radicals at the time of post ischemia reperfusion using electron paramagnetic resonance (EPR) spectroscopy in a macaque model. These free radicals may be formed as a result of reperfusion or may be an un-involved bystander. It is possible that they may be involved in reperfusion injury.

Animals↗
PubMed1994

Correlation between bleeding time and antithrombotic effect of platelet-suppressive agents in rat experimental model.

To examine whether the dosage of a platelet-suppressive agent at which an antithrombotic effect is adequate and bleeding tendency is not increased can be found, the antithrombotic effects, antiplatelet effects and bleeding times of ticlopidine and aspirin were investigated in the rat experimental thrombus formation model. Thrombus formation was determined by measuring the change in wet weight of a silk thread placed in a carotid arteriovenous shunt. Ticlopidine inhibited thrombus formation and platelet aggregation at rather low doses (50-100 mg/kg) without prolonging bleeding time. However, aspirin did not inhibit thrombus formation at even the highest examined dose (200 mg/kg), while bleeding time was prolonged at even the lowest dose (50 mg/kg). These results suggest that a dosage of antithrombotic agent that does not increase bleeding tendency can be easily established using ticlopidine, although it is relatively difficult using aspirin.

Animals↗
PubMed1993

Inhibitory effect of staphylokinase on platelet aggregation.

We investigated the effect of staphylokinase (SAK), which has specific thrombolytic properties, on human platelet aggregation. Platelet aggregation induced with collagen was observed following preincubation of platelets in platelet-rich plasma (PRP) or washed platelet suspension (WP) with SAK at 37 degrees C for 30 min. SAK inhibited platelet aggregation in PRP only at the highest examined concentration (1 x 10(-4) g/ml). Although SAK did not inhibit platelet aggregation in WP which contained fibrinogen, it did when the platelets had been preincubated with SAK and plasminogen. The most effective concentration in WP was 1 x 10(-6) g/ml. The effect could be inhibited by adding aprotinin or alpha 2-antiplasmin. The highest generation of plasmin in the same preincubation fluid was detected at 1 x 10(-6) g/ml SAK. We concluded that SAK can inhibit platelet aggregation in WP by generating plasmin and/or fibrinogen degradation products, but is only partially effective in PRP because of the existence of alpha 2-antiplasmin.

Amino Acid Sequence↗
PubMed1993

Failure of deferoxamine to reduce myocardial infarct size in a primate model of ischemia-reperfusion injury.

Baboons were subjected to treatment with deferoxamine (DF), a strong iron-chelating agent, to inhibit the iron-dependent production of hydroxyl radicals. Studies were then done to determine if this would result in a reduction in the size of myocardial infarct. Baboons underwent occlusion of the left anterior descending coronary artery for 2 hr followed by reperfusion for the next 22 hr. A treated group (n = 4) received a 2-hr preischemic intravenous infusion of DF (10 mg/kg/hr). This infusion continued throughout the ischemic phase and 2 hr into the reperfusion phase. A control group (n = 8) underwent the identical protocol minus the DF infusion. At the end of the reperfusion period, the hearts were sectioned and stained for histological examination. The treated animals had a 22% larger volume of infarct compared with those of the controls (P = 0.06). There was no statistically significant difference (P > 0.05) in hemodynamic or epicardial ST segment measurements between the two groups. In this primate model, there was no myocardial protection afforded by DF. Baboons are similar to humans in that both have minimal collateral circulation. In the literature, DF has been noted to actually contribute to the production of free radicals in certain circumstances. This experiment appears to indicate that caution should be exercised in the use of DF in the treatment of ischemia-reperfusion injury of the heart.

Animals↗
PubMed1993

Comparison of the antithrombotic effects of low molecular weight heparinoid KB-101 and heparin in a rat experimental model.

1. We compared the low molecular weight heparinoid KB-101 and heparin with regard to suppression of experimental thrombus formation and effects on bleeding time, prothrombin time (PT), and activated partial thromboplastin time (APTT) in rats. 2. KB-101 exerted a similar antithrombotic activity as that of heparin. 3. Heparin prolonged bleeding time, PT, and APTT more than KB-101 did. 4. These results suggested that KB-101 is superior to heparin as an anticoagulant.

Animals↗
PubMed1993

[Thrombotic state in antiphospholipid syndrome].

