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Biomedical subjects

K Fujii

Publications and source records attributed to K Fujii.

At least 631 records · Page 35Linked to original sources

Doppler echocardiographic quantitation of cross-sectional area under various hemodynamic conditions: an experimental validation in a canine model of supravalvular aortic stenosis.

The hemodynamic effects on cross-sectional area calculated with the continuity equation were assessed in canine experiments. In 13 open chest dogs, 46 supravalvular aortic stenoses were created by aortic root banding. The cross-sectional area of the stenosis was calculated by Doppler echocardiography with application of the continuity equation before and after the following hemodynamic interventions: protocol 1, atrial pacing at 90, 120, 150 and 180 beats/min after sinus node crush; protocol 2, preload reduction by mild and severe clamping of the inferior vena cava; and protocol 3, afterload augmentation by mild and severe clamping of the descending aorta. In each observation, a dimension of the stenosis was directly measured by two-dimensional echocardiography, and the cross-sectional area was determined as a reference standard. As a result of the hemodynamic interventions, significant changes were observed in stroke volume and pressure gradient (protocol 1), in cardiac output, stroke volume and pressure gradient (protocol 2) and in heart rate, cardiac output and pressure gradient (protocol 3). Despite these changes in hemodynamic variables, the Doppler-derived cross-sectional area showed no significant change for a given stenosis. In addition, areas calculated with the continuity equation (x) agreed well with those determined by two-dimensional echocardiography (y) (r = 0.96, p less than 0.001, y = 0.97x + 0.02, SEE = +/- 0.06 cm2). Thus, it is concluded that Doppler echocardiography with application of the continuity equation accurately predicts the stenotic cross-sectional area over a wide range of hemodynamic conditions in supravalvular aortic stenosis.

Animals↗

The effect of IgA immune complexes on the proliferation of cultured human mesangial cells.

To investigate the role of IgA-containing circulating immune complexes (IgA-CIC) in mesangial cell proliferation, human mesangial cells were cultured with sera or IgA isolates from IgA-CIC-positive IgA nephropathy patients and negative controls. A solid phase anti-C3d enzyme-linked immunosorbent assay (ELISA) was used for the detection of IgA-CIC. Sera stimulated the proliferation of the mesangial cells at both 24 and 72 hours' incubation. However, there was no difference in the proliferation of cells incubated with sera from IgA-CIC-positive patients and negative controls. IgA-CIC-positive and negative IgA isolates both stimulated proliferation of mesangial cells at 24 hours' incubation. Our data do not support the hypothesis that IgA-CIC are directly responsible for mesangial cell proliferation.

Antigen-Antibody Complex↗

Intraoperative localization of a cervicomedullary glioma from the killed end potential: illustrative case.

We recorded the intraoperative somatosensory evoked potentials directly from the upper cervical cord and medulla in a patient with an intrinsic tumor at the region of the cervicomedullary junction. The killed end potential, a large positive potential, was obtained at the caudal end of the tumor. This type of potential occurs when an impulse approaches but never passes beyond the recording electrode. Myelotomy guided by the killed end potential enabled appropriate spinal and medullary dissection and led to early encounter with the cervicomedullary tumor.

Adult↗

Tumors of the lateral ventricular wall, especially the septum pellucidum: clinical presentation and variations in pathological features.

The clinical and histopathological features of 19 patients with tumors involving the septum pellucidum are presented. These tumors predominantly affected young adults, and the clinical manifestations were usually the results of raised intracranial pressure related to obstructive hydrocephalus, mental abnormality, epileptic seizures, or a combination of these. Seventeen of the tumors grew mainly in the lateral and third ventricles, and the other 2 grew both into the lateral ventricle and the cerebral parenchyma. The direction of cellular differentiation of the tumor cells varied from patient to patient and consisted of 8 neurocytomas, 1 mature neuronal tumor with ganglionic and small round neuronal cells, 3 subependymomas, 3 subependymal giant cell astrocytomas, 2 pilocytic astrocytomas, 1 malignant astrocytoma, and 1 teratoma with embryonal carcinoma. These tumors were considered to have arisen from the multipotential cells in the subependymal plate or germ cell rests in the lateral ventricular wall, especially in the septum pellucidum. Because of the relatively inert biological behavior and histological features of most of these tumors, we favor the malformative theory of their origin. Either total or an extensive excision of the tumors in this series, which had developed mainly in the ventricular system, provided long-term survival in many cases.

Adolescent↗

Potassium channel blockers and the effects of cromakalim on the smooth muscle of the guinea-pig bladder.

