PubMed Health⌕ Search

Biomedical subjects

M Koide

Publications and source records attributed to M Koide.

At least 199 records · Page 11Linked to original sources
PubMed1987

Effects of a new vasodilator, nicorandil, on exercise-induced impairment of left ventricular function in patients with old myocardial infarction.

Hemodynamic effects of nicorandil on exercise-induced impairment of left ventricular function were studied in nine patients with old myocardial infarction but without angina pectoris. Hemodynamic data were obtained by symptom-limited supine multistage bicycle ergometer exercise testing before and 1 h after single oral administration of 15 mg of nicorandil. Systolic and diastolic blood pressure at rest decreased significantly after nicorandil administration (p less than 0.01). A most remarkable change in the hemodynamic response to supine dynamic exercise after nicorandil was a decrease in pulmonary artery wedge pressure (both at rest and at peak exercise, p less than 0.001). An index cardiac function, obtained from the relation between pulmonary artery wedge pressure and left ventricular stroke work index, improved significantly after nicorandil. The ration of pressure-rate product to coronary sinus flow, which is an index of the ratio of myocardial oxygen consumption to myocardial oxygen supply, decreased significantly (p less than 0.05) after nicorandil administration. Reproducibility of the testings was also studied in six patients with old myocardial infarction. Invasive hemodynamic variables between two successive symptom-limited supine leg exercise testings, except pulmonary artery wedge pressure, were reproducible in patients with old myocardial infarction but without angina pectoris. Only pulmonary artery wedge pressure at rest in the second exercise testing showed a significantly lower value (p less than 0.05). It is concluded that nicorandil is a useful drug for improvement of exercise-induced impairment of left ventricular function with an increase in myocardial oxygen supply.

Adult↗
PubMed1986

Effects of isosorbide-5-mononitrate on exercise-induced hemodynamic changes in angina pectoris.

Hemodynamic effects of isosorbide-5-mononitrate (ISMN) were studied in 14 patients with effort angina pectoris. Hemodynamic and echocardiographic data were obtained by angina-limited supine multistage bicycle ergometer exercise testing before and 120 minutes after single oral administration of 20 mg of ISMN. Compared with control exercise testing, the ST segment at peak exercise showed less depression after administration of ISMN (p less than 0.001). At rest, systolic and diastolic blood pressure decreased significantly after administration of ISMN (p less than 0.001 and p less than 0.01, respectively). At rest and at peak exercise, pulmonary artery wedge pressure (both p less than 0.001), left atrial volume (both p less than 0.001) and left ventricular end-diastolic volume (both p less than 0.05) decreased, whereas cardiac index, pressure-rate product and systemic vascular resistance did not change significantly after administration of ISMN. Average time to peak plasma ISMN concentration was 90 minutes and average peak plasma concentration was 460 ng/ml with an elimination half-life of 7 hours. These data suggest that the main mechanism of the antianginal action of ISMN is a reduction in left ventricular preload followed by diminution of myocardial oxygen requirements.

Adult↗
PubMed1986

Exercise P-vector magnitude changes in angina pectoris: Frank-Vectorcardiographic and hemodynamic correlations.

Multistage bicycle ergometer exercise testings with Frank vectorcardiogram and M-mode echocardiogram were performed on 12 patients with effort angina pectoris. The left atrial and left ventricular end-diastolic volume (LAV and LVEDV) were calculated as a cube of the left atrial and left ventricular end-diastolic dimension. The mean pulmonary artery wedge pressure (mPAWP) was measured with a Swan-Ganz catheter during the testing. At peak exercise a statistically significant increase was observed in mPAWP (p less than 0.001), LAV (p less than 0.005), the maximal horizontal P-vector magnitude (Hmax) (p less than 0.05) and the percent change in Hmax (%Hmax). %Hmax showed a significant correlation with the increment of mPAWP (delta mPAWP) (r = 0.66, p less than 0.05), the increment of LVEDV (delta LVEDV) (r = 0.83, p less than 0.01) and the increment of LAV (delta LAV) (r = 0.81, p less than 0.001). Multiple regression analysis was performed on %Hmax as a dependent variable with delta LAV, delta mPAWP, and the increment of heart rate (delta HR) as independent variables (r = 0.84, p less than 0.05), but the partial correlation coefficients of delta mPAWP and delta HR were not significant. The present study demonstrated that the increase in Hmax had a close relationship with the increase in mPAWP and LVEDV and that the preload of the left ventricle during exercise-induced anginal attack could be predicted noninvasively by %Hmax. The increase in Hmax was thought to be due to the increase in LAV during anginal attack.

