[Vectorcardiography and spathol velocity ECG in experimental diffuse myocardiopathy].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to Y Sakamoto.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
1. When the tissue impedance of the guinea-pig taenia coli was measured across a 2 mm sucrose gap in a longitudinal direction, the impedance locus could be fitted by two different circular arcs. Their characteristic frequencies were about 0-6 and 240 Hz after 60 min superfusion with sucrose solution. From the effects of changing the width of sucrose gap and of transection of tissue, and also from taking the difference between impedances measured at two distances, it was concluded that the low-frequency locus corresponds to the transverse impedance of the plasma membrane and the high-frequency locus to the longitudinal tissue impedance. 2. A change in the longitudinal tissue impedance was measured during superfusion with sucrose solution, using a frequency range between 5 Hz and 10 kHz. The admittance decreased with time of superfusion and this time course could be expressed by the sum of three exponential terms. The fastest component, having a time constant of 1-3 min at 10 kHz, was interpreted to correspond to a process of wash-out of extracellular medium. 3. Admittances at zero and infinite frequencies were obtained from the impedance locus. The decrease in these admittances with the time was analysed and the values at the start of washing were obtained by extrapolating the admittance change to zero time. 4. From these values it was estimated that the myoplasmic resistance was 214 omega cm, the junctional resistance 372 omega cm, and the junctional capacity 3-1 muF/cm at 25 degrees C. In these calculations the equivalent circuit of tissue was assumed to be expressed by two components in series: one for the myoplasmic resistance and the other for the junction which has the junctional resistance and capacity in parallel. 5. After 90 min superfusion with sucrose solution, the total tissue impedance measured at zero frequency was increased from 586 to 3034 omega cm. In the total impedance the myoplasmic resistance was increased from 214 to 914 omega cm and the junctional resistance from 372 to 2120 omega cm. Thus, the change in junctional resistance was greater than that in myoplasmic resistance during superfusion of sucrose solution.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Specific receptors for dexamethasone (11beta, 17alpha, 21-trihydroxy-9alpha-fluoro-16alpha-methyl-1,4-pregnadiene-3,20-dione) in the cytoplasm of the liver from AH 130 (solid type) tumor-bearing rats markedly increased in the advanced stage of tumor growth. The cytoplasmic receptors of the livers of normal and tumor-bearing rats differed in their affinities for dexamethasone, and their apparent equilibrium (dissociation) constants (K) for dexamethasone were 4.0 and 2.6 X 10(-9) M, respectively. The rates of dissociation of dexamethasone-receptor complexes and the heat denaturations of the receptors in the livers of normal and tumor-bearing rats were similar. The glucocorticoid receptors of tumor-bearing rat liver had slightly higher affinities than did those of normal liver for all the steroids tested. Only a trace amount of receptors for dexamethasone could be detected in the cytoplasm of AH 130 ascites cells.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Rat liver malate dehydrogenase (decarboxylating) (NADP) ((L-malate: NADP) oxidoreductase (oxaloacetate-decarboxylating), EC 1.1.1.40) was purified and crystallized from medium containing 30 mM Tris-HCl buffer (pH 7.7), 5 mM MgCl2 and 2 mM 2-mercaptoethanol. The enzyme formed rhomboid crystals free from coenzyme, and appeared homogeneous on isoelectric focusing. The crystalline enzyme had an isoelectric point of pH 6.3. Amino acid analysis showed that it contained more acidic amino acids than basic ones.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
1. The electrical properties of mouse pancreatic islet cells have been explored in vitro using a single intracellular micro-electrode for both voltage recording and current injection. 2. The frequency of spontaneous electrical activity induced in islet cells by concentrations of D-glucose greater than 2-8 mM was enhanced by depolarizing, and reduced by hyperpolarizing, current injection. Post-stimulus inhibition and facilitation were also observed. 3. Intracellular current injection evoked a spike potential in Krebs solution containing a low D-glucose concentration (2-8mM), and in glucose-free, but not Ca-free solution. Evoked spikes were observed in approximately 10% of the cell population impaled. 4. The relationship between the rate of rise of an evoked spike and membrane potential displacement by intracellular current injection a sigmoid curve suggesting the presence of an inactivation process in spike potential genesis. 5. High [K]o, 30-50mM, induced electrical activity rarely, and then only transiently, thereafter blocking it; conditioning hyperpolarizing current tended to restore spike activity. 6. D-600, 5 times 10-minus 5M, blocked the electrical activity induced by D-glucose, tolbutamide or current injection; these inhibitory effects were reversed by a threefold increase in [Ca]o to 7-68 mM. 7. From these results it is concluded that the electrical activity induced in islet cells by Dglucose, tolbutamide and current injection is due mainlu to Ca-2+ influx and is dependent on the level of the membrane potential
