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Biomedical subjects

T Enoki

Publications and source records attributed to T Enoki.

At least 19 recordsLinked to original sources

Relationship between variations in the circle of Willis and flow rates in internal carotid and basilar arteries determined by means of magnetic resonance imaging with semiautomated lumen segmentation: reference data from 125 healthy volunteers.

BACKGROUND AND PURPOSE: Volume flow rates in the feeding arteries of the brain are measured to evaluate blood flow dynamics in vascular disease. Although these flow values are thought to be effected by anatomic variations in the circle of Willis, few reports have described the effect. This study reports on the relationship between variations in the circle of Willis and volume flow rates in the bilateral internal carotid and basilar arteries of normal volunteers. METHODS: We prospectively examined 125 healthy volunteers by MR imaging. Variations in the circle of Willis were classified as "textbook" type, hypoplasia of the precommunicating segment of the anterior cerebral artery (A1), hypoplasia of the precommunicating segment of the posterior cerebral artery (P1), or "other." Volume flow rates were measured by 2D cine phase-contrast MR imaging. Lumen boundaries and volume flow rates were semiautomatically determined by pulsatility-based segmentation. RESULTS: Of the 117 subjects (61 men, 56 women; mean age, 23.6 years) considered suitable for flow measurement, 105 showed textbook type, and 6 each showed A1 hypoplasia and P1 hypoplasia. Total flow rates for the 3 variations were 781 +/- 151 mL/min (mean +/- SD), 744 +/- 119, and 763 +/- 129, respectively. Relative contributions by flow rates of the internal carotid arteries and the basilar artery for the 3 variations were 39.8%:38.9%:21.3%, 31.8%:49.1%:19.0%, and 46.6%:41.6%:11.7%, respectively, showing statistically significant differences. CONCLUSIONS: Variations in the circle of Willis correlate significantly with relative contributions by the flow rates of the bilateral internal carotid and basilar arteries.

Adult↗

Effect of hypercapnia on arterial hypotension after induction of anaesthesia.

We evaluated the effectiveness of intentional hypercapnia against hypotension after induction of anaesthesia with thiopental and isoflurane (TI) or propofol (P). For each group, 24 patients were anaesthetized with thiopental 4 mg kg(-1) (TI) or propofol 2 mg kg(-1) (P) for tracheal intubation and then lightly anaesthetized with isoflurane at 0.6% end-expiratory concentration (TI) or by 6 mg kg(-1) h(-1) infusion of propofol (P). In both anaesthesia groups, patients were randomly assigned to either normocapnia (end-tidal CO(2) = 35 mmHg) or hypercapnia (end-tidal CO(2) = 45 mmHg), which were achieved through adjusting the tidal volume. Systolic arterial pressure (SAP) 15 min after intubation was compared with the preanaesthetic baseline value. Under normocapnia, both TI and P induced a comparable, statistically significant suppression of SAP by approximately 20 mmHg from baseline. Hypercapnia prevented the decrease in SAP in TI but not in P. No patient in the TI-hypercapnia group experienced SAP below 100 mmHg, unlike those in the other groups. In conclusion, mild hypercapnia was effective in the prevention of hypotension in patients receiving thiopental followed by 0.6% end-expiratory isoflurane, but not in patients receiving 6 mg kg(-1) h(-1) propofol.

Adult↗

Ca(2+) channels activated by endothelin-1 in CHO cells expressing endothelin-A or endothelin-B receptors.

We compared the Ca(2+) channels activated by endothelin-1 (ET-1) in Chinese hamster ovary (CHO) cells stably expressing endothelin type A (ET(A)) or endothelin type B (ET(B)) receptors using the Ca(2+) channel blockers LOE-908 and SK&F-96365. In both CHO-ET(A) and CHO-ET(B), ET-1 at 0.1 nM activated the Ca(2+)-permeable nonselective cation channel-1 (NSCC-1), which was sensitive to LOE-908 and resistant to SK&F-96365. ET-1 at 1 nM activated NSCC-2 in addition to NSCC-1; NSCC-2 was sensitive to both LOE-908 and SK&F-96365. ET-1 at 10 nM activated the same channels as 1 nM ET-1 in both cell types, but in CHO-ET(A), it additionally activated the store-operated Ca(2+) channel (SOCC), which was resistant to LOE-908 and sensitive to SK&F-96365. Up to 1 nM ET-1, the level of the formation of inositol phosphates (IPs) was low and similar in both cell types, but, at 10 nM ET-1, it was far greater in CHO-ET(A) than in CHO-ET(B). These results show that, in CHO-ET(A) and CHO-ET(B), ET-1 up to 10 nM activated the same Ca(2+) entry channels: 0.1 nM ET-1 activated NSCC-1, and ET-1 > or = 1 nM activated NSCC-1 and NSCC-2. Notably, in CHO-ET(A), 10 nM ET-1 activated SOCCs because of the higher formation of IPs.