Adult↗
PubMed1986

Characterization of xylamine binding to proteins of PC12 pheochromocytoma cells.

PC12 pheochromocytoma cells take up 3,4-dihydroxyphenylethylamine (dopamine) and norepinephrine by a Na+-dependent, cocaine-sensitive system. The kinetics suggest that the same transporter functions for both substrates. Xylamine, a nitrogen mustard that blocks catecholamine uptake into neurons, irreversibly inhibited norepinephrine uptake into PC12 (IC50 = 15 microM). Pretreatment with 10 microM xylamine did not inhibit norepinephrine transport if 10 microM cocaine or 100 microM norepinephrine was also present during the pretreatment period or if Na+ was absent. These results indicate that xylamine must interact with the norepinephrine transporter to inhibit norepinephrine uptake. PC12 accumulated [3H]xylamine; this uptake had Na+-dependent and Na+-independent components. The Na+-dependent uptake was saturable (Km = 13 microM), and it was inhibited by cocaine (IC50 = 0.6 microM), desipramine (IC50 less than 1 nM), and norepinephrine (IC50 = 1 microM). Several proteins became prominently labeled when intact PC12 cells were incubated with [3H]xylamine; these proteins were enriched in a plasma membrane fraction and have molecular weights of 17,000, 24,000, 31,000, 33,000, 41,000, 42,000, 52,000, and 80,000. Other proteins were labeled less prominently. The labeling of all proteins was markedly decreased when the incubation with [3H]xylamine occurred in the presence of cocaine, desipramine, gramicidin D, or in a Na+-free buffer. These results indicate that xylamine must be transported into the cells for covalent binding to proteins to occur. [3H]Xylamine labeled essentially the same proteins when incubated with cell homogenates, but competition experiments with bretylium, desipramine, and cocaine failed to reveal which of the [3H]xylamine-labeled proteins is associated with the norepinephrine transporter.

Adrenal Gland Neoplasms↗
PubMed1986

Analysis of the exercise-induced orthogonal P wave changes in normal subjects and patients with coronary artery disease.

Near-maximal treadmill exercise testing was performed on 26 normal individuals (NL) and 78 patients with coronary artery disease (CAD) using a modified Bruce's protocol. Exercise-induced changes in orthogonal P wave measurements were made automatically, using an averaging technique, immediately before and 30 sec after treadmill exercise to assess their diagnostic significance in evaluation of left ventricular (LV) function in CAD patients. The maximal inferior and posterior components of the P wave and the maximal P-vector magnitude in the frontal and left sagittal planes showed a statistically significant increase after treadmill exercise both in NL and CAD patients. These changes were considered to be physiological responses of the P wave to dynamic exercise. The percent changes of the maximal horizontal P-vector magnitude (%Hmax) were significantly higher after treadmill exercise in CAD patients than in NL. In patients with effort angina pectoris and without a previous myocardial infarction, the %Hmax showed a highly significant negative correlation with the percent changes of the LV ejection fraction (r = 0.66, p less than 0.01), measured by exercise RI angiography. These results suggest that the exercise-induced increase in %Hmax reflects transient impairment of LV function during exercise. It was concluded that a %Hmax of more than 120% provided a useful, noninvasive index for assessing LV function in treadmill exercise testing.

Adult↗
PubMed1985

[Clinical and experimental studies on serum and urine amylase levels in carcinoma of the pancreas and periampullary region].

Serum and urinary amylase level are different between in cases with carcinoma of the pancreas head and in those with carcinoma of body or tail of the pancreas. In this study the relationship between elevation in serum and urinary amylase level and the portion of obstructed pancreatic duct by tumor was analysed in cases with pancreatic carcinoma was analysed and also this was investigated in experimental model of pancreatic duct ligated dog. In patients with carcinoma of the pancreas and periampullary region, the site of obstruction of the main pancreatic duct was estimated by ERP and serum and urinary amylase level were measured. The values of serum amylase level were different according to the site of obstruction of the pancreatic duct by the tumor and in cases with highly elevated serum amylase levels the main pancreatic duct was obstructed within 5cm from the duodenal papilla. Pathology of these cases revealed pancreatic fibrosis derived from pancreatitis accompanied by tumor was closely related to serum and urinary amylase level. In pancreatic ligated dogs similar findings were observed. These data suggested that elevated serum amylase level is due to the pancreatic duct obstruction in cases with carcinoma of the periampullary duodenum.

