Biomedical subjects

A Hara

Publications and source records attributed to A Hara.

654 records · Page 37Linked to original sources

PubMedDate not supplied

Experimental study on enzyme distribution and its relation to myocardial ischemic changes following coronary circulatory disturbances.

Coronary artery ligation of canine heart was performed to investigate the relationship between the lactate dehydrogenase (LDH) pattern in myocardium and the distribution of coronary flow, especially in the early stage of ligation and after reperfusion. In the myocardium of normal dogs, the LDH pattern was similar in the left ventricle, the interventricular septum, and the right ventricle; the average LD5:LD4 ratio was 1.1, 1.2, and 1.2, respectively, and consisted mainly of heart type. In the left and right auricles, however, the ratios were 0.3 and 0.2, respectively, lacking heart type. In the left ventricle, LD5:LD4 ratio in the subendocardium was different from that in the subepicardial layer. Blood flow distribution in canine myocardium was investigated by the fluorescent pattern on the cut surface of heart, in which 10% fluorescein sodium was injected into the cavity. By this method the evolution of the ischemic area from the endocardial layer to the epicardial side following coronary artery ligation and the effect of reperfusion on the ischemic area were clarified. Electron microscopic studies indicated that loss of mitochondrial function may account for the irreversibility of myocardial cell alteration. A new method for studying enzyme localization in tissues was introduced for studying LDH isoenzyme distribution in normal and injured myocardium.

Animals↗

PubMedDate not supplied

Studies on metabolism of bromazepam. VI. Reduction of 2-(2-amino-5-bromobenzoyl)pyridine, a metabolite of bromazepam, in the rabbit, rat, and guinea pig.

Three urinary metabolites that were formed by cleavage of the benzodiazepine ring of bromazepam, 2-(2-amino-5-bromobenzoyl)pyridine (ABBP), 2-(2-amino-5-bromo-3-hydroxybenzoyl)pyridine (3-OH-ABBP), and 2-amino-5-bromo-2'-azabenzhydrol (ABAB), were measured in urine of rabbits, rats, and guinea pigs. The major metabolite was 3-OH-ABBP in all animals given bromazepam orally. ABAB was also excreted in major amounts in the guinea pig, but was excreted in minor amounts in the rabbit and rat. Moreover, ABAB was excreted in the urine of all animals given ABBP orally. It may be concluded that ABAB was formed by reduction of the carbonyl group of ABBP. ABBP reduction was catalyzed by NADPH-dependent enzymes occurring in rabbit liver cytoplasm, and rat liver microsomes, and guinea pig liver cytoplasm and microsomes. The reductases were inhibited by sulfhydryl group reagents. The optimum pH of the cytoplasmic enzyme ranged from 7.2 to 7.8, and that of the microsomal enzyme was 6.5. The apparent KM value for the reduction of ABBP by guinea pig liver microsomes was the lowest among all of the liver preparations.

Animals↗

PubMedDate not supplied

Effect of nisoldipine on the oxymyoglobin level of myocardial cells in hypoxic, perfused rat hearts.

The effect of nisoldipine on the oxygen balance in the hypoxic myocardial cells was studied. The isolated rat heart, driven at 300 beats/min, was perfused with Krebs-Henseleit solution equilibrated with a gas mixture containing 95% O2 + 5% CO2 (normoxic perfusion solution) at a constant flow rate (9 ml/min) according to the Langendorff's technique. The myocardial oxygenation level of myoglobin (reflecting intracellular oxygen tension) of the cells locating on the ventricular surface was continuously determined by means of an optical technique. Hypoxic perfusion (perfused with Krebs-Henseleit solution equilibrated with a gas mixture containing 30% O2 + 5% CO2 + 65% N2) decreased the oxymyoglobin level (MbO2), left ventricular pressure (LVP), and perfusion pressure (PP). Nisoldipine was infused into the aortic cannula for 10 min during the hypoxic perfusion. Larger doses of nisoldipine (282.9 and 141.5 nM expressed in terms of the final concentration in the perfusion solution) increased the MbO2 level and decreased LVP, without affecting PP. Smaller doses (70.7 and 35.4 nM) did not have a marked effect on these parameters. These results suggest that nisoldipine, in larger doses, improves the oxygen balance of the hypoxic myocardial cells, probably because of decrease in LVP hence oxygen demand, and that nisoldipine does not dilate further coronary vessels that have been dilated by hypoxia.

Animals↗

PubMedDate not supplied

Simple approach to secondary posterior chamber intraocular lens implantation in patients without a complete posterior lens capsule support.

We describe a simple new method of implanting secondary posterior chamber intraocular lenses (PC-IOLs) with ciliary sulcus fixation in patients with complete posterior lens capsule support. Two pairs of PC-9 needles (Alcon Surgical, Fort Worth, Tex) are involved, each pair connected by the Girth Hitch method, with a guiding needle on one end and a tying needle on the other. This ab externo technique overcomes many of the disadvantages noted in previous reports on secondary PC-IOL implantation.

Cataract Extraction↗

PubMedDate not supplied

Effect of K-7259, a novel derivative of dilazep, on cardiovascular actions of adenosine: comparison with dilazep.

The effect of K-7259, a novel derivative of dilazep, on the cardiovascular action of adenosine was studied in the aortic ring and isolated perfused heart in guinea-pigs, and compared with that of dilazep. Adenosine produced a concentration-dependent relaxation in phenylephrine (2 x 10(-6) M)-contracted aortic rings and exhibited a negative chronotropic effect in the isolated perfused heart. Dilazep (10(-8), 10(-7) and 10(-6) M) potentiated significantly the relaxing action of adenosine on the aortic ring in a concentration-dependent way. K-7259 (10(-6) M), however, did not potentiate the relaxing action of adenosine, although the high concentration of K-7259 (10(-5) M) potentiated it slightly but significantly. The negative chronotropic effect of adenosine was also potentiated by dilazep (10(-7) and 10(-6) M), but not by K-7259 (10(-6) M). These results suggest that the potentiating action of K-7259 on the cardiovascular effects of adenosine is very weak when compared with that of dilazep.

Adenosine↗

PubMedDate not supplied

The combination of different types of antitumor topoisomerase II inhibitors, ICRF-193 and VP-16, has synergistic and antagonistic effects on cell survival, depending on treatment schedule.

VP-16 and ICRF-193 are different types of antitumor topoisomerase II inhibitors, being cleavable and non-cleavable complex-stabilizing types, respectively. To examine the possibility of enhancing the efficacy of combination chemotherapy, we carried out simultaneous and sequencial treatment of cells with the two drugs. When KB cells were exposed continually to low concentrations (0.05 - 0.2 microM) of the drugs, the effects were synergistic. In contrast, when the cells were treated with high concentrations of ICRF-193 and VP-16 for 1 hour, the VP-16-induced cytotoxicity was prevented by ICRF-193 and the degree of prevention was increased by the pretreatment of cells with ICRF-193, while post-treatment with ICRF-193 had little effect on the cytotoxicity of VP-16. ICRF-193 at 1 microM was found to interact with about half molecules of topisomerase IIa and II beta in cells, as judged by increased amounts of a salt-stable complex. ICRF-193 inhibited in vitro VP-16-induced cleavable complex formation, but a much higher concentration was needed to reverse the cleavage already generated by VP-16. Thus, the antagonistic or synergistic effects of ICRF-193 and VP-16 depend on the concentration of the drug, as it may be critical as to how many molecules of cellular topoisomerase II interact with the drugs.

Antineoplastic Combined Chemotherapy Protocols↗