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Biomedical subjects

Y Hirano

Publications and source records attributed to Y Hirano.

At least 253 records · Page 14Linked to original sources
PubMed1987

Development of capillary networks from rat microvascular fragments in vitro: the role of myofibroblastic cells.

A new model useful for studying capillary growth in vitro is described. When the microvessel fragments and accompanying single cells (myofibroblastic cells) from rat epididymal fat pads were co-cultivated, the myofibroblastic cells initially began to grow and reached confluence. A few days later, endothelial cells started to sprout from the vessel fragments, forming cellular cord networks on and in the multilayered myofibroblastic cells. Ultrastructurally, the lumina, surrounded by the endothelial cells having intercellular junctions, were observed at cross-sectioned cellular cords. The growth of cellular cords from the fragments always occurred after the myofibroblastic cells had reached confluence. The medium conditioned to isolated rat myofibroblastic cells stimulated not only the proliferation of the endothelial cells from the bovine capillary and human vein but also the migration of bovine capillary endothelial cells in vitro. Moreover, the extracellular matrix produced by rat myofibroblastic cells modulated the morphology of bovine capillary endothelial cells to a cordlike shape. These observations strongly suggest that the formation of the capillary in vitro is induced by myofibroblastic cells.

Animals↗
PubMed1987

Effect of acetylcholine on aconitine induced delayed afterdepolarisation in the frog atrium and ventricle.

The effect of acetylcholine on the aconitine induced delayed afterdepolarisation and triggered electrical activities under nominally calcium free conditions were studied in frog atrium and ventricle. The changes in intracellular potassium activity were also examined. The aconitine induced delayed afterdepolarisation and triggered electrical activities in atrial muscles were transiently suppressed by acetylcholine. This inhibition was correlated with the time course of the development of hyperpolarisation in the resting membrane potential during acetylcholine application. Propranolol did not abolish the transient inhibition of delayed afterdepolarisation during continuous application of acetylcholine, whereas atropine completely inhibited this effect of acetylcholine. Intracellular potassium activity decreased with time after acetylcholine application, whereas the resting potential became hyperpolarised at an early stage, showing slow recovery thereafter. These results indicate that the transient inhibition of delayed afterdepolarisation by acetylcholine is associated with transient hyperpolarisation of the membrane potential, which is assumed to be caused by potassium accumulation or desensitisation of the muscarinic receptor, or both.

Acetylcholine↗
PubMed1987

Possibility of elevated parathyroid function in patients with calcium-containing nephrolithiasis as compared with normal controls.

109 patients with calcium-containing nephrolithiasis and 10 normal controls underwent oral calcium load test. After thorough examination, 6 of the 109 patients were diagnosed as having primary hyperparathyroidism (PHPT) and the remainder as having normocalcemic nephrolithiasis without PHPT. Following the oral calcium load test, the latter were operationally divided into 3 groups - normocalciuric nephrolithiasis (NN), n = 78; absorptive hypercalciuria (AH), n = 10, and renal hypercalciuria (RH), n = 15 - according to the criteria reported by Pak et al. Before the oral calcium load test, nephrogenous adenosine 3',5'-monophosphate (NcAMP), urinary adenosine 3'-5'-monophosphate (urinary cAMP), and plasma immunoreactive parathyroid hormone (iPTH) were determined to evaluate parathyroid function. This function, as assessed by mean basal NcAMP in the NN, AH and RH groups as well as the PHPT group, was significantly increased as compared with that in the normal controls. Within the NcAMP-elevated 4 groups, the mean basal NcAMP was highest in the PHPT group followed by the RH, AH and NN groups. In view of the mean basal NcAMP, disregarding the PHPT group, the NN and AH groups seemed to be intermediate types between the normal controls and the RH groups. Similar, but less distinctive results were obtained in the determination of urinary cAMP and plasma iPTH. On the other hand, when leaving the PHPT group out, the mean basal urinary calcium creatinine ratio (Ca/Cr) was highest in the RH group followed by the AH and NN groups, and lowest in normal controls, suggesting that the NN and AH groups were intermediate between normal controls and the RH group. The mean basal urinary Ca/Cr ratio in the PHPT group was moderately elevated but not remarkable. Almost similar tendencies were observed in 24-hour urinary calcium excretions on a calcium-restricted diet. A weakly positive correlation (r = 0.232, p less than 0.05) between basal NcAMP and basal urinary Ca/Cr ratio was observed in accumulated cases of the NN, AH and RH groups, whereas a negative correlation (r = -0.664, p less than 0.05) was obtained in normal controls. It is concluded that a possible abnormal calcium metabolism is suggested in stone formers without PHPT. Additionally, it is speculated that 'relative hypercalciuria' in NN and hypercalciuria in AH and RH might be accounted for in a single line of a primary renal leak of calcium.