1. The K+ channel blocking drugs tetraethylammonium Cl (TEA), procaine, 4-aminopyridine (4AP) and quinidine all produced concentration-dependent contractions of strips of smooth muscle from the guinea-pig urinary bladder. Apamin and glibenclamide caused little increase in the mechanical activity, and tolbutamide inhibited it. 2. TEA, procaine, 4AP, quinidine and apamin all increased the frequencies of spontaneous action potentials recorded with microelectrodes. TEA, quinidine and procaine all caused prolongation of the falling phase of the spike, and procaine and apamin completely abolished the after-hyperpolarization. 3. TEA and procaine increased K+ efflux from the tissue, an effect blocked by nifedipine. TEA and apamin increased, whereas quinidine, procaine and 4AP decreased K+ uptake. 4. Cromakalim caused a concentration-dependent hyperpolarization of the membrane, abolished spike activity, increased K+ fluxes and relaxed the smooth muscle. The relaxant effect of cromakalim was unaffected by apamin, and in its presence the effects of cromakalim on membrane potential and K+ fluxes were unchanged. Procaine abolished all the effects of cromakalim, and TEA at high concentrations reduced but did not abolish these effects. Quinidine reduced the effects of cromakalim on tension and membrane potential, but its actions were surmounted by higher concentrations of cromakalim. The effects of 4AP on tension and membrane properties were transitory, but it had some effects on the actions of cromakalim. Glibenclamide and tolbutamide reversed the relaxant effects of submaximal cromakalim concentrations, tolbutamide only transiently. 5. It is concluded that the channels opened by cromakalim are not those involved in generating the spike after-hyperpolarization. They have properties similar to the delayed rectifier K+ channels responsible for spike repolarization, and also are similar to the ATP-dependent K channels in vascular smooth muscle.

4-Aminopyridine↗

Ionic mechanisms in spontaneous vasomotion of the rat basilar artery in vivo.

1. The goal of this study was to examine ionic mechanisms that modulate spontaneous rhythmic changes in vascular calibre or 'vasomotion' in the basilar artery in vivo. 2. Diameter of the basilar artery was measured through a craniotomy in anaesthetized rats under control conditions and during topical application of antagonists or alteration in the ionic composition of artificial cerebrospinal fluid (CSF). 3. Both Ca2(+)-free CSF and the Ca2+ channel blocker, nimodipine, produced moderate dilatation of the basilar artery and abolished vasomotion. Increasing the concentration of Ca2+ in CSF from 1.7 to 5.0 mM did not affect the frequency of vasomotion, although the amplitude was increased slightly. 4. Both K(+)-free CSF and ouabain produced mild to moderate vasoconstriction and abolished vasomotion. In contrast, increasing the concentration of K+ in CSF produced vasodilatation of the basilar artery and decreased or abolished vasomotion depending on the degree of vasodilatation. 5. Tetrodotoxin had no effect on vasomotion. 6. These results suggest that vasomotion of the basilar artery in vivo is dependent on extracellular Ca2+ and K+, and on the activity of Na(+)-K(+)-ATPase, and not dependent on Na+ channel.

Animals↗

Vasomotion of basilar arteries in vivo.

Vasomotion is a rhythmic change in vascular caliber that has been described in vivo mainly in peripheral arterioles. In this study, we have characterized vasomotion in a large artery of the brain in vivo. In anesthetized rats, spontaneous vasomotion was observed in 38 of 47 basilar arteries visualized through a cranial window. Base-line arterial diameter was 259 +/- 9 (means +/- SE) microns. Under control conditions, the frequency of vasomotion was 4.8 +/- 0.2 cycles/min, and the amplitude was 19 +/- 2% of the mean diameter. Vasomotion usually occurred simultaneously along the entire length of the vessel, but in some arteries it propagated in either direction. Moderate hypertension (phenylephrine) or vasoconstriction induced by topical application of serotonin, vasopressin, or the thromboxane analogue U 46619 increased the frequency of vasomotion. Moderate hypotension or vasodilation induced by nitroglycerin, adenosine, or acetylcholine decreased the frequency. Marked hypertension, hypotension, or vasodilatation abolished vasomotion. Thus vasomotion of the basilar artery in vivo 1) is common and of relatively large amplitude, 2) does not seem to be driven by a single pacemaker, and 3) is dependent on vessel diameter or vasomotor tone.

Animals↗

Cerebral blood flow and metabolism in normotensive and hypertensive patients with transient neurologic deficits.

