Biomedical subjects

N Sekiguchi

Publications and source records attributed to N Sekiguchi.

At least 37 records · Page 2Linked to original sources

PubMed1996

Coronary angioplasty ameliorates hypoperfusion-induced endothelial dysfunction in patients with stable angina pectoris.

OBJECTIVES: This study sought to investigate the effect of coronary angioplasty on chronic hypoperfusion-induced endothelial dysfunction in patients with coronary heart disease. BACKGROUND: The endothelium is an important component for organ flow regulation. Ischemia with or without reperfusion is known to cause endothelial dysfunction. We tested the hypothesis that chronic hypoperfusion impairs endothelial function in the angiographically normal coronary artery segment distal to stenosis and that the impairment by chronic hypoperfusion is reduced by coronary angioplasty. METHODS: In 13 patients with stable angina pectoris, substance P (10, 30 and 100 pmol) and nitroglycerin (200 micrograms) were sequentially infused into the coronary artery in a cumulative manner on the day after coronary angioplasty. In 10 of these patients, vascular responses to these agents were again investigated 3 months after angioplasty. Changes in vascular diameter were evaluated in vessels located proximal and distal to the target lesion, both of which were angiographically normal, by performing computer-assisted quantitative coronary angiography. In five patients, the transstenotic pressure gradient was also measured with a pressure sensor-mounted guide wire before angioplasty. RESULTS: On the day after angioplasty, the magnitude of dilation by substance P in distal segments was significantly less than that in proximal segments and inversely correlated with the transstenotic pressure gradient (p < 0.05) and lesion stenosis (p < 0.05). There was no difference in nitroglycerin-induced vasodilation between the two vessel segment groups. Three months later, the impaired response to substance P in the distal segment was restored to normal. CONCLUSIONS: We conclude that chronic hypoperfusion impairs endothelium-dependent dilation of coronary artery distal to critical stenosis in patients with ischemic heart disease and that coronary angioplasty ameliorates the endothelial dysfunction within 3 months.

Aged↗

PubMed1996

Prostacyclin-stimulating factor, novel protein, and diabetic angiopathy.

We recently purified and cloned a new protein that stimulates the synthesis of prostacyclin (PGI2) by the vascular endothelial cells (ECs). We have termed this protein "PGI2-stimulating factor" (PSF). The present study evaluated the expression of PSF mRNA in tissues of Wistar rats, including the kidneys of rats with streptozotocin-induced diabetes, and in cultured cells. Furthermore, we evaluated the presence of PSF in human sera and the immunohistochemical localization of PSF in tissues of patients obtained at autopsy. The latter included a coronary atherosclerotic lesion of a patient who died of acute myocardial infarction. PSF was observed by Northern blot analysis to be expressed in all rat tissues examined (brain, lung, liver, kidney, skeletal muscle, and fat tissue) and was expressed in cultured vascular ECs, smooth muscle cells (SMCs), and fibroblast cells (FCs). A decreased expression of PSF was observed in the kidneys of diabetic rats versus those of normal rats. The presence of PSF in human serum was confirmed by Western blot analysis. In humans, PSF was mainly localized in vascular ECs and SMCs of arterial media and in SMCs of bronchi. Reduced staining for PSF was found in an atherosclerotic versus a normal coronary artery of humans. PSF may be involved in the production of PGI2 in the vessel wall and may participate in the maintenance of vascular homeostasis. PSF abnormalities may be involved in the development of such vascular lesions as atherosclerosis and diabetic angiopathy.

Amino Acid Sequence↗

PubMed1995

Vasodilatory effect of nicorandil on coronary arterial microvessels: its dependency on vessel size and the involvement of the ATP-sensitive potassium channels.

We aimed to clarify the size dependency of nicorandil-induced dilation in coronary microcirculation and the involvement of adenosine triphosphate (ATP)-sensitive potassium channels. Coronary arterial microvessels were observed through a microscope equipped with a floating objective in anesthetized open-chest dogs (n = 29). Heart rate and mean aortic pressure were maintained at control level. In 16 dogs, nicorandil was infused into the coronary in a cumulative fashion (0.1, 1.0, 10, and 100 micrograms/kg/min, for 5 min for each dose). In 13 dogs, glibenclamide (10 microM) was topically applied onto the observed area, and nicorandil was similarly infused. Nicorandil dilated vessels < 100 microns in diameter at all applied doses in a dose-dependent manner. Glibenclamide abolished the dilation of these vessels at the lower two doses. Vessels > 100 microns in diameter dilated only at the two higher doses and the dilation was not affected by glibenclamide. These data suggest that the vessels < 100 microns are more sensitive to this agent than other size vessels, and that ATP-sensitive potassium channels are involved in the nicorandil-induced dilation of vessels smaller than 100 microns, whereas the dilation of other size vessels occurs independently of this channel.

Adenosine Triphosphate↗

PubMed1994

Effect of an ATP sensitive potassium channel opener, levcromakalim, on coronary arterial microvessels in the beating canine heart.

