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Biomedical subjects

Y Abiko

Publications and source records attributed to Y Abiko.

At least 253 records · Page 14Linked to original sources
PubMed1986

Effect of dilazep on decrease in myocardial pH during ischemia in dogs.

The present study was undertaken in order to examine whether dilazep (1,4-bis-[3-(3,4,5-trimethoxybenzoyloxy)propyl]perhydro-1, 4-diazepine dihydrochloride monohydrate) attenuates myocardial acidosis induced by coronary artery occlusion in dogs. In dogs with nonischemic normal heart, dilazep (300 or 500 micrograms/kg i.v.) increased blood flow in the left anterior descending coronary artery (LAD) with a decrease in heart rate and diastolic blood pressure. In other dogs, LAD flow was reduced by an occluder by 57 to 68% (partial occlusion) for 90 min. Partial occlusion for 30 min decreased myocardial pH by 0.67 to 0.87 pH units, increased ST segment of the surface electrocardiogram, and decreased regional myocardial contractile force. Dilazep was injected i.v. 30 min after partial occlusion. The decrease in myocardial pH induced by partial occlusion was attenuated by the injection of 300 micrograms/kg of dilazep insignificantly and by that of 500 micrograms/kg of dilazep significantly. Restoration of myocardial [H+] induced by dilazep was calculated from the myocardial pH data. Dilazep (500 micrograms/kg) restored myocardial [H+] induced by partial occlusion by 56.7%, and saline solution restored it by 27.4% 60 min after the drug injection, the actual restoration induced by dilazep being 29.3%. Dilazep, however, did not restore the ST segment elevation and contractile force decrease. It is concluded that dilazep attenuates myocardial acidosis during ischemia.

Animals↗
PubMed1985

Inhibition with NCO-700, a protease inhibitor, of degradation of cardiac myofibrillar proteins during ischemia in dogs.

NCO-700 is a newly synthesized inhibitor of both cathepsin B and calcium-activated neutral protease. We examined whether NCO-700 inhibits degradation of myofibrillar proteins induced by cardiac ischemia in dogs anesthetized with pentobarbital. Cardiac ischemia was produced by complete occlusion of the left anterior descending coronary artery (LAD) for 3 or 6 hr. Myofibrils were prepared from the ischemic myocardium, in which LAD was occluded, and from the nonischemic myocardium, in which LAD was not occluded. Electrophoresis of myofibrils prepared from the ischemic myocardium revealed that there were many degradation bands of myofibrillar proteins as well as the bands corresponding to alpha-actinin (AN), the 55 kDa protein (55 K), actin (A), tropomyosin (TM), troponin I (TN I), myosin light chain 1 (LC1) and myosin light chain 2 (LC2). In addition, the content of AN, 55 K, A, TM, TN I, LC1 and LC2 in the ischemic myofibrils was lower than that in the nonischemic myofibrils. Treatment with NCO-700 at the total dose of 20 mg/kg, which was injected intravenously before and during ischemia, inhibited both appearance of the degradation bands and the decrease in the content of A, TM, TN I, LC1 and LC2 being produced by cardiac ischemia. NCO-700, however, did not inhibit the decrease in the content of 55K and AN being induced by ischemia.

Animals↗
PubMed1985

Fibrinolytic action of a new semi-synthetic polysaccharide sulfate, galactan polysulfate (DH 6322), in the rat.