We used positron emission tomography to examine retrospectively the effects of blood pressure on regional cerebral blood flow and oxygen metabolism in seven normotensive and eight hypertensive patients with a history of transient neurologic deficits. In the hypertensive patients, a decrease in regional cerebral blood flow was closely related to blood pressure; these changes were most pronounced in the supratentorial structures, especially the striatum and thalamus. In contrast, the regional cerebral metabolic rate for oxygen was less related to blood pressure. Consequently, the regional oxygen extraction fraction was increased in the hypertensive patients, while regional cerebral blood volume and the regional cerebral blood flow volume ratio were unchanged. Multivariate regression analysis confirmed that hypertension was an independent factor affecting regional cerebral blood flow. The analysis also disclosed that age, sex, hematocrit, smoking, and PaCO2 affected regional cerebral blood flow. These findings suggest that the hemodynamic reserve in hypertensive individuals is reduced, which may predispose them to cerebral ischemia and perhaps stroke, even during small decreases in cerebral perfusion pressure.

Blood Pressure↗

Effects of neuromedin B and GRP-10 on gastrin and insulin release from cultured tumor cells of a malignant gastrinoma.

A study relating to gastrin release from gastrinoma cells by neuromedin B and C-terminal decapeptide of gastrin releasing peptide (GRP-10) has not yet been reported. Therefore, we studied the effects of neuromedin B and GRP-10 on gastrin release from cultured dispersed cells prepared from both the primary tumor in the pancreas and the metastatic tumor in the liver from a case of malignant Zollinger-Ellison syndrome. Both the primary and metastatic tumors obtained by a curative operation contained similar concentrations of gastrin and glucagon, whereas the primary tumor contained 10 times more insulin than the metastatic tumor. Gastrin release from cultured cells of both tumors was suppressed by 0.1 and 10 nM neuromedin B and tended to be suppressed by 0.1-10 nM GRP-10. However, insulin release from cultured cells of the pancreatic tumor was stimulated by GRP-10, but not by neuromedin B. These results might suggest that receptor function for the bombesin family peptides is abnormal in gastrinoma cells in both primary and metastatic tumors, and that a major source of insulin secretary cells is the contaminated normal islet cells in the primary tumor.

Adult↗

[A case of advanced thoracic esophageal cancer with marked response to bleomycin absorbed on activated carbon particles (BLM-CH44), methotrexate, and cisplatin].

A 67-year-old women, who suffered from advanced esophageal cancer with left main bronchus and azygous vein involvement, was treated by combined administration of bleomycin absorbed on activated carbon particles (BLM-CH44, 10 mg/body), methotrexate (30 mg/body i.m.), and cisplatin (75 mg/body i.v.). BLM-CH44 was injected around tumor and total dose of BLM was 120 mg, that of MTX was 180 mg, and that of CDDP was 225 mg. After therapy, the sign of extra-esophageal spread disappeared and a radical operation was performed. Microscopically, the lesion of the esophagus was almost disappeared, and CH44 staining lymph node involvement was completely disappeared.

Aged↗

Mesenteric lymphatic vasomotion following hemorrhage and retransfusion in the rat.

The effect of hemorrhage and retransfusion on the rhythmic contraction of mesenteric lymphatic vessels was studied in 24 rats, anesthetized with pentobarbital. The rats were divided into four groups according to the amount of blood withdrawn: 0.5ml/100g body weight (BW), 1ml/100g, 2ml/100g, and 2.5ml/100g. Immediately following hemorrhage at the rate of 0.5ml/100g/min, lymphatic contraction frequencies were decreased to 67 +/- 12.5, 45 +/- 24.7, 43 +/- 33.1, and 31 +/- 17.8% of the prehemorrhage values in each of the above four groups, respectively (p less than 0.01). Twenty minutes after hemorrhage, lymphatic contraction frequencies were decreased to 70 +/- 17.2, 46 +/- 36.8, and 34 +/- 41.3% in the 0.5ml/100g, 2ml/100g, and 2.5ml/100g, respectively (p less than 0.05). Immediately following hemorrhage, the lymphatic contracted diameters were also reduced to 77 +/- 9.7 and 61 +/- 9.0% of the prehemorrhage values in the 1ml/100g and 2.5ml/100g groups, respectively (p less than 0.01). Twenty minutes after hemorrhage, all withdrawn blood was reinfused. Lymphatic contraction frequency and contracted diameter recovered after retransfusion in each group but 20 minutes after retransfusion, the lymphatic contraction frequency in the 2ml/100g group was still decreased to 42 +/- 30.3% (p less than 0.01). Lymphatic contraction frequency not only decreased proportionately with hypotension during hemorrhage but after retransfusion contraction frequency correlated directly with the mean arterial pressure 20 min after hemorrhage. These data suggest that mean arterial pressure and by inference capillary blood flow and tissue oxygenation are major factors regulating lymphatic vasomotion.