1. Responses of the membrane electrical characteristics of mouse pancreatic islet cells to ionic environmental changes have been used to assess the role of [Na]0 and [K]0 in the control of membrane potential, i.e. by electrodiffusion or via an electrogenic sodium pump. Islet cell electrical properties were measured in vitro with intracellular glass micro-electrodes. 2. Substitution of LiCl for extracellular NaCl did not change the islet cell membrane potential significantly in low (2.8 mM) glucose solutions, but readmission of NaCl caused a transient hyperpolarization (membrane potential maximum: -70 mV) in high glucose; when choline chloride was substituted for NaCl no hyperpolarization was observed on NaCl re-admission. 3. Superfusion with K-free solution gave no marked change in membrane potential during 30 min incubation in either low (2-8 mM) or high (28 mM) glucose concentrations but longer periods of exposure to K-free solutions caused progressive depolarization. 4. Readmission of K+ induced a transient hyperpolarization of up to 30 mV magnitude and 10 min duration in the presence of high (28 mM) but not low glucose (2-8 mM) concentrations. At the level of maximum hyperpolarization the membrane potential reached -60 mV, the electrical activity induced by the high glucose concentration being concurrently completely blocked. Replacement of [Cl]0 by isethionate accentuated these effects. 5. Ouabain, 10(-3) M, or a decrease in temperature from 37 to 7 degrees C depolarized the islet cells and blocked the transient hyperpolarization induced by readmission of K+. 6. Diphenylhydantoin, 1-5 times 10(-4) M, caused a significant hyperpolarization of the islet cells in low glucose (2-8 mM) and inhibited the electrical activity induced by high glucose (28 mM) or tolbutamide (0-7 mM). 7. It is concluded from these results that both an electrogenic and ionic component contribute to the membrane potential of the mouse pancreatic islet cell although electrodiffusional control normally predominates; acceleration of the Na-K exchange pump by diphenylhydantoin inhibits glucose-induced electrical activity. These findings are discussed in relation to the permeability characteristics of the islet cell membrane and the mechanism of insulin release.
1. The effects of monosaccharides, glycolytic intermediates, metabolic inhibitors and anxia, have been studied on the membrane electrical activity of mouse pancreatic islet cells in vitro using a single intracellular micro-electrode for both voltage recording and current injection. 2. In addition to D-glucose (28mM), D-mannose (16-6mM), and L-leucin (10mM), the substances D-glyceraldehyde (11mM), and acetoacetate (20 mM), induced action potentials in islet cells but other glucos analogues and metabolic intermediates including L-glucose dod not. 3. Mannoheptulose 20 mM), but not D-galactose or 2-deoxy-D-glucose, antagonized the electrical activity induced in islet cells by D-glucose, 28mM. Prior treatment of the cells with mannoheptulose caused them to hyperpolarize and completely prevented the appearance of electrical activity on subsequent exposure to D-glucose. 4. Electrical activity induced by D0glucose 28mM, was progressively inhibited by phloridzin, 10mM, if the cells were exposed to D-glucose and inhibitor simultaneously, and abolished on pretreatment with inhibitor for 30-60 min. Phloridzin also caused depolarization of the islet cells which was independent of extracellular glucose. 5. Anoxia completely blocked the electrical activity induced by glucose but not that evoked by D-glyceraldehyde, L-leucine, tolbutamide or glibenclamide. 6. Iodoacetic acid, 5 mM, rapidly blocked glucose-induced electrical activity whilst that elicited by tolbutamide was relatively resistant to inhibition. 7. The nature and possible location of the glucoreceptor in pancreatic islet cells is discussed in relation to the origin and functional significance of glucose-induced electrical activity and insulin secretion.
The slow wave in the circular muscle of guinea-pig stomach was investigated with the double sucrose-gap method. 2. The amplitude of the slow wave was reduced by depolarization, and it was increased by a small hyperpolarization (5-10 mV). With hyperpolarization greater than 15 mV the amplitude decreased, and the slow wave became reduced, and less dependent on polarization. This residual was not abolished by strong hyperpolarizing current pulses. 3. The frequency of the slow waves was not much affected by membrane polarization. The change was only 15-20% by depolarization or hyperpolarization of 12mV. 4. Rythmic inward currents could be recorded under voltage-clamp conditions. The frequency of the inward currents was the same as that of the slow wave. The intensity of inward current was little affected by membrane polarization. 5. Lowering the temperature reduced the frequency of the slow wave. The rates of rise and fall of the component which remained during strong hyperpolarization were similarly decreased by lowering the temperature. The Q10 of the frequency was about 2-7. 6. It is suggested that the slow wave consists of two different components. One is generated by a potential independent process, and triggers the second component which is potential dependent. The first component may be controlled by some metabolic process.