Acetamides↗

Frustrations in polymer conformation in gels and their minimization through molecular imprinting.

We report an experimental realization of a gel system in which frustrations exist and can be minimized, thus meeting two crucial criteria predicted to enable memory of conformations in polymers. The gels consist of a thermosensitive major monomer component and two minor components. One minor component is positively charged and will form complexes around negatively charged target molecules placed in solution. The complexes can be imprinted into the gel by then cross-linking the second minor component, which will form cross-links additional to those in the major polymer matrix. The complexes are destroyed and reformed upon swelling and reshrinking of the gels, showing that memorization has been achieved.

Arylsulfonates↗

Gel catalysts that switch on and off.

We report development of a polymer gel with a catalytic activity that can be switched on and off when the solvent composition is changed. The gel consists of two species of monomers. The major component, N-isopropylacrylamide, makes the gel swell and shrink in response to a change in composition of ethanol/water mixtures. The minor component, vinylimidazole, which is capable of catalysis, is copolymerized into the gel network. The reaction rate for catalytic hydrolysis of p-nitrophenyl caprylate was small when the gel was swollen. In contrast, when the gel was shrunken, the reaction rate increased 5 times. The activity changes discontinuously as a function of solvent composition, thus the catalysis can be switched on and off by an infinitesimal change in solvent composition. The kinetics of catalysis by the gel in the shrunken state is well described by the Michaelis-Menten formula, indicating that the absorption of the substrate by the hydrophobic environment created by the N-isopropylacrylamide polymer in the shrunken gel is responsible for enhancement of catalytic activity. In the swollen state, the rate vs. active site concentration is linear, indicating that the substrate absorption is not a primary factor determining the kinetics. Catalytic activity of the gel is studied for substrates with various alkyl chain lengths; of those studied the switching effect is most pronounced for p-nitrophenyl caprylate.

Acrylamides↗

Disordered magnetism at the metal-insulator threshold in nano-graphite-based carbon materials

The magnetism of activated carbon fibers composed of a disorder network of nanographites was investigated, where each nanographite has about 1 edge-inherited localized spin. The susceptibility, for samples situated around the metal-insulator threshold, shows a cusp around 4-7 K in addition to the presence of a field-cooling effect. These behaviors are explained in terms of disordered magnetism caused by random strengths of inter-nano-graphite antiferromagnetic interactions mediated by pi-conduction carriers.

Journal Article↗

Thiopental induces contraction of rat aortic smooth muscle through Ca(2+) release from the sarcoplasmic reticulum.

UNLABELLED: Little is known about the mechanism of thiopental-induced contraction in vascular smooth muscle. This study aimed to clarify this question by conducting isometric tension experiments and (45)Ca(2+) flux measurements in endothelium-denuded rat aortic rings. Thiopental induced a concentration-dependent contraction under basal tension. This contraction was enhanced when rings were precontracted with phenylephrine in the presence of verapamil. In Ca(2+)-free solution, thiopental-induced contraction was reduced but not abolished with high concentrations. Ca(2+) store depletion with a maximum dose of caffeine in Ca(2+)-free solution further reduced the contraction by subsequent thiopental. Ca(2+) store depletion with thapsigargin completely abolished contraction by thiopental. (45)Ca(2+) influx experiment in the presence of verapamil showed that thiopental could not induce any Ca(2+) influx with or without phenylephrine prestimulation. The (45)Ca(2+) efflux experiment showed more evidence of thiopental-induced Ca(2+) release, which was abolished by thapsigargin. In conclusion, thiopental induces contraction in rat aortic smooth muscle by releasing Ca(2+) from the sarcoplasmic reticulum without Ca(2+) influx. IMPLICATIONS: This is the first study providing evidence that thiopental-induced vascular contraction is caused by Ca(2+) release from the sarcoplasmic reticulum of the smooth muscle.

Animals↗

Comparative contractile effects of halothane and sevoflurane in rat aorta.