The effect of plasma or IgG fraction obtained from patients with antiphospholipid syndrome (APS) on platelets, coagulation system, and also prostacyclin were examined. APS plasma or IgG fraction induced the activation of platelet aggregation, ATP release, and calcium mobilization. These effects were thought to be related to the enhancement of the direct binding of IgG fraction on platelet surface. In the study of coagulation system, although APS IgG inhibited factor X activation by the neutralization of phospholipid, a result indicating thrombotic state in APS could not be determined. APS plasma inhibited the prostacyclin synthesis in cultured endothelial cells, and the prostacyclin stability in APS plasma was reduced. These activating effect on platelets or inhibitory effect on prostacyclin of APS plasma or IgG fraction was thought to be one of the factors causing thrombotic state in APS.

Adult↗
PubMed1992

Vasorelaxant effect of trapidil on human basilar artery.

We have investigated the vasorelaxant effect of trapidil on human isolated basilar artery. Trapidil (10(-5)-10(-4) M) dose-dependently caused relaxation in vascular strips with or without endothelium, with no significant difference between the two types of strips. The relaxation responses were not inhibited by atropine, propranolol or methylene blue. Trapidil increased the concentration of 6-keto-PGF1 alpha, a prostacyclin degradation product, released from an artery ring in the incubation medium, but trapidil-induced relaxation was not inhibited by indomethacin. Pretreatment of vascular strips with 10(-5) M trapidil increased the relaxation responses to forskolin and dibutyryladenosine cyclic monophosphate but not to sodium nitroprusside or 8-bromoguanosine cyclic monophosphate. Trapidil induced a significant increase in the cAMP concentration but not in the cGMP concentration in artery strips. These results suggest that the relaxation response to trapidil is not caused by prostacyclin release or an increase in cGMP in the smooth muscle, but possibly by an increase in the cAMP levels, probably via an inhibitory effect on cAMP phosphodiesterase.

6-Ketoprostaglandin F1 alpha↗
PubMed1991

Clinical significance of new coagulation and fibrinolytic markers in ischemic stroke patients.

BACKGROUND AND PURPOSE: We investigated plasma levels of D-dimer products of crosslinked fibrin degradation products, thrombin-antithrombin III complex, and plasmin-alpha 2-antiplasmin complex for detecting coagulation system activation in ischemic stroke patients to determine the possible effect of age on these marker levels. METHODS: We measured plasma levels of these three markers in 54 acute ischemic stroke patients within 5 days of stroke onset, in 44 chronic ischemic stroke patients over 3 months from onset, and in 50 age-matched healthy subjects. We divided the stroke patients into two subgroups, those with visible occlusion and those with nonvisible occlusion having obstruction of the major cerebral artery. RESULTS: The plasma levels of these three markers were significantly (p less than 0.01) higher in the stroke patients than in controls. Significant differences did not exist at any level between the patients and controls in the younger-aged subjects (less than or equal to 64 years of age), but did exist in the older-aged subjects (greater than or equal to 75 years of age). An age-related increase of the marker levels was noted between stroke patients and controls. No significant difference in the three markers was found among any of the stroke patients. CONCLUSIONS: Increased levels of these markers in stroke patients seem to be related mostly to age.

Aged↗
PubMed1991

[Clinical usefulness of the measurement of plasma D-dimer levels].

To evaluate the clinical usefulness of D-dimer, various effects on the measurement of D-dimer were examined. Although both fibrinolytic and fibrinogenolytic products were detected by the measurement of FDP, only fibrinolytic products were detected by the measurement of D-dimer. In patients with DIC and other thrombo-embolic diseases, plasma D-dimer levels were significantly higher than in normal persons. A significant positive correlation between plasma D-dimer and serum FDP was found in DIC patients. In patients with DIC associated with acute promyelocytic leukemia, which is thought to be an increased fibrinogenolysis state, serum FDP was higher than the plasma D-dimer which suggests that increased fibrinogenolysis affects the result of serum FDP measurement. Plasma D-dimer significantly increased 5 minutes after endoscopic embolization with thrombin in the patients with esophageal varices. However serum FDP increased 30 minutes after the treatment, which suggests that the D-dimer is more useful for rapid detection of coagulo-fibrinolytic change than serum FDP. Plasma D-dimer was significantly higher in patients with cerebral infarction and increased with age. These finding suggest the usefulness of plasma D-dimer measurement for the specific and rapid evaluation of coagulo-fibrinolytic activation and thrombo-embolic state.

Adult↗