Galactan polysulfate, DH 6322, when added to rat plasma, shortened euglobulin clot lysis time through both increase in the recovery of plasminogen activator activity in euglobulin precipitates and direct acceleration of fibrinolysis. DH 6322 treatment also resulted in accelerating plasma clot lysis induced by urokinase. The effect of DH 6322 was further studied with a purified system composed of bovine fibrinogen and plasminogen. In this system, DH 6322 was found to be a potent stimulator of both fibrinolysis and fibrinogenolysis induced by urokinase. The activation process of plasminogen was not affected by DH 6322 even in the presence of fibrin or fibrinogen. The accelerating effect of DH 6322 on fibrinolysis in the purified system was scarcely affected by addition of plasma antifibrinolytic factors. DH 6322 also stimulated fibrin clot lysis induced by a low concentration of purified plasmin in place of plasminogen and urokinase, and its accelerating effect was not observed in the presence of tranexamic acid. Formation of fibrin clot susceptible to generated plasmin was observed at relatively high concentrations of DH 6322 above 80 micrograms/ml. Additional experiments indicated that DH 6322 increased the amount of plasminogen bound to fibrin. These results suggested that DH 6322 stimulated fibrinolysis through increasing the binding of plasminogen or plasmin to fibrin.

Animals↗
PubMed1985

Antithrombotic and thrombolytic effects of galactan polysulfate (DH 6322) in rats.

Anticoagulant, fibrinolytic and thrombolytic effects of galactan polysulfate (DH 6322), a new semi-synthetic polysaccharide sulfate of bacterial origin, were studied in the rat in vitro, ex vivo and in vivo. Addition of DH 6322 to citrated plasma gave a 50% reduction in euglobulin lysis time at around 50 micrograms/ml and a 2-fold prolongation in plasma recalcification time at 40 micrograms/ml. Intravenous injection of DH 6322 caused significant acceleration of euglobulin clot lysis and urokinase-induced plasma clot lysis at doses as low as 2 mg/kg, and also significant prolongation of plasma recalcification time. Oral application of the compound gave similar effects only at an extremely high dose of 3 g/kg. When injected intravenously before induction of pulmonary thrombosis by lactic acid infusion, DH 6322 was found to be effective in preventing thrombus formation. In progressive venous thrombosis induced by insertion of a steel coil into the inferior vena cava, DH 6322 treatment also caused a significant reduction of thrombus size together with increase in the serum levels of fibrin degradation products. The findings indicate that the antithrombotic effects of DH 6322 result from its enhancement of the fibrinolytic potential as well as its anticoagulative action.

Animals↗
PubMed1985

Effect of NCO-700, an inhibitor of protease, on myocardial pH decreased by coronary occlusion in dogs.

During myocardial ischemia in dogs effects of NCO-700, a protease inhibitor on myocardial pH, were investigated. Ischemia was produced for 90 min by partial occlusion of the left anterior descending coronary artery (LAD). Myocardial pH was measured by a micro glass pH electrode inserted in the subendocardium of the LAD area. Before partial occlusion, myocardial pH was 7.50-7.67. It decreased by 0.65 to 0.86 pH units after partial occlusion. NCO-700 was injected intravenously after 30 min partial occlusion. At a dose of 5 or 20 mg/kg NCO-700 increased myocardial pH, which had been decreased by LAD partial occlusion, by 0.26 or 0.31 pH units, respectively. In the nonischemic myocardium pH increased only 0.03 units. Drug-induced restoration of myocardial [H+] was then calculated. At a dose of 5 or 20 mg/kg NCO-700 restored myocardial [H+], which had been increased by partial occlusion. However, NCO-700 did not attenuate the ischemia-induced elevation of ST segment of the surface electrocardiogram. These observations demonstrate that NCO-700 attenuates myocardial pH depressed by partial occlusion of LAD.

Animals↗
PubMed1985

Glycylprolyl dipeptidylaminopeptidase from Bacteroides gingivalis.

Dipeptidyl aminopeptidase activity was found in the culture medium of Bacteroides gingivalis 381. The enzyme, hydrolyzing glycylprolyl-4-methylcoumaryl-7-amide, was purified 750-fold from culture medium by ammonium sulfate precipitation, Sephadex G-200 gel filtration, and DEAE Bio Gel A column chromatography. The molecular weight, determined by gel filtration, was approximately 160,000. The isoelectric point of the enzyme, estimated by isoelectric focusing using polyacrylamide disk gel electrophoresis, was about pH 6.2. The optimum pH of the enzyme was about 8.0, and the Km value was 0.05 mM. The enzyme activity was strongly inhibited by phenylmethylsulfonylfluoride and diisopropylfluorophosphate. The purified enzyme specifically cleaved glycylprolyl dipeptide from partially digested type I collagen.