Animals↗

A comparative study on reductive dehalogenation of halothane in liver, kidney and lung of the rabbit.

The contents of cytochrome P-450 (P-450) and cytochrome b5, and the activity of NADPH-cytochrome c reductase and the reductive metabolites of halothane, 2-chloro-1, 1-difluoroethylene (CDE) and 2-chloro-1, 1, 1-trifluoroethane (CTE) were measured in microsomes from the liver, kidney and lung of phenobarbital (PB) pretreated and untreated Japanese white strain rabbits. Microsomal P-450 levels in the liver, kidney (renal cortex) and lung of the rabbits were 1.91 +/- 0.35, 0.19 +/- 0.04 and 0.42 +/- 0.11 nmol/mg protein (mean +/- SD), respectively. In vivo phenobarbital pretreatment (PB-pretreatment) increased the content of P-450 to 2.95 +/- 0.40 nmol/mg protein (154%) in the liver and to 0.40 +/- 0.11 nmol/mg protein (211%) in the kidney, but had little effect in the lung. The activity of CDE formation was 0.72 +/- 0.10, 0.08 +/- 0.04 and 0.03 +/- 0.01 nmol/mg protein/min in the liver, kidney and lung, respectively. PB-pretreatment enhanced the activity of CDE formation to 1.59 +/- 0.49 nmol/mg protein (221%) in the liver, and to 0.29 +/- 0.16 nmol/mg protein/min (363%) in the kidney, but showed little enhancement in the lung. The activity of CTE formation was 1.30 +/- 0.19, 0.12 +/- 0.04 and 0.09 +/- 0.02 nmol/mg protein/min, in the liver, kidney and lung, respectively. PB-pretreatment enhanced the activity of CTE formation to 1.80 +/- 0.44 nmol/mg protein/min (138%) in the liver, but caused only slight enhancement in the kidney and lung. PB-pretreatment markedly enhanced the activity of CDE formation in the kidney. The authors conclude that cytotoxicity by reductive dehalogenation of halothane is possible not only in the liver but also in the kidney with PB-pretreatment.

Animals↗

Effects of in vivo pretreatment with various barbiturates on anaerobic halothane metabolism in rat liver microsomes.

The effects of in vivo pretreatment with phenobarbital (PB), thiopental (TP), thiamylal (TA), pentobarbital (PT), and secobarbital (SB) on hepatic microsomal enzymes, and the effects on anaerobic halothane dehalogenation, aminopyrine N-demethylation, and aniline hydroxylation in the microsomes were studied in male Wistar rats. Three hundred twenty mumol/kg (0.1 ml) of PB, TP, TA, PT, SB, or 0.1ml of 0.9% saline were administered daily, intramuscularly, for periods of one day up to ten days. Daily administration of PB, TP, TA, or PT induced cytochrome P-450, NADPH-cytochrome P-450 reductase and/or cytochrome b5. However, administration of SB did not induce these enzymes. The potency of these enzyme inductions ranged in descending order as follows: PB, TP, TA, and PT. After five days of daily administration of PB, TP, or TA, the production of the anaerobic halothane metabolite, CDFE, increased to 187%, 134%, and 130% of the control, respectively. The production of another halothane metabolite, CTFE, likewise increased to 197%, 168%, and 163%. However, pretreatment with PT or SB had no effect on anaerobic halothane dehalogenation. Aminopyrine N-demethylation also increased after five days of daily administration of PB, TP, and TA. However, aniline hydroxylation decreased after five days of daily administration of TA. Other barbiturates had no effect on aniline hydroxylation. In this study we showed that whereas PT and SB did not enhance anaerobic halothane dehalogenation, PB, TP and TA did. We conclude that not only PB, and also TP and TA, may be enhancing factors in halothane hepatotoxicity. We recommend that, if barbiturates are necessary, SB and PT be used in the preadministration of halothane anesthesia.

Anaerobiosis↗

[A study on disintegration of posterior composite resins caused by long-term water immersion].

