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Y Kono

Publications and source records attributed to Y Kono.

At least 199 records · Page 11Linked to original sources
PubMed1983

[Analysis of coronary hemodynamics in exercise by T1-201 scintigraphy: examination of rates of change of cardiac output, myocardial blood flow distribution, coronary blood flow and coronary vascular resistance].

From our observation that initial distribution of 201T1 in tissue is mainly dependent on blood flow distribution, we designed the method to obtain the rates of change of coronary blood flow and coronary vascular resistance and applied it to the analysis of coronary hemodynamics in patients with ischemic heart disease during submaximal exercise. We measured the rates of change of cardiac output (delta CO) and myocardial blood flow distribution (delta Fract ) in two occasions by the sequential two injections of T1, and obtained the rate of change of coronary blood flow (delta Flow) from delta CO and delta Fract . Using the rate of change of mean blood pressure, we calculated also the rate of change of coronary vascular resistance (delta CVR). The initial components of histograms of the right ventricle by the first and second injections of T1 were fitted into gamma function curve. S1 and S2 were the areas bounded by the curve and baseline of the first and second injections, and then the cardiac output ratio was estimated by R X S1/S2, where R was the dose ratio measured by another camera system. The five min count rates on the myocardium by the first (H1) and second (H2) injections of T1 were calculated five min after the injection. H2 was approximately H1 X R in the same condition of T1 injection but H2 was not equal to H1 X R, when the T1 injection was done in the different loading condition. Therefore the rate of change of myocardial blood flow distribution was calculated as delta Fract = (H1 X R-H2)/H2.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Output↗
PubMed1983

Impaired glucose tolerance related to changes in the energy metabolism of the remnant liver after major hepatic resection.

In 70% hepatectomized rabbits, the glucose tolerance patterns after an oral glucose load were characterized by a longstanding increase of blood glucose for more than 180 min (a linear pattern) at 24 hr after hepatectomy and by a return toward normal range within 180 min (a parabolic pattern) at 96 hr later. At the linear stage, the concentrations of pyruvate and lactate of the remnant liver increased to 192% and 203%, respectively, of sham-operated controls at 1 hr after an oral glucose load. At 3 hours after glucose load, the concentrations of glucose-6-phosphate, fructose-6-phosphate, pyruvate, and lactate increased to 191%, 192%, 174% and 298%, respectively. By contrast, at the parabolic stage, no significant changes were observed. On the other hand, the energy charge level of the remnant liver decreased to 0.767 at the linear stage and returned to near normal levels at the parabolic stage. The ketone body ratio (acetoacetate/beta-hydroxybutyrate) in the arterial blood decreased to 0.415 at the linear stage, concomitant with the increase in total ketone body and NEFA concentrations, and returned to near normal levels at the parabolic stage. These findings suggest that the reduced mitochondrial redox potential, reflected by the decrease in ketone body ratio, inhibits pyruvate dehydrogenase. This prevents the entrance of pyruvate into the Krebs cycle and results in the inhibition of glucose oxidation, leading to a linear pattern after an oral glucose load.

Animals↗
PubMed1982

Changes in antibody titers in cattle infected clinically and subclinically with bovine leukemia virus.

Changes in titers of antibodies to protein and glycoprotein antigens of bovine leukemia virus (BLV) were investigated by immunodiffusion in two groups of cattle. In one group of cattle (10 head) which developed enzootic bovine leukosis during the observation period of 3 years, seven showed a gradual increase in antibody titers following a period of level antibody titers that persisted for several months to several years. The titer was finally eight to 32 times higher than the initial titer. The remaining three showed little change in titer. Of the 10 animals with tumors, three showed a decrease in the titer when they were in extremis. In contrast, in the second group of cattle (110 head), which were infected with BLV subclinically, the change in the titers during 1 and 3 years ranged from no change to four times the lowest titer that was observed during the period. Of the cattle which had a low level of antibody to one of the BLV antigens, a few became negative reactors to the respective antigen.

Animals↗
PubMed1982

Superoxide radical inhibits catalase.

Catalase was inhibited by a flux of O2- generated in situ by the aerobic xanthine oxidase reaction. Two distinct types of inhibition could be distinguished. One of these was rapidly established and could be as rapidly reversed by the addition of superoxide dismutase. The second developed slowly and was reversed by ethanol, but not by superoxide dismutase. The rapid inhibition was probably due to conversion of catalase to the ferrooxy state (compound III), while the slow inhibition was due to conversion to the ferryl state (compound II). Since neither compound III nor compound II occurs in the catalatic reaction pathway, they are inactive. This inhibition of catalase by O2- provides the basis for a synergism between superoxide dismutase and catalase. Such synergisms have been observed in vitro and may be significant in vivo.