Bacteroides↗
PubMed1985

Difference in the time course between increases in coronary flow and in effluent adenosine concentration during anoxia in the perfused rat heart.

The isolated rat heart was perfused by Langendorff's technique with either an oxygenated (95% O2 and 5% CO2) or an anoxic (95% N2 and 5% CO2) solution. Anoxia increased coronary flow and effluent adenosine concentration, but the time course of these changes was discordant; coronary flow increased transiently (the maximum increase in flow was observed within 1-2 min after the onset of anoxia), whereas the effluent adenosine concentration increased as a function of the time during anoxia. The concentration of effluent adenosine reached 3 microM 10 min after anoxia. The tissue (myocardial) adenosine content changed in parallel with the effluent adenosine concentration. An infusion of adenosine increased coronary flow dose-dependently, and the maximum increase was obtained when 0.27 microM of adenosine was infused. Effluent adenosine concentration was 0.05-0.3 microM in both anoxia and adenosine infusion experiments at the time when the maximum increase in coronary flow occurred. An increase in concentrations of adenosine above 0.05-0.03 microM in the effluent was not accompanied by an increase in coronary flow. These results raise a question about the role of adenosine in regulating coronary circulation during anoxic perfusion, though there is a possibility of vasodilatory function of adenosine in early period of anoxic perfusion.

Adenosine↗
PubMed1985

Attenuation by atenolol of myocardial acidosis during ischemia in dogs: contribution of beta-1 adrenoceptors to myocardial acidosis.

Coronary artery occlusion produces myocardial acidosis, which can be attenuated by propranolol or sotalol. The present study was undertaken to determine which beta adrenoceptors, beta-1 or beta-2, contribute to the ischemic myocardial acidosis. Dogs anesthetized with pentobarbital were used. In the first series of experiments, blood flow in the left anterior descending coronary artery was reduced by an occluder to about one-third of the original flow. Myocardial pH was measured by means of a micro pH electrode inserted into the left anterior descending coronary artery area at the depth of about 8 mm. The myocardial pH decreased from 7.44 to 7.55 to 6.73 to 6.89, 30 min after partial occlusion being the time immediately before an i.v. injection of drugs. Atenolol (1 mg/kg) attenuated significantly the decrease in myocardial pH that had been induced by partial occlusion, whereas IPS 339 (360 micrograms/kg) and ICI 118,551 (300 micrograms/kg) did not. The pH effect of atenolol was confirmed even in the paced heart. In the second series of experiments, the antagonistic action of these drugs on the isoproterenol-induced increase in heart rate and myocardial contractile force and the decrease in diastolic blood pressure was investigated. By this experiment, it was confirmed that atenolol has the beta-1 adrenoceptor antagonistic action, and the IPS 339 and ICI 118,551 have the beta-2 antagonistic action. These results suggest that the activation of beta-1 adrenoceptors contribute to the myocardial acidosis during ischemia.

Acidosis↗
PubMed1985

Effect of cinpropazide on ischemic myocardial acidosis in dogs.

In dogs anesthetized with pentobarbital, the left anterior descending coronary artery (LAD) was occluded by an occluder so that the LAD flow could be set to about half the original flow (partial occlusion). Partial occlusion of the LAD continued for 90 min, and myocardial pH decreased by 0.71 pH unit 30 min after the start of partial occlusion. Cinpropazide, a coronary vasodilator, was injected intravenously 30 min after partial occlusion. Cinpropazide at the dose of 1 mg/kg, which increased LAD flow insignificantly in the nonischemic normal heart, attenuated the myocardial pH that has been reduced by partial occlusion, with a slight reduction in diastolic blood pressure. Restoration of myocardial [H+] 60 min after the injection of cinpropazide was 75.3%, and that of saline solution was 29.5%, indicating that cinpropazide restored the myocardial [H+] by 45.8% during ischemia. The effect of cinpropazide to increase myocardial pH was not observed in the dog with nonischemic heart, however. It is concluded that cinpropazide attenuates myocardial acidosis during ischemia.