BACKGROUND: Volatile anesthetic agents have been shown to have contractile effects in vascular tissues during specific conditions. This study compared contractile effects of halothane and sevoflurane in rat aorta treated with verapamil. This study also tried to elucidate the mechanism of the contraction. METHODS: Endothelium-denuded rat thoracic aorta was used for recording of isometric tension and measurement of influx of 45Ca2+. All experiments were performed in the presence of verapamil. In recording of tension, rings were precontracted with a submaximum dose of phenylephrine, followed by exposure to halothane or sevoflurane. For measurement of influx of 45Ca2+, rat aortic strips were exposed to phenylephrine and then to additional halothane or sevoflurane. Influx of Ca2+ was estimated by incubating the strips in 45Ca2+-labeled solution for 2 min. RESULTS: Halothane (0.5-4.0%) induced contraction in a dose-dependent manner, whereas sevoflurane (1-4%) had no effect on tension. Influx of 45Ca2+ was strongly enhanced by halothane at 1% and 2%, but only slightly at 4%, and was not affected by 1-4% sevoflurane. SK&F 96365, a blocker of voltage-independent Ca2+ channels, abolished contraction and influx of 45Ca2+ by 1% halothane. Depletion of Ca2+ from the sarcoplasmic reticulum with ryanodine or thapsigargin reduced the contraction induced by halothane at 4% but not that at 1% and 2%. CONCLUSION: Halothane is suggested to cause contraction by enhancing influx of Ca2+ via voltage-independent Ca2+ channels at concentrations up to 2% and by inducing release of Ca2+ at 4%. Sevoflurane (1-4%) is devoid of these contractile effects.

Anesthetics, Inhalation↗

[Effect of Down's syndrome on perioperative and long-term prognosis after ventricular septal defect repair].

In this study, we investigated perioperative and long-term prognosis and the risk of major complications after repair of ventricular septal defect in 48 patients with Down's syndrome who underwent ventricular septal defect repair between May 1980 to August 1999 were compared with those in 48 patients with normal chromosomes matched for age and time period. Pp/Ps were significantly lower after the operation in both groups; however perioperative and postoperative Pp/Ps of Down's syndrome group were significantly higher than that those of control group. The duration of intubation was significantly longer in the Down's syndrome group and the case-control study revealed that the risk of long intubation (> or = 7 days) was significantly higher in the Down's syndrome group, but the incidence of PH crisis did not differ between the 2 groups. The main reasons of prolonged intubation period were respiratory complications such as pneumonia or atelectasis. In Down's syndrome group, a 5 months old boy died of heart failure on the 5th postoperative day. All other patients were survived through a mean follow-up period of 122.4 months (the follow-up rate was 95.8%). In conclusion, the perioperative and long-term prognosis after ventricular septal defect repair in patients with Down's syndrome were similar to those in patients with normal chromosome.

Cardiac Surgical Procedures↗

Reversible molecular adsorption based on multiple-point interaction by shrinkable gels.

A general approach is presented for creating polymer gels that can recognize and capture a target molecule by multiple-point interaction and that can reversibly change their affinity to the target by more than one order of magnitude. The polymers consist of majority monomers that make the gel reversibly swell and shrink and minority monomers that constitute multiple-point adsorption centers for the target molecule. Multiple-point interaction is experimentally proven by power laws found between the affinity and the concentration of the adsorbing monomers within the gels.

Adsorption↗

Combined right hepatic and retrohepatic caval resection with reconstruction using a polytetrafluoroethylene graft for primary leiomyosarcoma of the liver: report of case.

We present herein the case of a 53-year-old woman who underwent successful surgical treatment for a leiomyosarcoma of the liver that originated from the posterior hepatic segment and involved the retrohepatic inferior vena cava (IVC). A computed tomographic scan and magnetic resonance imaging demonstrated a large tumor, with rich vascularity, in the liver. The IVC was found to be occluded on these scans, which was confirmed by venacavography. The patient underwent a combined right hepatic and caval resection with reconstruction using an expanded polytetrafluoroethylene graft. The tumor consisted of spindle-shaped cells with cigar-shaped nuclei. It also had a moderate degree of cellularity and ten mitotic figures per ten high-power fields. Immunohistologically, desmin and alpha-smooth muscle actin were stained positive in the tumor cells, implying that the tumor was derived from smooth muscle cells. The patient is alive and well 15 months after her operation.

Blood Vessel Prosthesis Implantation↗

Activation of three types of voltage-independent Ca2+ channel in A7r5 cells by endothelin-1 as revealed by a novel Ca2+ channel blocker LOE 908.

