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Biomedical subjects

Y Abiko

Publications and source records attributed to Y Abiko.

At least 289 records · Page 16Linked to original sources
PubMed1982

A neural factor involved in increase of the glycogen phosphorylase activity after coronary ligation in both ischemic and nonischemic areas of the dog heart.

We performed experiments to determine whether or not extracardiac factors are involved in the increase of the glycogen phosphorylase activity after coronary artery ligation in dog hearts. A branch of the left anterior descending coronary artery (LAD) was ligated for 1.5 minutes. The glycogen phosphorylase activity was determined in the endo- and epicardial layers. LAD ligation significantly increased the glycogen phosphorylase activity in both LAD (ischemic) and circumflex (nonischemic) areas. Pretreatment with reserpine (1 mg/kg, im, 24 hours before experiments) or hexamethonium (3 mg/kg, iv) prevented the LAD ligation-induced increase in the glycogen phosphorylase activity, but adrenalectomy did not. In the heart-lung preparation and stellectomized dogs, LAD ligation did not increase the glycogen phosphorylase activity in both ischemic and nonischemic areas. Changes in the glycogen phosphorylase activity in the endocardial layers were not essentially different from those in the epicardial layers. In other dogs, metabolic intermediates and ST segment of the surface electrocardiogram were measured. LAD ligation significantly decreased the tissue level of creatine phosphate and increased that of lactate in the ischemic but not in the nonischemic area. An elevation of ST segment occurred only in the ischemic area. Thus ischemic and nonischemic areas were confirmed. The ATP level, however, did not change in any of the ischemic and nonischemic areas. It is suggested that LAD ligation increases the glycogen phosphorylase activity in both ischemic and nonischemic areas probably by an increase in the efferent cardiac sympathetic nerve activity.

Adrenal Glands↗
PubMed1982

Insulin releasing action of 2-[2-(4,5-dihydro-1H-imadazol-2-yl)-1-phenylethyl] pyridine dihydrochloride sesquihydrate (DG-5128), a new, orally effective hypoglycaemic agent.

2-[2-(4,5-dihydro-1H-imidazol-2-yl)-1-phenylethyl] pyridine dihydrochloride sesquilhydrate (DG-5128) is a new orally effective hypoglycaemic agent structurally unrelated to the known hypoglycaemics. DG-5128 was found to decrease blood glucose levels by stimulating insulin release, like the sulphonylurea hypoglycaemics. However, the study with the rat Langerhans islets in vitro indicated a great difference in mode of stimulation of insulin release between DG-5128 and a sulphonylurea hypoglycaemic, tolbutamide. DG-5128 significantly reversed alpha-adrenergic inhibition of the glucose-primed insulin release from the islets, while tolbutamide did not. From the comparison with the effects of phentolamine, yohimbine and prazosine, DG-5128 was strongly suggested to stimulate the glucose-primed insulin release through antagonizing at alpha 2-adrenoreceptors on the B cells.

Administration, Oral↗
PubMed1982

Crossover plot study of glycolytic intermediates in the ischemic canine heart.

Effects of regional ischemia on myocardial glycolysis were studied by measuring the levels of glycolytic intermediates in the endo- and epicardial layers of the left ventricle in dogs anesthetized with pentobarbital. Regional ischemia was induced by ligating a small branch of the left anterior descending coronary artery. The myocardial tissue samples were removed before and 1.5, 3, 7, or 30 min after coronary artery ligation. Based on a crossover plot study of the glycolytic intermediates, it is suggested that the activity of glycogen phosphorylase was accelerated, while that of phosphofructokinase was inhibited in ischemic myocardium samples removed 1.5, 3, 7, and 30 min after ligation. When the frozen myocardium was allowed to stand at room temperature for 10 min, the crossover plot study revealed acceleration of phosphofructokinase activity. The metabolic response to regional ischemia of the endocardial layers was more marked than that of the epicardial. During ischemia the levels of adenine nucleotides did not change significantly, but those of citrate and hydrogen ions increased significantly. It appears that inhibition of myocardial phosphofructokinase activity during ischemia is partly due to an increase in the levels of citrate and hydrogen ions in the ischemic tissue.

Adenine Nucleotides↗
PubMed1982

Effect of diltiazem, a calcium antagonist, on myocardial pH in ischemic canine heart.