Acidosis↗
PubMed1984

Purification and some properties of rat alpha 2-plasmin inhibitor.

alpha 2-Plasmin inhibitor was purified from rat plasma by the procedures including sequential lysine-Sepharose chromatography, ammonium sulfate precipitation and plasminogen-Sepharose, DEAE-Sephadex, concanavalin A-Sepharose, and Sephadex G-200 chromatographies. The final preparation was homogeneous as judged by sodium dodecyl sulfate polyacrylamide gel- and immuno-electrophoresis. It was a single polypeptide chain with a molecular weight of about 7.1 X 10(4) daltons and was found to possess fast-acting antiplasmin activity. There existed other molecular forms of alpha 2-plasmin inhibitor-related antigen with molecular weight of 6.3 X 10(4) and 6.1 X 10(4) daltons. The latter was found to be inactive in binding to plasminogen and in inhibiting plasmin activity. Normal plasma level of alpha 2-plasmin inhibitor in rats was immunologically determined to be 7.9 +/- 0.8 mg/dl. Indirect evidence was obtained that rat alpha 2-plasmin inhibitor was incorporated into cross-linked fibrin during blood clotting.

Animals↗
PubMed1984

Physiological role of alpha 2-plasmin inhibitor in rats.

For understanding the physiological role of rat alpha 2-plasmin inhibitor (alpha 2-PI), the effect of alpha 2 PI deficiency on the fibrinolytic system was studied in rats in vitro and in vivo. Selective removal of alpha 2 PI from plasma was achieved in vitro and in vivo by immune complex formation with specific anti-rat alpha 2 PI rabbit gamma-globulin and the F(ab')2 fragments derived from specific anti-rat alpha 2 PI rabbit IgG, respectively. Depletion of alpha 2 PI from plasma resulted in almost complete loss of the fast-acting antiplasmin activity of the plasma and in a marked acceleration of urokinase-induced plasma clot lysis. A similar acceleration of thrombus dissolution was also observed, when a thrombus isolated from a thrombosed rat was incubated in alpha 2 PI-deficient serum in vitro. The effect was found to be inversely proportional to the alpha 2 PI levels in plasma or serum. When alpha 2 PI deficiency was induced in rats with experimental venous thrombosis, thrombus size was markedly decreased in association with elevation of serum fibrin degradation products and reduction of plasma plasminogen, indicating enhanced fibrinolysis in vivo. In addition, alpha 2 PI deficiency for a longer period induced a mild bleeding tendency at the sites of venipuncture. These results indicate that alpha 2 PI plays an important role as a stabilizer of fibrin in rats, as in humans.

Animals↗
PubMed1984

Beta-lactam antibiotics resistant Rothia dentocariosa from infected postoperative maxillary cyst: studies on R-plasmid and beta-lactamase.

A cephalexin and penicillin G resistant strain of Rothia dentocariosa was clinically isolated from pus of infected postoperative maxillary cyst. The strain contained multiple plasmids. Plasmid curing tests with rifampicin eliminated cephalexin and penicillin G resistant phenotypic functions and 47 megadalton plasmids from the strain. Beta-Lactamase isolated from the strain hydrolyzed cephalosporin more efficiently than penicillin.

Actinomycetaceae↗
PubMed1984

Fibronectin mediated human gingival fibroblasts attachment to bone.