Adult↗
PubMed1984

[Effect of diuretic, azosemide (SK-110), in combination with antibiotic, cephaloridine, on kidney].

This study was performed to compare the acute-renal toxicity of azosemide (SK-110) or furosemide (FM) treatment in combination with cephaloridine (CER). 1) Initially, the acute-renal toxicity of CER was studied after a subcutaneous administration at dose levels of 500, 1000, 1500 and 2000 mg/kg. The values of BUN, creatinine and relative kidney weights were increased in rats given CER at dose levels above 1500 mg/kg. consequently, it was considered that the threshold of CER with regard to acute-renal toxicity was 1000 mg/kg. 2) Secondarily, the acute-renal toxicity of SK-110 or FM were studied after oral administration of 40, 80, 160 or 320 mg/kg doses alone or in combination with CER. Acute-renal toxicity was evident in the 320 mg/kg-treated rats after both SK-110 and FM alone, as revealed by analysis of a number of parameters, i.e., BUN, serum creatinine, urine sediment and composition and pathological data composing both kidney weights and studies at the microscope level. However, the increase of BUN and relative kidney weights values, elevated numbers of epithelial cells in the urine and necrosis observed in the uriniferous-tubular epithelium on histopathological examination of kidneys were noted in rats given at dose levels of only 80 mg/kg with SK-110 + CER, whereas they were seen in animals treated with FM even at the lowest applied dose of 40 mg/kg in combination with CER. In conclusion, this study showed that the minimum dose of SK-110 or FM in combination with CER which causes acute-renal toxicity were, respectively, 80 mg/kg or less than 40 mg/kg.

Administration, Oral↗
PubMed1984

[Effect of azosemide (SK-110) and its metabolites on mouse liver].

The effect of azosemide (SK-110), and its metabolites, 5-(2'-amino-4'-chloro-5'-sulfamoylphenyl)-tetrazole (M-1), 2-thiophenecarboxylic acid (TC), on mouse liver was investigated using biochemical and pathological parameters as indices of hepatotoxicity. The effects were compared with that of furosemide (FM) administration. A single dose of each compound was administered orally, or intraperitoneally, while multiple oral dosing was carried out once daily for a week. The results are summarized as follows: 1) SK-110 did not produce hepatotoxicity even after a single p.o. dose as high as 5000 mg/kg, a single i.p. dose of 400 mg/kg, or multiple p.o. doses of 700 mg/kg/day. 2) M-1 also did not produce hepatotoxicity even after a single p.o. dose of 4000 mg/kg or multiple p.o. doses of 550 mg/kg/day. TC did not exert hepatotoxicity after a single i.p. dose of 150 mg/kg or multiple p.o. doses of 250 mg/kg/day, but did produce hepatotoxicity after a single p.o. dose of more than 1000 mg/kg. However, it was presumed that, in vivo, TC formed as a metabolite of administered SK-110 would hardly produce hepatotoxicity. 3) FM produced hepatotoxicity after a single p.o. dose of more than 800 mg/kg, or a single i.p. dose of more than 200 mg/kg, but not after multiple p.o. doses of 700 mg/kg/day. Based on these findings, it was concluded that, in contrast to FM, SK-110 had no hepatotoxic effect on the mouse liver.

Administration, Oral↗
PubMed1983

Phosphatidylethanolamine methyltransferase activity in developing, demyelinating, and diabetic mouse brain.

The catalysis by phosphatidylethanolamine methyltransferase (PEMT) of phosphatidylcholine (PC) synthesis by the successive methylation of phosphatidylethanolamine in the presence of S-adenosylmethionine (AdoMet) as methyl donor, was detected in actively myelinating mouse brains. PEMT activity in the microsome fraction of fetal mouse brain at 17 days of gestation was 253 mu u/mg protein and that of adult brain after 7 days of remyelination following 6 weeks cuprizone administration was 148 mu u/mg. These figures are much higher than found in normal adult brains (1.7 mu u/mg). An increase in PEMT activity was observed in the brains of genetically transmitted diabetic mice, C57BL/KsJ-db/db, and streptozotocin-induced diabetic mice; 16.3 and 9.2 mu u/mg, respectively. The methyl group of mecobalamin was transferred to homocysteine producing AdoMet and was further metabolized into choline and acetylcholine in brain slices. These results suggest that in the diabetic state, an increase in PC synthesis is probably required in order to replace damaged myelin or to supply choline or acetylcholine essential to for nerve functions. Mecobalamin might serve as the source of the methyl group utilized for PC synthesis.

Animals↗