1. We have shown that in addition to voltage-operated Ca2+ channel (VOC), endothelin-1 (ET-1) activates two types of Ca2+-permeable nonselective cation channel (NSCC) in A7r5 cells: its lower concentrations (< or = 1 nM; lower [ET-1]) activate only an SK&F 96365-resistant channel (NSCC-1), whereas its higher concentrations (> or = 10 nM; higher [ET-1]) activate an SK&F 96365-sensitive channel (NSCC-2) as well. 2. We now characterized the effects of a blocker of Ca2+ entry channel LOE 908 on NSCCs and store-operated Ca2+ channel (SOCC) in A7r5 cells, and using two drugs, clarified the involvement of these channels in the ET-1-induced increase in the intracellular free Ca2+ concentrations ([Ca2+]i). Whole-cell recordings and [Ca2+]i monitoring with fluo-3 were used. 3. LOE 908 up to 10 microM had no effect on increases in [Ca2+]i induced by thapsigargin or ionomycin, but SK&F 96365 abolished them. 4. In the cells clamped at -60 mV, both lower and higher [ET-1] induced inward currents with linear iv relationships and the reversal potentials of -15.0 mV. Thapsigargin induced no currents. 5. In the presence of nifedipine, lower [ET-1] induced a sustained increase in [Ca2+]i, whereas higher [ET-1] induced a transient peak and a sustained increase. The sustained increases by lower and higher [ET-1] were abolished by removal of extracellular Ca2+, and they were suppressed by LOE 908 to 0 and 35%, respectively, with the LOE 908-resistant part being abolished by SK&F 96365. 6. These results show that LOE 908 is a blocker of NSCCs without effect on SOCC, and that the increase in [Ca2+]i at lower [ET-1] results from Ca2+ entry through NSCC-1 in addition to VOC, whereas the increase at higher [ET-1] involves NSCC-1, NSCC-2 and SOCC in addition to VOC.

Acetamides↗

Pharmacological characterization of Ca2+ entry channels in endothelin-1-induced contraction of rat aorta using LOE 908 and SK&F 96365.

We have recently shown that endothelin-1 (ET-1) activates two types of Ca2+-permeable nonselective cation channels (designated NSCC-1 and NSCC-2) and store-operated Ca2+ channel (SOCC). These channels can be pharmacologically discriminated using Ca2+ channel blockers such as SK&F 96365 and LOE 908. Here we characterized Ca2+ entry channels involved in ET-1-induced contractions of rat thoracic aortic rings and increases in the intracellular free Ca2+ concentration ([Ca2+]i) of single smooth muscle cells using these blockers. LOE 908 or a blocker of voltage-operated Ca2+ channel nifedipine had no effect on the contractions and increases in [Ca2+]i induced by thapsigargin or ionomycin, whereas SK&F 96365 abolished them. The contractions and increases in [Ca2+]i induced by ET-1 depended on extracellular Ca2+ but were resistant to nifedipine. The responses to lower concentrations (< or =0.1 nM) of ET-1 were abolished by either SK&F 96365 or LOE 908. The responses to higher concentrations (> or = 1 nM) were abolished by SK&F 96365, but were partially resistant to LOE 908. SK&F 96365 inhibited the LOE 908-resistant contractions induced by higher concentrations of ET-1 with IC50 values similar to those for contractions induced by thapsigargin or ionomycin. These results show that the contractions and increases in [Ca2+]i of rat aortic smooth muscles at lower concentrations of ET-1 involve only one Ca2+ entry channel which is sensitive to SK&F 96365 and LOE 908 (NSCC-2), whereas those at higher concentrations of ET-1 involve another Ca2+ entry channel which is sensitive to SK&F 96365 but resistant to LOE 908 (SOCC) in addition to the former channel.

Acetamides↗

Activation of two types of Ca2+-permeable nonselective cation channel by endothelin-1 in A7r5 cells.

