Regime of improved confinement in neutral-beam-heated limiter discharges of a tokamak.
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Biomedical subjects
Publications and source records attributed to T Shoji.
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A gas chromatographic-mass spectrometric (GC-MS) method using single ion monitoring (SIM) is described for the determination of residual macrolide antibiotics, oleandomycin, kitasamycin, spiramycin and tylosin, in beef and pork. For GC-MS determination, oleandomycin is acid hydrolysed to desoleandomycin and acetylated, in the same way as erythromycin. However, for elution from a GC column, the carbon-carbon double bonds in the antibiotics must be hydrogenated to single bonds before acid hydrolysis. Kitasamycin and spiramycin are therefore converted into hydroforocidine acetate and tylosin into hydro-O-mycaminosyl tylonolide acetate, which are determined by GC-MS with SIM.
Human and rat alpha-calcitonin gene-related peptides (CGRPs) caused relaxation of porcine coronary arterial strips precontracted by 10(-5) M of prostaglandin (PG) F2 alpha at low concentrations. pD2 values for human and rat CGRPs in endothelium-preserved strips were 8.41 +/- 0.03 (n = 5) and 8.49 +/- 0.03 (n = 5), respectively. The same concentrations of CGRPs relaxed the endothelium-depleted preparations. CGRPs were much more potent and had steeper concentration-response curves than isoproterenol, nitroglycerin (GTN), isobutylmethylxanthine (IBMX), verapamil and nifedipine. Like isoproterenol, GTN and IBMX, but in contrast to the calcium antagonists, the relaxing potencies of human and rat CGRPs were greatly reduced in the strips precontracted by 50 mM of KCl. The relaxation caused by human CGRP was not affected by treatment with propranolol (10(-6) M) or cimetidine (10(-5) M). Human CGRP (1.6 X 10(-8) M) caused a significant (about 2-fold) elevation of the content of cyclic AMP in coronary tissue but did not cause any change in the content of cyclic GMP. CGRP-like immunoreactive fibers were found to be localized in the adventitia but not in the media or intima of the coronary artery. These results indicate a direct and endothelium-independent potent relaxant action of CGRP in coronary vessels. This relaxation could be caused by a mechanism not shared by calcium antagonists but associated with the rise in cyclic AMP.
In an attempt to define the effects of a calcium antagonist, nitrendipine, on renal function, intrarenal hemodynamics, and renin release, we infused the drug into the renal artery of anesthetized dogs. Infusion of nitrendipine at a rate of 5 micrograms/min in both hydropenic and hydrated dogs resulted in a significant increase in renal blood flow (RBF), glomerular filtration rate (GFR), urine flow and renin release, with no change in systemic blood pressure, indicating a significant renal vasodilation. The urinary excretion rate of sodium increased by the same proportion as that of calcium. The intrarenal blood flow as measured by hydrogen washout rate showed that the outer cortical flow increased by the same proportion as the inner cortical flow. During nitrendipine infusion, free water reabsorption rate (TcH2O) in hydropenic dogs or free water clearance (CH2O) in hydrated dogs increased in proportion to the urine flow. Neither the ratio of TcH2O nor that of CH2O to osmolar clearance changed throughout the experiment. These data suggest that nitrendipine may not inhibit sodium transport in the medullary portion of the ascending limb of Henle and may induce an enhancement of the delivery of sodium to the Henle loop. Thus, nitrendipine exerts its diuretic and natriuretic actions via the alteration of renal hemodynamic and the inhibitory effect on proximal sodium reabsorption.
The time course of the loss of myoglobin from the rat ventricular myocardium in the early phase of ischemia was studied with the use of an immunohistochemical technique and an image analyzer. The loss of myoglobin, as an index of myocardial injury, was evident in the left ventricular subendocardium as early as 0.5 hr after occlusion of the left main coronary artery. A clear-cut demarcation of the myoglobin-depleted area helped quantification of the injured areas with an image analyzer. The area with depleted myoglobin became transmural and reached maximum after 2 and 3 hr of occlusion, respectively. Electron microscopic observation of the myoglobin-depleted region revealed amorphous dense bodies in the mitochondria, indicating irreversible damage to the myocardial cells. On the other hand, no irreversible changes could be detected with hematoxylin-eosin stain until 6 hr after the start of the ischemia, and the distinction between the reversible and irreversible areas was unclear. We suggest that depletion of myoglobin from the myocardium serves as a marker for irreversible ischemic injury. Quantitative assessment of the injured areas by immunohistochemical staining for myoglobin together with an image analyzer could be of great value for the evaluation of early ischemic myocardial damage.