The purpose of this study is to clarify a cause of disintegration for posterior composite resins by long-term immersion in distilled water during the 3-year period. Three kinds of posterior composite resins [Bellfirm P (BP), Clearfil Posterior (CP) and Micro Jar (MJ)] and one conventional anterior composite resin [Clearfil FII (FII)] were prepared as to specimens with 20 mm diameter, and 1 mm in thickness. These specimens were immersed in distilled water at 37 +/- 1 degree C for 3 years. These specimens were observed by scanning electron microscope (SEM). The residuces in distilled water were analyzed by X-ray microdiffractometry, infrared (IR) and nuclear magnetic resonance (NMR) spectrometers. One posterior composite resin (microparticle filled resin) was eluted in water more than the other posterior and anterior composite resins with conventional fillers. In SEM observations, many air bubbles were found inside all sections of the four composite resins, because of all mixing type composite resins. The subsurface layer of all four composite resins showed signs of disintegration, but the center layer of the specimens was not disintegrated. Three cured composite resins except MJ had crystalline X-ray diffraction patterns before water immersion, but the cured MJ alone was amorphous. These peaks of crystals showed fillers of these composite resins respectively. X-ray diffraction patterns of the dissolved substances for three composite resins except BP were also crystalline, but the peaks of the crystals except CP were different from the peaks of the fillers respectively. In IR and 1H-NMR spectra of dissolved substances, an unreacted monomer could be detected in one posterior composite resin (BP), but not in the other composite resins. In 1H-NMR spectra of dissolved substances, new signals not found originally were observed in all four composite resins. Therefore, the progress of disintegration was demonstrated clearly. The dissolved substances of all four composite resins were shown as the disintegrated substances between resin matrixes and silane coupling agents. It is suggested that the disintegration of these composite resins by long-term water immersion is derived from hydrolysis.

Composite Resins↗

[Experiences in general anesthesia of patients with scoliosis presupposed to have difficulties in airway maintenance].

We experienced general anesthesia of two patients with cerebral palsy presupposed to have difficulties in tracheal intubation by reason of scoliosis. Case 1 is a 26-year-old woman. Chest X-ray photography and respiratory sounds in both pulmonary areas indicated neither airway stricture nor respiratory distress, but severe scoliosis presupposed difficult tracheal intubation. However, under the impression of possible intubation obtained by preoperative laryngoscopy, orotracheal intubation was tried with rapid induction. Epiglottis deviation to the left noted upon developing larynx made the glottis direct invisible, but some compression of cricoid from outside barely succeeded in intubation. The fixation of the endotracheal tube found much difficulties in its proper positioning so as to make stethoscopy uniform in both pulmonary areas, but trial rotations of the tube both in various directions and at various depths barely managed to find a position of uniform stethoscopy in both pulmonary areas, in which position the tube was fixed as proper positioning. Anesthesia was performed by nitrous oxide.oxygen.halothane; peroperative hemodynamics remained stable and arterial blood gas analysis presented no problems. Case II is a 16-year-old man. Resting respiration presented stridor and chest X-ray photography indicated scoliosis and laryngeal stricture. Patient's lack in the degree of cooperation made laryngoscopy impossible. Thus, in view of a high possibility of difficult tracheal intubation, orotracheal intubation was tried under the control of spontaneous respiration. While the intubation was being carried out by means of a stylet without developing larynx, severe bronchostriction was palpable at the point when the tube barely passed through the glottis, making the intubation impossible. However, the tube barely managed to be inserted while rotating with the stylet being extracted. Anesthesia was carried out by nitrous oxide.oxygen.halothane; peroperative hemodynamics underwent no remarkable change and arterial blood gas analysis presented no problems.

Adolescent↗

MR imaging of the liver before and after transcatheter hepatic chemo-embolization for hepatocellular carcinoma.

Transcatheter chemo-embolization (TCE) in hepatocellular carcinoma (HCC) was performed in 38 patients. The patients were examined by MR imaging before TCE as well as one week and 4 to 5 weeks after TCE. The tumor signal intensity in T2 weighted images increased in 13 cases and decreased in 19 cases after TCE. Increased intensity seemed to reflect intra-tumoral hemorrhage or liquefaction accompanying tumor necrosis. Decreased intensity seemed to reflect coagulation necrosis. In 9 of 18 cases followed over a 2-month period the signal intensity had decreased in both T1 and T2 weighted images. In these patients the tumor showed no recurrence at angiography and the decreased signal seemed to reflect the completion of coagulation necrosis. A hyper- and/or hypointense rim around the tumor appeared in 22 cases. These changes were thought to be perifocal edema or granulation tissue around the tumor. MR imaging was useful in evaluating the necrotic process of the tumor after TCE.

Aged↗