The effect of diltiazem on ischemic myocardial acidosis was studied in the canine heart whose left anterior descending coronary artery was partially occluded to reduce coronary flow to about one-third (partial occlusion). Myocardial pH was measured by use of a micro glass pH electrode. The pH decreased from 7.53 to 6.93 by partial occlusion and appeared to reach a steady state within 30 min. Saline or drugs were injected i.v. 30 min after partial occlusion. The decreased pH increased spontaneously by 34% of the total reduction of pH in the next 60 min after saline injection. Diltiazem (100 micrograms/kg) potentiated the increase in pH; the pH increased by 76% 60 min after the injection. Propranolol (1 mg/kg) also potentiated the increase in pH that had been decreased by partial occlusion. The relation between pH decrease and the tissue levels of metabolites was also studied. The reduction of myocardial pH from 7.5 to 6.8 was accompanied by a 2-fold increase in the tissue lactate content and by decreases in the ATP and creatine phosphate contents. There was a significant correlation between the hydrogen ion concentration calculated from the pH and each of the lactate, ATP and creatine phosphate contents. The present study indicates that diltiazem attenuates ischemic myocardial acidosis.

Adenosine Triphosphate↗
PubMed1982

Hypoglycemic action of 2-[2-(4,5-dihydro-1H-imidazol-2-yl)-1-phenylethyl]pyridine dihydrochloride sesquihydrate (DG-5128), a new hypoglycemic agent.

2-[2-(4,5-Dihydro-1H-imidazol-2-yl)-1-phenylethyl]pyridine dihydrochloride sesquihydrate (GD-5128) is a new hypoglycemic agent structurally unrelated to the known hypoglycemics. It was effective in reducing fasting blood glucose levels in mice, rats, dogs and monkeys at a single oral dose ranging from 5 to 25 mg/kg. DG-5128 was also effective in suppressing hyperglycemia induced by oral and subcutaneous glucose load in mice, rats and monkeys. In addition, it was interesting to find that DG-5128 effectively suppressed glucose-induced and post-prandial hyperglycemia in genetically diabetic mice of AyKK strain which were resistant to the action of tolbutamide, and that it strongly and specifically inhibited adrenaline-induced platelet aggregation. The hypoglycemic activity was not affected by simultaneous administration of other drugs including mefenamate, sulfamonomethoxine, cefazolin, dicoumarol, furosemide and clofibrate. DG-5128 did not cause lactic acidosis in rats even after repeated administration of large doses. These findings suggest usefulness of DG-5128 as a new anti-diabetic agent.

Animals↗
PubMed1981

Comparative study on the effects of a hypoglycemic 2-substituted-2-imidazoline derivative (DG-5128) and tolbutamide on insulin secretion from and insulin synthesis in the isolated rat pancreatic islets.

2[2-(4,5-Dihydro-1H-imidazol-2-yl)-1-phenylethyl]pyridine dihydrochloride sesquihydrate (DG-5128) was found to stimulate the glucose-primed insulin secretion from the isolated rat pancreatic islets throughout the incubation period, unlike tolbutamide which stimulated it only in the initial phase of incubation. The effect of DG-5128 was more pronounced at a higher glucose concentration (5 mg/ml). In the islet perifusion study, DG-5128 was also found to stimulate the glucose-induced insulin secretion in both the first and the second phases of the reaction, in contrast to tolbutamide which stimulated only the first phase of insulin secretion from the perifused islets. DG-5128 gave no significant effect on the glucose-stimulated increase in incorporation of [3H]leucine into the proinsulin and insulin fractions, while tolbutamide significantly inhibited the incorporation especially at a low glucose concentration (1 mg/ml). These and the previous findings indicate that DG-5128 is a new class of hypoglycemic agent with a unique mode of action different from the known hypoglycemics ever reported.

Animals↗
PubMed1981

Effect of probucol on serum lipoprotein levels in normal and dyslipoproteinemic mice.

The effect of probucol was studied on serum lipoprotein levels in normal and cholesterol-fed, hypercholesterolemic mice. In normal mice, probucol caused a significant reduction in LDL + VLDL cholesterol at daily doses above 25-50 mg/kg and also in HDL cholesterol at higher doses. In cholesterol-fed mice, probucol treatment decreased LDL + VLDL cholesterol at daily doses exceeding 200 mg/kg and also HDL cholesterol at a daily dose of 800 mg/kg. The ratio of LDL + VLDL cholesterol to HDL cholesterol was significantly reduced by treatment at 25-100 mg/kg in normal mice and at 200 mg/kg in hypercholesterolemic mice. The ratio was not reduced at doses above these ranges. These dose-effect relationships were not modified by duration of probucol treatment. These findings suggest that there is an optimum dosage of probucol to lower LDL + VLDL cholesterol and the atherogenic index, and that the actual optimum dosage for the beneficial effect depends on blood lipid levels or types of hyperlipidemia. This may be important in the clinical application of this drug, because a negative correlation has been demonstrated between HDL cholesterol levels and ischemic heart disease. Clofibrate treatment did not affect serum lipid levels significantly in either normal or cholesterol-fed mice. Probucol was again effective in lowering LDL cholesterol values in cholesterol-fed mice which had previously been treated with clofibrate for 2 weeks without any beneficial effect. In an additional experiment, it was found that the probucol-induced reduction in cholesterol returned to the pre-treatment levels gradually over several days, depending on the dose and without rebound elevation after withdrawal of the drug.