1. In A7r5 cells loaded with the Ca2+ indicator fura-2, we examined the effect of a Ca2+ channel blocker SK&F 96365 on increases in intracellular free Ca2+ concentrations ([Ca2+]i) and Mn2+ quenching of fura-2 fluorescence by endothelin-1 (ET-1). Whole-cell patch-clamp was also performed. 2. Higher concentrations (> or = 10 nM) of ET-1 (higher [ET-1]) evoked a transient peak and a subsequent sustained elevation in [Ca2+]i: removal of extracellular Ca2+ abolished only the latter. A blocker of L-type voltage-operated Ca2+ channel (VOC) nifedipine at 1 microM reduced the sustained phase to about 50%, which was partially sensitive to SK&F 96365 (30 microM). 3. Lower [ET-1] (< or = 1 nM) evoked only a sustained elevation in [Ca2+]i which depends on extracellular Ca2+. The elevation was partly sensitive to nifedipine but not SK&F 96365. 4. In the presence of 1 microM nifedipine, higher [ET-1] increased the rate of Mn2+ quenching but lower [ET-1] had little effect. 5. In whole-cell recordings, both lower and higher [ET-1] induced inward currents at a holding potential of -60 mV with linear I-V relationships and reversal potentials close to 0 mV. The current at lower [ET-1] was resistant to SK&F 96365 but was abolished by replacement of Ca2+ in the bath solution with Mn2+. The current at higher [ET-1] was abolished by the replacement plus SK&F 96365. 6. In a bath solution containing only Ca2+ as a movable cation, ET-1 evoked currents: the current at lower [ET-1] was sensitive to Mn2+, whereas that at higher [ET-1] was partly sensitive to SK&F 96365. 7. These results indicate that in addition to VOC, ET-1 activates two types of Ca2+-permeable nonselective cation channel depending on its concentrations which differ in terms of sensitivity to SK&F 96365 and permeability to Mn2+.

Animals↗

Effects of isoflurane on receptor-operated Ca2+ channels in rat aortic smooth muscle.

We have investigated the effects of isoflurane on receptor-operated Ca2+ channels (ROC) in vascular smooth muscle. In isolated rat thoracic aortic rings denuded of endothelium, the effects of isoflurane on phenylephrine-induced contraction and Ca2+ influx were evaluated in the presence of supramaximal doses of nifedipine or verapamil. Under isometric tension recording, the aortic rings were precontracted by phenylephrine 300 nmol litre-1 and exposed to 1.2%, 2.3% or 3.5% isoflurane. Phenylephrine-induced precontraction was enhanced with 2.3% isoflurane by mean 8.1 (SD 9.3)% (P < 0.05 vs 0% isoflurane). The constrictor effect of 2.3% isoflurane was not inhibited by depletion of intracellular Ca2+ stores with ryanodine 20 mumol litre-1, but was abolished in a Ca(2+)-free solution or by SK&F 96,365 30 mumol litre-1, an ROC blocker. Isoflurane-induced contraction was accompanied by increased intracellular free Ca2+ concentration, monitored using fura PE3. Unidirectional 45Ca2+ influx measurement in phenylephrine-stimulated aortic strips revealed that the mean amount of Ca2+ influx was significantly (P < 0.05) enhanced by 1.2% and 2.3% isoflurane, which were 117.1% and 119.7% of control values, respectively. Our results strongly suggest that isoflurane enhanced Ca2+ influx through ROC that had been submaximally activated by phenylephrine.

Anesthetics, Inhalation↗

Transcranial magnetic stimulation over the posterior cerebellum during smooth pursuit eye movements in man.

Recent neurophysiological experiments in the monkey have demonstrated that the flocculus and the posterior vermis, lobules VIc-VII (oculomotor vermis), are involved in the generation of pursuit eye movements. Whereas the functions of the flocculus in the control of smooth pursuit have been intensively investigated, sufficient data are not available for a profitable discussion of the functions of the oculomotor vermis in the control of smooth pursuit. We previously indicated that the posterior vermis can be electrically stimulated by a focal transcranial magnetic stimulation (TMS) device through the skull in man, and that focal TMS of the posterior vermis can modulate saccadic eye movements. In this study we investigated the effects of cerebellar stimulation on smooth pursuit metrics in man using a focal TMS device. Focal TMS was applied over the posterior cerebellum in an area approximately 7 mm lateral and caudal to the inion, where saccadic eye movements are modulated by TMS, during horizontal smooth pursuit elicited by a step-ramp target with a constant velocity of 15 degrees/s in four normal subjects. The TMS device was triggered after the onset of smooth pursuit during the initial acceleration phase (latency range = 40-80 ms) or the steady-state tracking phase (latency range = 300-340 ms). We investigated the effect of TMS on the velocity and acceleration of smooth pursuit. For smooth pursuit directed ipsilateral to the stimulation side (ipsiversive), focal TMS of the posterior cerebellum produced abrupt acceleration of pursuit in both initial acceleration and steady-state tracking phases. On the other hand, TMS produced abrupt deceleration of contraversive pursuit in both initial acceleration and steady-state tracking phases. These findings suggest that the posterior vermis controls smooth pursuit velocity in a direction-selective manner in both initial acceleration and steady-state tracking phases.

Adult↗