[Correction of complete endocardial cushion defect (Rastelli C) using a modified "endocardial cushion prosthesis"].
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Biomedical subjects
Publications and source records attributed to K Nishigaki.
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Improved 4-aminoantipyrine (4-AA) colorimetry was developed for the detection of minute quantities of residual hydrogen peroxide in several kinds of food. Hydrogen peroxide in the sample was stabilized with potassium bromate and extracted with cold methanol. The methanol extract was diluted with phosphate buffer, protein was eliminated with zinc sulfate, and the extract was reacted with phenol, 4-AA, and peroxidase to the stable quinoneimine dye. The weak color solution was purified with Florisil column chromatography, concentrated, and determined by colorimetry. Recoveries of hydrogen peroxide from samples fortified at 0.5, 2, and 10 ppm ranged from 70.7 +/- 8.9 to 98. 5 +/- 1.2%. Color development was linear with amount of H2O2 from 0.5 to 20 micrograms, corresponding to 0.05-2 ppm in samples.
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A new antibiotic, setomimycin, was isolated from the culture broth of strain AM-2947, which was identified as Streptomyces pseudovenezuelae. The compound is a weakly acidic substance, and has UV-absorption at 228, 268 and 422 nm and a molecular formula of C34H28O9 (MW 580). It is active against Gram-positive bacteria including Mycobacteria, and has antitumor activity against Sarcoma-180 solid tumor in mice.
BACKGROUND: To evaluate cardiac sympathetic activity, a simple method should be developed to replace such complex methods as the spillover rate of tritiated norepinephrine (3H-norepinephrine) or microneurography of sympathetic nerve activity. The goal of this study is to evaluate cardiac sympathetic activities by analyzing the washout of I-123 meta-iodobenzylguanidine (123I-MIBG), a radiolabeled norepinephrine analogue, in Dahl salt-sensitive (DS) rats as it relates to the progression of hypertension. METHODS AND RESULTS: Dahl salt-resistant (DR) rats and DS rats were fed an 8 % salt diet starting at age 5 weeks. Marked hypertension and cardiac hypertrophy developed in the DS rats, whereas DR rats remained normotensive. Then the time-activity curves of 123I-MIBG from 15 to 200 minutes were obtained from both DS and DR strains at ages 8, 11, and 13 weeks using dynamic scintigraphic analysis. We also examined the nonneuronal washout of 123I-MIBG using dynamic scintigraphic studies in desipramine pretreated normal rats. In the preliminary study with desipramine pretreatment, the majority of the nonneuronal 123I-MIBG washout occurred by 90 minutes after injection. Therefore the late-phase washout in the control rats was found to reflect the neuronal washout. We then applied exponential curve fitting to the time activity curves acquired in the 90- to 200-minute period after 123I-MIBG injection in both DR and DS rats. When we compared the coefficients of these washout curves in the DS and DR rats as an index of cardiac sympathetic activities, the coefficient values remained high during all stages in DS rats, whereas they decreased with age in DR rats. CONCLUSION: Measurement of late-phase 123I-MIBG washout may be a useful tool for assessing the change in sympathetic activity in the progression of hypertension without the influence of extraneuronal washout of 123I-MIBG and left ventricular hypertrophy.
The interaction of alpha 1- and alpha 2-adrenoceptor constriction of isolated rat cremaster small arteries (mean diameter +/- SEM, 114 +/- 5 microns) with the myogenic mechanism was examined with in vitro videomicroscopy. Microdissected vessels were double-cannulated with glass micropipets in a tissue bath, and intraluminal pressure was set at 65 mm Hg baseline pressure. Norepinephrine (NE) concentration-response curves were obtained alone and in the presence of prazosin or rauwolscine to establish the concentration of NE required to selectively stimulate alpha 1- or alpha 2-adrenoceptors. A bimodal response was produced by NE alone, indicating interaction with more than one receptor population. Rauwolscine and prazosin each produced dextral displacement at low (< 0.1 microM) NE concentrations. However, while prazosin exhibited competitive antagonism, rauwolscine did not antagonize NE at concentrations > or = EC50 value. Thus, both alpha 1- and alpha 2-adrenoceptors mediate constriction at low NE concentrations, but only alpha 1-receptors contributed to constriction at intermediate and high concentrations. These data are in contrast to previous findings for the same vessels studied in vivo. Diameter responses to increases and decreases in transmural pressure from baseline were examined in the relaxed (passive) state with nitroprusside present, during spontaneous intrinsic tone, and during induced alpha 1- or alpha 2-tone (EC20 concentration of NE plus rauwolscine or prazosin). Myogenic constriction during increases in lumen pressure and myogenic inhibition of tone during decreases in pressure were greatest during alpha 2-tone, less during intrinsic tone and least during alpha 1-tone.(ABSTRACT TRUNCATED AT 250 WORDS)
The left atrium (LA) stores part of the right ventricular stroke volume during ventricular systole for passive release into the left ventricle (LV) during ventricular early diastole and active release during ventricular late diastole (passive and active contraction). The rest of the right ventricular stroke volume flows through the LA from the pulmonary vascular bed to the LV (LA conduit function). The factors affecting these LA functions were evaluated during ventricular diastole by left atrial angiography and left ventriculography in 21 patients with normal LV ejection fraction (0.53-0.76), but without coronary artery disease and valvular heart disease, aged 40-70 years. LV stroke volume was calculated from left ventriculograms. The maximal LA volume, minimal LA volume, and LA volume at the beginning of the left atrial active contraction were calculated from the left atrial angiograms, and further corrected by a regression equation (true volume = 0.91 x calculated volume -1.1). The LA reservoir volume, LA passive contraction volume, LA active contraction volume, and LA conduit volume were obtained. LA conduit volume correlated significantly with LV stroke volume (r = 0.97), but not with maximal LA volume and LA reservoir volume. LA active contraction volume correlated significantly with LA reservoir volume, LA volume at the beginning of LA active contraction, and maximal LA volume (r = 0.85, 0.60, 0.54, respectively). LA passive contraction volume did not correlate with any factor, and was grossly independent of LV stroke volume. LA conduit volume may be associated with LV diastolic function, and LA active contraction volume appears to increase with increased LA volume.