Animals↗
PubMed1981

Cyclic guanidines. 14. Imidazo[1,2-a]thienopyrimidin-2-one derivatives as blood platelet aggregation inhibitors.

A series of novel 1,2,3,5-tetrahydroimidazo[1,2-a]thieno[2,3-d]-, -[3,2,-d]-, and -[3,4-d]pyrimidin-2-one derivatives has been prepared and tested for the activity of inhibiting platelet aggregation in rats in vitro and ex vivo. These compounds were synthesized through the following reactions: sodium borohydride reduction of 2,4-dichlorothienopyrimidines, followed by ethoxycarbonylmethylation and successive amination. Most of the compounds were found to be potent inhibitors of blood and platelet aggregation. Structure-activity relationships have indicated the essential contribution of the lactam structure and lipophilic substituents on the thiophene ring to the effective interaction of the compounds with a receptor site on the platelet. Among the compounds studied, 1,2,3,5,6,7,8,9-octahydro-[1]benzothieno[2,3-d]imidazo[1,2-a]pyrimidin-2-one (9m) exhibited the most favorable activity.

Animals↗
PubMed1981

Characterization of the Streptococcus mutans plasmid pva318 cloned into Escherichia coli.

We further characterized the cryptic plasmid pVA318 of Streptococcus mutans. It had a contour length of 5.64 +/- 0.26 kilobases and a guanine-plus-cytosine content of 32 to 34 mol %. Upon cloning the pVA318 plasmid into the vector pBR322 in Escherichia coli, we made the following observations. The expression of tetracycline resistance by HindIII-cloned chimeras, where the insert was in the tetracycline resistance promotor, depended on the orientation of the pVA318 insert. Both HindIII-cloned chimeras segregated from polA(Ts) cells at a nonpermissive temperature. Chimeric molecules cloned with PstI initially showed much instability; the reason for this is unknown, although stable variants were obtained. Both HindIII-cloned variants and a PstI-cloned chimera produced a pVA318-specific protein of approximately 20,000 molecular weight in E. coli minicells. The biological function of this protein is not known; it had no bacteriocin activity against S. mutans or group A Streptococcus indicator strains, and it did not appear in the E. coli periplasm. We constructed a map of pVA318 for restriction endonucleases HindIII, HpaI, PstI, and HaeIII. A previously reported BamHI site in pVA318 did not appear in the pVA318 portion of any of our chimeric clones.

Cloning, Molecular↗
PubMed1981

Acute changes of myocardial norepinephrine and glycogen phosphorylase in ischemic and non-ischemic areas after coronary ligation in dogs.

The myocardial norepinephrine (NE) content and glycogen phosphorylase activity were measured before and after coronary artery ligation in dogs anesthetized with pentobarbital. Coronary artery ligation was performed by ligating a branch of the left anterior descending coronary artery (LAD). Before coronary artery ligation, the NE content in the circumflex area (778.05 +/- 37.83 ng.g-1 wet tissue) was significantly higher than that in the LAD area (630.57 +/- 35.75 ng.g-1 wet tissue). The NE content in the circumflex area (non-ischemic area) decreased significantly 1.5, 3, 30. 60, and 420 min after coronary artery ligation, while that in the LAD area (ischemic area) did not decrease significantly except for the NE level obtained after 420 min of coronary artery ligation. The glycogen phosphorylase activity increased significantly 1.5 min after coronary artery ligation in both non-ischemic and ischemic areas. From the foregoing results, it is suggested that NE release occurs in both ischemic and non-ischemic areas within at least 1.5 min after coronary artery ligation, and that within 60 min after coronary artery ligation the NE content decreases in the non-ischemic area but not in the ischemic area probably because of very limited washout of the released NE in the ischemic area.

Animals↗