A recently developed highly sensitive radioimmunoassay method for detecting plasma kinin was used to re-evaluate the results of previous studies, in which plasma kinin had been measured with a bioassay method. To clarify the mechanism of plasma kinin release in global myocardial ischaemia the left main coronary artery was cannulated using a Griggs type autoperfusing cannula after pentobarbital anaesthesia in open chest dogs. The animals were divided into a non-coronary constricted group (n = 4) and a moderately coronary constricted group (n = 7). Cardiac sympathetic nerve stimulation (10 V, 4 Hz, 2 ms duration) was given to both groups. Haemodynamic recordings and blood samples were taken before and after coronary constriction as well as after sympathetic nerve stimulation. The arterial and coronary sinus plasma kinin concentrations were determined with the new radioimmunoassay method. After sympathetic nerve stimulation apparent myocardial ischaemia occurred and the plasma kinin concentration in coronary sinus blood increased significantly in the constricted group. In the non-constricted group, however, myocardial ischaemia did not appear and no significant change in coronary sinus plasma kinin concentrations was seen. These findings show that there was a pronounced release of plasma kinin from the heart when apparent myocardial ischaemia occurred.
We investigated the effects of captopril on the plasma atrial natriuretic polypeptide (ANP) level and the renin angiotensin system in rats. A single oral administration of captopril decreased the plasma ANP level and increased the plasma renin activity (PRA). Chronic administration of captopril for 2 weeks caused no changes in plasma ANP level, but PRA was increased. This suggests the hypothesis that the hemodynamic changes rather than changes in the renin angiotensin system caused by captopril may affect the plasma ANP level.
Effects of a new antiarrhythmic agent, E-0747, on action potentials of swine cardiac Purkinje fibers were studied using standard microelectrode techniques. E-0747 decreased the maximum rate of rise (Vmax) of action potentials at concentrations higher than 3 X 10(-7) M at a frequency of 1 Hz without change in resting membrane potential. E-0747 (3 X 10(-6) M) shifted the steady-state relationship between the Vmax and the resting membrane potential in a hyperpolarizing direction by 9.2 +/- 0.9 mV. E-0747 depressed the Vmax in a rate-dependent manner. At a concentration of 3 X 10(-6) M, the depression was approximately 50% at a stimulation of 3.3 Hz. E-0747 (3 X 10(-6) M) did not depress the Vmax of the first action potential after a rest period of approximately 30 min, but subsequently reduced the Vmax with successive stimulations reaching a new steady level after approximately 20 min. The time course of recovery from inactivation of the Vmax in the presence of E-0747 (10(-6) M) did not differ from that of the control. E-0747 shortened the action potential duration (APD), but did not affect the ratio of effective refractory period (ERP) to APD. These results suggest that E-0747 depresses the Vmax by closely associating with open and/or inactivated sodium channels. It may be classified as an antiarrhythmic agent of class 1C type of the Vaughan Williams' classification.
We have reported a case of malignant lymphoma in associated with Hashimoto's disease arising in the right lobe of thyroid of a 57-year-old woman. The pre-operative aspirated biopsy was valuable for diagnosis Immuno-histochemical observations revealed the localization of anti B cell antibody in the cell surface of lymphoma cells and anti thyroglobulin antibody in intactly follicular epithelium within the lymphoma tissue. This lymphoma was diagnosed as diffuse, medium cell and B cell type. Radiation and chemotherapy were performed for multiple metastasis of liver and brain, but this case had died of DIC and diffuse hyaline membrane disease of lung.
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A case of traumatic occlusion of the bilateral vertebral arteries associated with fracture of the cervical spine is reported. A 34-year-old man, having no previously noted medical problems, fell to the bottom of a bathtub with a depth of 80 cm, and hit the vertex fronto-parietal region of his head. He was transferred to our hospital 6 hours after his fall with a crush fracture of the cervical spine at the C6 level. On admission he was alert, but having pain in the vertex region, dysarthria, blurred vision and hemiparesis. Roentgenograms confirmed a crush fracture of the C6 vertebral body. Computed tomograms of the brain revealed a high density of basilar artery. Cervical traction with a Halo brace was then carried out. Twelve hours after the trauma, left oculomotor and right facial palsy appeared followed by bilateral oculomotor palsy and respiratory difficulty. At the 14th hour, he displayed bilateral Babinski's signs and tetraparesis. Tetraparesis became complete with right-side Horner's syndrome at 16 hours. Cerebral arteriograms performed 20 hours after the trauma showed a complete occlusion of the right vertebral artery and an incomplete occlusion of the left vertebral artery at the C6-7 intervertebral disk space. Conscious level deteriorated to a 200 level on the Japan coma scale 28 hours after the trauma and to a 300 level after 32 hours. Computed tomograms revealed a marked low density on the cerebellum and brain stem 38 hours after the accident. He expired on the 22nd day after the trauma.(ABSTRACT TRUNCATED AT 250 WORDS)
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