Acetaldehyde↗
PubMed1982

Oxygen Enhancement of bactericidal activity of rifamycin SV on Escherichia coli and aerobic oxidation of rifamycin SV to rifamycin S catalyzed by manganous ions: the role of superoxide.

Oxygen enhanced the bactericidal activity of rifamycin SV to Escherichia coli K12. Anaerobically grown cells, which had a low level of superoxide dismutase, were more susceptible to the bactericidal activity than aerobically grown cells, which contained a high level of superoxide dismutase. Oxygen also enhanced the inhibition of RNA polymerase activity of rifamycin SV, when Mn2+ was used as a cofactor. Rifamycin S was reduced to rifamycin SV by NADPH catalyzed by cell-free extracts of Escherichia coli K12. These results indicate that the inhibition of bacterial growth by rifamycin SV is due to the production of active species of oxygen resulting from the oxidation-reduction cycle of rifamycin SV in the cells. The aerobic oxidation of rifamycin SV to rifamycin S was induced by metal ions, such as Mn2+, Cu2+, and Co2+. The most effective metal ion was Mn2+. In the presence of Mn2+, accompanying the consumption of 1 mol of oxygen and the oxidation of 1 mol of rifamycin SV, 1 mol of hydrogen peroxide and 1 mol of rifamycin S were formed. Superoxide was generated during the autoxidation of rifamycin SV. Superoxide dismutase inhibited the formation of rifamycin S, but scavengers for hydrogen peroxide and the hydroxyl radical did not affect the oxidation. A mechanism of Mn2+-catalyzed oxidation of rifamycin SV is proposed and its relation to bactericidal activity is discussed.

Aerobiosis↗
PubMed1982

Electron spin resonance studies on the oxidation of rifamycin SV catalyzed by metal ions.

The formation of Mn2+- or Cu2+-rifamycin SV complex and the semiquinone radical of rifamycin SV was studied by electron spin resonance spectroscopy. The results indicate that: (1) the complexes Mn2+-rifamycin SV (g parallel = 2.265, g perpendicular = 2.087, A parallel = 177 x 10(-4) cm-1) were formed; (2) in Cu2+-rifamycin SV, Cu2+ was of square-planar type and was ligated to oxygen atoms; (3) the semiquinone radical of rifamycin SV (g = 2.0031) was formed only under aerobic conditions and its formation was inhibited by superoxide dismutase. The formation of hydroxyl radicals during the autoxidation of rifamycin SV was detected by the spin trapping method using N-t-butyl-alpha-phenylnitrone. Superoxide dismutase, mannitol and EDTA inhibited the development of the signal of the spin adduct, indicating that the hydroxyl radical is formed in via the Fenton-type reaction.

Benzoquinones↗
PubMed1982

Aerobic oxidation of rifamycin SV to rifamycin S catalyzed by horseradish peroxidase.

The aerobic oxidation of rifamycin SV to rifamycin S was catalyzed by horseradish peroxidase. The oxidation rate increased with increasing pH. The oxidation was inhibited by catalase, but superoxide dismutase enhanced the oxidation rate of rifamycin SV. Superoxide inhibited the oxidation and superoxide dismutase relieved the inhibition of oxidation by superoxide. An oxidation mechanism of rifamycin SV catalyzed by horseradish peroxidase which accounts for these data is proposed and a convenient positive assay for superoxide dismutase, using the rifamycin SV-horseradish peroxidase-O2 system, is described.

Aerobiosis↗
PubMed1982

Significance of mitochondrial enhancement in restoring hepatic energy charge after revascularization of isolated ischemic liver.

The critical point of reversibility in hepatic ischemia was investigated. Immediately after the liver was isolated, the hepatic energy charge decreased rapidly from the control level of 0.85 to 0.28 and remained at a constant value during 30-, 60-, and 90-min ischemic periods. After revascularization of the liver, the rapidity toward the normalization of the energy charge and the mitochondrial phosphorylative activity were different according to the ischemic time. The livers after 30- and 60-min exclusion showed a normalization of the energy charge and the enhancement of mitochondrial phosphorylative activity, while the livers after 90-min exclusion showed only a slight increase of energy charge, which remained far from the normal value, and the enhancement of mitochondrial phosphorylative activity was not observed. From these results, it is suggestive that a rapid enhancement in phosphorylative activity of the liver mitochondria after revascularization plays a decisive role on the restoration of the viability of isolated ischemic liver.