Adult↗
PubMed1987

Aconitine-induced delayed afterdepolarization in frog atrium and guinea pig papillary muscles in the presence of low concentrations of Ca2+.

Aconitine will induce arrhythmias after the fiber has been completely repolarized. This arrhythmia is generally facilitated in the presence of high Ca2+ solution, yet the aconitine-induced arrhythmia occurs even in the presence of low Ca2+ solutions. We studied aconitine-induced arrhythmia (particularly the amplitude of delayed afterdepolarization) in the frog atrium or guinea-pig papillary muscles in Ca2+-free solution, in the presence or absence of Ca2+ channel blocking agents. In Ca2+-free solution, aconitine (10(-5) g/ml) decreased the resting potential, overshoot, Vmax, and shortened the duration of the 90% action potential, before the onset of delayed afterdepolarization in frog atrial preparations. Tetrodotoxin (TTX) (2 X 10(-7) g/ml) blocked these aconitine-induced electrical changes. Verapamil (10(-6) g/ml) in nominally Ca2+-free solution blocked neither the generation of delayed afterdepolarization nor the triggered activity, while LaCl3 (0.5 mM) or TTX halted it. Delayed afterdepolarization appeared following the aconitine-induced transient increase in twitch tension. This transient increase in twitch tension was blocked by LaCl3 and TTX but not by verapamil. Delayed afterdepolarization in Ca2+-free solution demonstrated the voltage dependence of a U shape between -40 and -80 mV and was inhibited by low Na+ and high K+. Under the influence of aconitine in the guinea pig papillary muscle exposed to the Ca2+-free solution, depolarizing clamp pulses produced a transient inward current, and here the sigmoid time- and voltage-dependent characteristics were similar to those seen in the case of digitalis intoxication. These results suggest that intracellular Na+ loading plays an important role in the aconitine-induced delayed afterdepolarization and transient inward currents in low Ca2+ solution.

Aconitine↗
PubMed1987

Protective effect of acute ethanol administration on endotoxin-induced liver injury.

The effect of acute administration of ethanol on endotoxin-induced liver injury was studied. Biochemical and histological results indicated that ethanol pretreatment protected endotoxin-induced liver injury through the improvement of hepatic blood circulation, which is probably associated with an inhibitory effect of ethanol on platelet functions and coagulation system.

Alanine Transaminase↗
PubMed1987

Analysis of 3-sulfated and nonsulfated bile acids by one-step solvolysis and high performance liquid chromatography.

A facile solvolysis procedure of 3-sulfated bile acid was devised using trifluoroacetic acid, tetrahydrofuran, and methanol. The sulfate esters were completely solvolyzed within only 2 hr by the present method. The clinical utility of the solvolysis procedure and high performance liquid chromatography using immobilized 3 alpha-hydroxysteroid dehydrogenase was demonstrated in the analysis of bile acids in serum of patients with obstructive jaundice. The quantities of 3-sulfated bile acids were calculated from the difference in the amount of bile acids before and after solvolysis. A significantly large proportion of 3-sulfated glycochenodeoxycholic acid, i.e., 21.9 to 31.3% of total glycochenodeoxycholic acid, was found in the serum of patients with obstructive jaundice. Thus, the present method permits simultaneous quantitation of 3-sulfated as well as nonsulfated bile acids in biological samples.

Bile Acids and Salts↗
PubMed1987

[Liver metastasis of thymoma--report of two cases].

We experienced two cases of liver metastasis resulting from thymoma, which is reported to be rare in Japan. Case 1 was a 57-year-old man who was admitted because of hepatomegaly. US, CT and angiography revealed multiple tumors in the liver which were thought to be liver metastasis from an unknown origin. He died of cardiac tamponade one year later. An autopsy revealed thymoma with metastasis to the liver, lung and pericardium. Case 2 was a 32-year-old female who visited our hospital complaining of right hypochondriac pain, US detected several large hyperechoic masses in the liver. A us-guided liver biopsy confirmed metastasis from thymoma. Histological tests of the liver of these two cases showed epithelial type of thymoma.