OBJECTIVE: The aim was to clarify the site in the coronary microcirculation that is dilated by an ATP sensitive potassium channel opener, levcromakalim, and to examine whether the magnitude of dilatation is size dependent. METHODS: Coronary arterial microvessels were observed through an intravital microscope equipped with a floating objective in beating canine left ventricles in situ. Flow velocity of the left anterior descending coronary artery was measured with a suction-type Doppler probe. Heart rate and aortic pressure were maintained at control levels throughout the experiments. Three doses of levcromakalim (0.01-1.0 microgram.kg-1.min-1) or a single dose (1.0 microgram.kg-1.min-1) were infused into the coronary artery in groups, with or without intracoronary glibenclamide pretreatment (200 or 400 micrograms.kg-1). The effect of levcromakalim on different sized vessels was assessed by dividing them into three groups according to control diameter (small, internal diameter < 100 microns; medium, > or = 100, < 200 microns; large, > or = 200 microns). RESULTS: The lowest dose of levcromakalim dilated only the small vessels. The two higher doses dilated vessels of all sizes, but the magnitude of dilatation was greater in the small vessel group than in the other two groups. Coronary resistance significantly decreased dose dependently during the infusion of 0.1 and 1.0 microgram.kg-1.min-1 of levcromakalim. Pretreatment with glibenclamide markedly attenuated the levcromakalim induced dilatation of all vessel groups and the reduction in coronary vascular resistance. CONCLUSIONS: Levcromakalim heterogeneously dilates coronary arterial microvessels via the opening of ATP sensitive potassium channels, and small vessels are more sensitive to levcromakalim.

Animals↗

PubMed1994

Effect of calcitonin gene-related peptide on coronary microvessels and its role in acute myocardial ischemia.

BACKGROUND: Calcitonin gene-related peptide (CGRP) is a potent dilator of epicardial conduit vessels and is released during myocardial ischemia in humans. However, the effect of CGRP on coronary arterial microvessels is still unclear, and it is unknown if CGRP modulates the tone of coronary arterial microvessels during acute myocardial ischemia. METHODS AND RESULTS: Epimyocardial microvessels were observed through a microscope equipped with a floating objective system in anesthetized open-chest dogs. Heart rate and aortic pressure were maintained at control levels. Flow velocity of the left anterior descending coronary artery (LAD) was measured with a suction-cup Doppler probe. When CGRP was cumulatively infused into the LAD (0.05, 0.5, 5.0, and 50 pmol/kg per minute) or superfused (0.03, 0.3, 3.0, and 30 nmol/L) over the left ventricular surface, arterial control microvessels > 100 microns in diameter dilated dose dependently at dosages of 0.5 to 50 pmol/kg per minute (infused) or 0.3 to 30 nmol/L (superfused), but those < 100 microns dilated only at the highest dose, and those > 100 microns had greater dilation in both groups. Only the highest dose of CGRP (infused) significantly increased coronary flow. The superfusion of CGRP(8-37) (CGRP receptor antagonist, 300 nmol/L) did not affect the control diameters of coronary arterial microvessels but completely abolished CGRP-induced vasodilation at the same doses (infused and superfused). However, 300 nmol/L of CGRP(8-37) did not affect the response of coronary arterial microvessels to the LAD occlusion in any size. CONCLUSIONS: CGRP preferentially dilates the coronary arterial microvessels > 100 microns in diameter but has only a small effect on those < 100 microns. Endogenous CGRP does not modulate the tone of coronary arterial microvessels during acute myocardial ischemia in beating canine hearts.

Animals↗

PubMed1994

Pertussis toxin-sensitive G protein mediates coronary microvascular control during autoregulation and ischemia in canine heart.

GTP-binding regulatory proteins (G proteins) regulate various biological functions, but their participation in controlling coronary microvascular tone has not been established yet. The goal of the present study was to elucidate the role of pertussis toxin (PTX)-sensitive G protein in regulating coronary microvascular tone during autoregulation and ischemia. In 42 open-chest dogs, coronary arterial microvessels on the surface of the left ventricle were directly observed by epi-illuminated fluorescence microangiography using a floating objective system. PTX (300 ng/mL) was superfused onto the surface of the left ventricle for 2 hours to block Gi and G(o) protein in epimyocardial coronary microvessels in vivo. PTX superfusion caused no change in the resting diameters of microvessels and significantly blocked the vasoconstriction induced by BHT 920 (a selective alpha 2-agonist). After pretreatment with PTX or its vehicle, the left anterior descending coronary artery (LAD) was occluded by a hydraulic occluder to reduce coronary perfusion pressure (CPP) in a stepwise fashion. A mild stenosis (CPP, 60 mm Hg), a severe stenosis (CPP, 40 mm Hg), and complete occlusion were sequentially produced. Coronary flow velocity in the LAD distal to the stenotic site was continuously monitored. In both PTX and vehicle groups, flow velocity did not significantly decrease during mild stenosis, proving that transmural coronary autoregulatory function was well preserved in the preparation. During severe stenosis and complete occlusion, the coronary flow velocity significantly decreased. In the vehicle group, microvessels < 100 microns in inner diameter significantly dilated in response to the reduction in perfusion pressure (mild stenosis, 6.2 +/- 1.9%; severe stenosis, 21.1 +/- 4.4%; and complete occlusion, 16.8 +/- 5.9%; P < .05 versus baseline diameters). In the PTX group, microvessels did not dilate during each occlusion level (mild stenosis, -2.0 +/- 0.9%; severe stenosis, -3.9 +/- 1.9%; and complete occlusion, -13.4 +/- 2.9%; P < .05 versus vehicle group). PTX did not affect the microvascular dilation caused by nitroprusside. The present data indicate that PTX-sensitive G protein is crucially involved in microvascular control during autoregulation and ischemia.