Adenine Nucleotides↗
PubMed1982

Haemagglutination by bovine leukaemia virus.

Bovine leukaemia virus (BLV) was found to agglutinate mouse erythrocytes. Under optimal conditions, including the use of neuraminidase-treated erythrocytes, 200 microgram/ml of BLV purified from the supernatant fluid of BLV-infected bat cells had haemagglutinating titres of about 512 units. BLV haemagglutination was drastically affected by pH and temperature; maximum agglutination occurred at pH 6 and 4 degrees C. That the BLV haemagglutinin is a glycoprotein was suggested by the fact that trypsin, potassium periodate or neuraminidase, but not lipid solvents or phospholipase C, significantly reduced the haemagglutinating (HA) activity of purified BLV. Furthermore, purified BLV glycoprotein of mol. wt. 51 000 (gp51) had HA activity. The receptors for BLV on mouse erythrocytes were inactivated by proteolytic enzymes but not by sodium deoxycholate or potassium periodate. Neuraminidase treatment of erythrocytes increase their agglutinability fourfold. Haemagglutination is a relatively sensitive test for detecting BLV glycoprotein because 0.4 microgram/ml of glycoprotein can be detected by this method. The pH and temperature sensitivity of the BLV HA reaction and specificity for mouse erythrocytes distinguish BLV from that of equine infectious anaemia virus and murine leukaemia virus, the other C type retroviruses known to have HA activity.

Animals↗
PubMed1982

Clinical experience of postoperative hepatic failure treatment with pig or baboon liver cross-hemodialysis with an interposed membrane.

The present study emphasizes the principle of using liver support to restore the blood ketone body ratio (acetoacetate/beta-hydroxybutyrate), which reflects the redox potential of liver mitochondria and correlates with hepatic energy charge (ATP + 0.5ADP/ATP + ADP + AMP). Eleven surgical patients with grade IV hepatic coma were treated by an ex vivo pig or baboon liver cross-hemodialysis with an interposed Cuprophan membrane when their blood ketone body ratios had decreased to below 0.4 compared with the normal of above 0.7. Three patients were treated by cross-hemodialysis using a standard Cuprophan membrane dialyzer without increase of blood ketone body ratio and without marked beneficial effect. However, five of eight patients who had blood ketone body ratios of above 0.25 became fully alert after treatment by cross-hemodialysis using the larger pore size and greater surface area Cuprophan membrane, concurrent with a rise in the decreased blood ketone body ratio, and three of them were later discharged. By contrast, in the three patients with blood ketone body ratios below 0.25, there was no restoration of consciousness and no improvement in their blood ketone body ratios by this liver support. It is suggested that, as long as the blood ketone body ratio remained over 0.25, this metabolic liver support is effective in restoring grade IV hepatic coma.

Aged↗
PubMed1982

The effects of heterologous liver cross-hemodialysis on adenylate energy charge of the remnant liver after major hepatic resection.

The effect of liver support on the adenylate energy charge (ATP + 0.5ADP)/(ATP + ADP + AMP) of the remnant liver after major hepatic resection was studied in rabbits. The present study emphasized the principle of restoring the decreased energy charge level of the remnant liver after major hepatic resection by use of an ex vivo heterologous liver cross-hemodialysis with an interposed Cuprophan membrane. The energy charge level provides the cell with a very sensitive intracellular control mechanism. Regulatory enzymes from biosynthetic sequences exhibit very little activity at low levels of energy charge, and their activities increase sharply at high-energy charge levels. The energy charge level of the remnant liver maximally decreased from the control level of 0.860 to 0.767 at 24 hours after 70% hepatectomy. The energy charge level increased from 0.767 to 0.857 after two hours of cross-hemodialysis with an interposed Cuprophan membrane between the 24-hour, 70% hepatectomized rabbit and an ex vivo pig liver with high energy charge. The above results suggest that this ex vivo pig cross-hemodialysis may be effective for biosynthesis in the regenerative processes of the remnant liver.

Adenosine Monophosphate↗
PubMed1982

The pathophysiology of septic shock: acute renal failure in rats following live E coli injection. A histochemical study of the proximal tubules.