Adult↗
PubMed1987

New abnormalities in the morphology, cell surface receptors, and electrolyte metabolism of In(Lu) erythrocytes.

The In(Lu) phenotype is inherited as an autosomal dominant trait and is characterized by suppression of the Lutheran, P1, i, and Aua erythrocyte blood group antigens. We have developed a monoclonal antibody (L21) that strongly agglutinates all erythrocytes except In(Lu), and we have identified eight In(Lu) individuals among 42,000 blood donors tested. Studies of two families confirmed the dominant mode of inheritance and revealed several new features of this phenotype. The erythrocytes of all five affected individuals from the two families exhibited diminished hemagglutination by the lectin concanavalin A, although they reacted normally with several other lectins. The erythrocytes of two affected individuals in one family exhibited marked acanthocytosis. The erythrocytes of the proposita of the other family exhibited a mild degree of poikilocytosis, but the cells of the other two affected individuals in this family had normal morphology. The osmotic fragility of fresh In(Lu) erythrocytes was normal, but after incubation for 24 hours at 37 degrees C in plasma the In(Lu) cells exhibited a marked increase in resistance to osmotic lysis. During the incubation period the erythrocytes lost K+ and their total cation content was diminished. These data indicate that in addition to the suppression of blood group antigens noted previously, the In(Lu) phenotype includes a variety of morphological abnormalities and a defect in electrolyte metabolism. The use of L21 and similar monoclonal antibodies provides a more sensitive means of detecting In(Lu) erythrocytes than typing with human anti-Lub antisera.

Antibodies, Monoclonal↗
PubMed1986

Changes in passive electrical properties of guinea-pig ventricular muscle exposed to low K+ and high Ca2+ conditions.

Changes in passive electrical properties of guinea-pig papillary muscle exposed to low K+, high Ca2+ conditions were examined using a single sucrose gap technique. While quiescent preparations exposed for 5 mins did not develop delayed afterdepolarizations, those placed in the test solution for 30 mins with or without stimulation developed afterdepolarizations. Changes occurring during a short exposure to low K+, high Ca2+ solution were increases in membrane resistance, membrane time constant and space constant by 47%, 83% and 17% compared with the control, respectively. There were no significant changes in internal longitudinal resistance and membrane capacity. During long exposure to the test solution (30 mins), delayed afterdepolarizations developed. There were similar increases in membrane resistance and in time constant as found during the short exposures. Internal longitudinal resistance was calculated to have increased by 24% during the long exposure. A 19% increase in membrane capacity was also found during the test condition. High Ca2+ or low K+ alone did not cause a significant increase in internal longitudinal resistance. The conduction velocity in the longitudinal direction decreased from 107 +/- 23 cm/s during the control to 80 +/- 7 cm/s during the test period for 30 mins. These results suggest that, in addition to the abnormal impulse formation based on afterdepolarizations, low K+, high Ca2+ solution changes the passive electrical properties of the fibers, resulting in a lower rate of impulse conduction.

Action Potentials↗
PubMed1986

Changes in K+ currents induced by Ba2+ in guinea pig ventricular muscles.

Effects of Ba2+ on the K+ currents of guinea pig ventricular muscle were studied using the single sucrose-gap voltage-clamp technique. Ba2+ decreased the late (1- or 2-s) current at any potential level, with stronger suppression in the slope conductance at resting potential level than at depolarized voltages above 0 mV. During depolarizing pulses beyond -40 mV, Ba2+ reduced both the time-dependent and time-independent current components, indicating suppression of both outward and background K+ currents (IK and IK1, respectively), whereas tail currents after repolarization to -40 mV increased, with their time courses having double exponentials. These apparent conflicting results between IK and the tail current could not be explained by extracellular K+ fluctuation, because 20 mM Cs+ alone depressed both factors, but an additional application of Ba2+ caused an increase in both components compared with those in the former condition. On hyperpolarization below -60 mV, a time-dependent decrease in the inward current was observed after Ba2+ application without an activation of If. The decrease was stronger and faster at negative potential levels. These results are compatible with a time- and voltage-dependent blocking action of Ba2+ on the inward rectifier K+ current reported in other cardiac and noncardiac tissues. In two components of the tail currents after repolarization from depolarizing voltage steps during Ba2+ application, the faster one can probably be attributed to this blocking action of IK1, whereas the slower one can be attributed to the deactivation of IK. This time-dependent component of IK1 may contribute to the generation of Ba2+-induced automaticity at the depolarized state.

Animals↗