Experiments were undertaken to examine the effects of acid and fibronectin treatments on the human gingival fibroblast attachment to bone in vitro. The binding of [125I]fibronectin to bone powders was dependent on concentration of fibronectin and incubation time. The optimum pH of [125I]fibronectin attachment to bone powders was 6.0 using phosphate buffer. Acid treatment on bone powders in low concentration such as 10 mM of citric acid enhanced [125I]fibronectin binding. The attachment of [3H]thymidine labelled human gingival fibroblasts to bone was enhanced 1.5, 2.0 and 2.5-fold by citric acid, fibronectin and citric acid + fibronectin treatment, respectively. Scanning electron microscopic observations confirm that citric acid and/or fibronectin treatment enhanced the cell number and rapidity of fibroblast attachment to bone surfaces.

Animals↗
PubMed1984

Changes in cardiac ultrastructure and myofibrillar proteins during ischemia in dogs, with special reference to changes in Z lines.

This study was designed to examine whether or not coronary ligation produces changes in myofibrillar proteins, especially Z line proteins including alpha-actinin and the 55 kDa protein, in the dog. Changes in ultrastructure of the myocardium after coronary ligation were also studied. A branch of the left anterior descending coronary artery was ligated for a period of 3, 6, 24 or 72 h. Coronary ligation produced ultrastructural changes in Z lines (characterized by broader and wavy Z lines) as well as changes in glycogen granules, mitochondria, and nuclei. Myofibrils were isolated from the myocardium that had been made ischemic by coronary ligation. The yield of myofibrils was reduced as the ischemic period was increased. Phase microscopic examination of the isolated myofibrils from the ischemic myocardium revealed that there were spread Z lines with wider I bands, these changes being essentially the same as those observed by the electron microscope in the ischemic myocardium. The effect of coronary ligation on the myofibrillar proteins was studied by means of polyacrylamide gel electrophoresis. In the isolated myofibrils from the myocardium 3 h after coronary ligation, there were decreases in the percentage of actin, alpha-actinin and the 55 kDa protein, and these changes progressively increased with lengthening of the ischemic period. These results suggest that coronary ligation decreases actin, alpha-actinin and the 55 kDa protein, in association with ultrastructural changes of the Z lines.

Actinin↗
PubMed1984

Nicorandil attenuates myocardial acidosis during coronary occlusion in dogs.

In dogs anaesthetized with pentobarbitone, the left anterior descending coronary artery (LAD) was partially occluded. Before and 30 min after partial occlusion, the myocardial pH was 7.52-7.54 and 6.89-6.91, respectively. Nicorandil (50 micrograms kg-1, i.v.) increased the pH that had been reduced by partial occlusion and this effect lasted at least 60 min. Thus nicorandil attenuates ischaemic myocardial acidosis.

Acidosis↗
PubMed1984

Is ischemia-induced pH decrease of dog myocardium respiratory or metabolic acidosis?

Ischemia causes myocardial acidosis and elevation of myocardial CO2 tension (PCO2). We performed the present study to examine whether accumulation of hydrogen ion is a cause or result of accumulation of CO2. The myocardial pH and PCO2 were measured simultaneously in the dog heart, and the concentration of HCO-3 [( HCO-3]) was calculated according to the Henderson-Hasselbalch equation. Ischemia was induced by either partial or complete occlusion of the left anterior descending coronary artery (LAD). After LAD occlusion, the myocardial pH decreased with a marked decrease in [HCO-3], indicating that metabolic acidosis occurred. We ascertained in experiments with blood sample in vitro that an addition of lactic acid into blood decreased both [HCO-3] and pH (metabolic acidosis), whereas an addition of CO2 gas into blood increased [HCO-3] and decreased pH (respiratory acidosis). These findings suggest that ischemic acidosis is not respiratory in nature, but metabolic. The myocardial pH decrease due to ischemia, however, cannot be explained by the tissue lactate accumulation alone, because the decrease of [HCO-3] is far greater than the increase of lactic acid during ischemia.

Acidosis↗