Acute renal failure was induced in rats by injection of a lethal dose of live Escherichia coli. Enzyme activities of the proximal tubule were studied histochemically at three, six, and 12 hours following E coli injection. The enzymes examined were alkaline phosphatase (A1Pase), acid phosphatase (AcPase), adenosine triphosphatase (ATPase), succinate dehydrogenase (SDH), glucose-6-phosphatase (G6Pase), and glucose-6-phosphate dehydrogenase (G6PDH). At three hours, ATPase activity was slightly decreased, while other enzymes showed no changes in activities at this time. At six hours, a slight increase in AcPase activity was seen in the pars recta. At this time, although A1Pase showed no change in activity, other enzymes revealed slight decreases in activities: G6Pase and SDH in the pars convoluta, ATPase in the pars convoluta and pars recta, and G6PDH in pars recta. At 12 hours after treatment, all enzymes showed decreases in activities; however, no necrotic tubule changes were detectable by light microscopy. Since sodium reabsorption in proximal tubules requires a sodium pump consisting of Na-K ATPase, early histochemical changes in ATPase activity in proximal tubule following bacteremia may be related to early changes in sodium reabsorption causing polyuria and to the subsequent development of acute renal failure.

Acute Kidney Injury↗
PubMed1982

A study of oxidative phosphorylative activity and calcium-induced respiration of rat liver mitochondria following living Escherichia coli injection.

Mechanisms of subcellular dysfunction of the liver in sepsis are still obscure. The present study investigates changes in oxidative phosphorylative activity and calcium-induced respiration of rat liver mitochondria following live Escherichia coli injection (E coli, Serotype: 0--18. A 1.25--1.5 X 10(9)/100 gm body wt inoculum of E coli bacteria was injected via the tail vein, causing a 100% mortality rate within 24 hours after injection. In order to determine alteration of liver mitochondrial membrane permeability, serum ornithine carbamoyltransferase activity was measured following E coli injection. This activity increased ten to 100-fold over that of controls with time following injection. However, the yield of liver mitochondria from treated rats, estimated by the amount of collected mitochondrial protein and the recovery rate of succinate dehydrogenase activity in the final mitochondrial suspensions, was not significantly different from that of controls. Mitochondrial oxidative phosphorylative activity measured using glutamate as a substrate was enhanced throughout all period to death (P less than 0.01 at three and six hours, P less than 0.05 in the fatal stage) and was associated with concomitant increases in respiratory control ratios. Similar results were obtained using beta-hydroxybutyrate as a substrate. This enhancement was accompanied by an increase in 2-4-dinitrophenol-stimulated ATPase activity (160% at three hours and 130% in the fatal stage). Calcium-induced stimulation of mitochondrial respiration as well as initial calcium uptake rate linked to respiration, using glutamate as a substrate, were higher in liver mitochondria from rats with E coli treatment than in those of controls throughout all periods (P less than 0.01 or less). These results suggest the coexistence of hyperfunctioning as well as deteriorated mitochondria following lethal treatment with E coli.

3-Hydroxybutyric Acid↗
PubMed1982

[Treatment of unresectable liver cancer with intrahepatic arterial infusion chemotherapy].

Intra-arterial infusion chemotherapy was performed in 50 patients with cancer of the liver including 12 primary hepatoma and 38 metastatic cancers, at Kurashiki Central Hospital from December 1977 through December 1981. B.D. Fomocath 5 French catheter was inserted through the lateral femoral circumflex artery and advanced retrogradely to the common hepatic or proper hepatic artery using a loop catheter technique and the catheter was connected to the tube of infusion pump. The dose of 5-Fluorouracil and Mitomycin C was 250 mg per day and 4-10 mg once a week, respectively. The patients had average survival of 8.2 months in hepatoma and 4.8 months in metastatic tumor. The results were unfortunately not encouraging but this regimen occasionally provides excellent results and has no contraindication.

Adult↗
PubMed1981

Hemagglutination of several strains of equine infectious anemia virus.

Six strains of equine infectious anemia (EIA) virus propagated in equine leukocyte cultures were found to agglutinate horse erythrocytes. Concentrated virus material containing about 20 units of complement fixation (CF) titer showed hemagglutinating (HA) titers ranging from 4 to 8 units. The HA activity remained stable after ether treatment and was reduced by trypsin, formaldehyde and KIO4. Cesium chloride equilibrium density gradient centrifugation revealed two populations of hemagglutinin, one in the density range of 1.15-1.16 g/ml coinciding with a peak of CF antigen and the other at round 1.27 g/ml. However, after the antigen was treated with ether, hemagglutinin showed a single peak at about 1.27 g/ml. Hemagglutinin receptors on the erythrocytes were inactivated by trypsin and formaldehyde but their activity was enhanced by neuraminidase. Hemagglutination was inhibited by sera from horses infected with homologous strain for EIA virus. The hemagglutinin showed immunological properties similar to those of the hemagglutinin of guinea pig erythrocytes as reported in our previous paper.

Animals↗