Adrenergic alpha-Agonists↗

PubMed1993

Acute promyelocytic leukemia with t(15;17) abnormality after chemotherapy containing etoposide for Langerhans cell histiocytosis.

BACKGROUND: Epipodophyllotoxins, etoposide and teniposide, have been shown to be implicated in the development, of acute myelogenous leukemia in patients treated for solid tumors or acute lymphoblastic leukemia. Etoposide has been shown to be an effective agent against Langerhans cell histiocytosis (LCH) and has gained wider use recently for first-line and salvage chemotherapy in cases of systemic LCH. METHODS: The authors report two patients with secondary acute promyelocytic leukemia (APL) with a t(15;17) abnormality after chemotherapy that included etoposide for the treatment of LCH. RESULTS: Patient 1, a 6-year-old girl, had APL develop 11 months after cessation of therapy that included vinblastine, prednisolone, and etoposide (9600 mg/m2 in total dose) for LCH. Patient 2, a 3-year-old girl, had APL develop 9 months after cessation of therapy that included vincristine, methotrexate, prednisolone, cyclophosphamide (10,800 mg/m2), and etoposide (4800 mg/m2) for LCH. CONCLUSIONS: The authors have experience with four patients treated with etoposide for LCH and suggest that there is a predisposition to secondary APL with t(15;17) for patients with LCH treated with etoposide. The authors warn against the imprudent use of etoposide as a first-line therapy for LCH.

Child, Preschool↗

PubMed1993

Color, contrast sensitivity, and the cone mosaic.

This paper evaluates the role of various stages in the human visual system in the detection of spatial patterns. Contrast sensitivity measurements were made for interference fringe stimuli in three directions in color space with a psychophysical technique that avoided blurring by the eye's optics including chromatic aberration. These measurements were compared with the performance of an ideal observer that incorporated optical factors, such as photon catch in the cone mosaic, that influence the detection of interference fringes. The comparison of human and ideal observer performance showed that neural factors influence the shape as well as the height of the foveal contrast sensitivity function for all color directions, including those that involve luminance modulation. Furthermore, when optical factors are taken into account, the neural visual system has the same contrast sensitivity for isoluminant stimuli seen by the middle-wavelength-sensitive (M) and long-wavelength-sensitive (L) cones and isoluminant stimuli seen by the short-wavelength-sensitive (S) cones. Though the cone submosaics that feed these chromatic mechanisms have very different spatial properties, the later neural stages apparently have similar spatial properties. Finally, we review the evidence that cone sampling can produce aliasing distortion for gratings with spatial frequencies exceeding the resolution limit. Aliasing can be observed with gratings modulated in any of the three directions in color space we used. We discuss mechanisms that prevent aliasing in most ordinary viewing conditions.

Color Perception↗

PubMed1993

Pharmacological action of (-)-(2S,3aR,7aS)-1-[(S)-N-[(S)-1-carbonyl-3- phenylpropyl]alanyl]hexahydro-2-indolinecarboxylic acid (trandolaprilat) in isolated smooth muscle preparations.

1. Trandolaprilat was found to inhibit angiotensin I (Ang I)-induced contraction of the rat thoracic aorta, and to augment bradykinin(BK)-induced contraction of the guinea pig ileum. In inhibitory activity (IC50) on the Ang I induced contraction of the rat thoracic aorta, trandolaprilat was about 2.4 times as potent as enalaprilat. Concerning the augmenting activity (AC50) on bradykinin-induced contraction of the guinea pig ileum, the activity of trandolaprilat was similar to that of enalaprilat. 2. Trandolaprilat had no effect on contractions induced by norepinephrine, PGF2 alpha, 5-HT or CaCl2 in the thoracic aorta of rats. 3. Trandolaprilat produced endothelium-dependent relaxation. This relaxation was inhibited by NG-methyl-L-arginine treatment, suggesting that endothelium-dependent relaxation of trandolaprilat is related to endothelium-derived-relaxation-factor(EDRF/NO). Like trandolaprilat, captopril also produced endothelium-dependent relaxation, whereas enalaprilat had no effect.

Angiotensin I↗

PubMed1993

Aberration-free measurements of the visibility of isoluminant gratings.

We developed a new apparatus and psychophysical technique to extend isoluminant contrast-sensitivity measurements to high spatial frequencies. The apparatus consists of two identical laser interferometers that are designed to produce phase-locked two-color interference fringes on the retina without the influence of diffraction and most aberrations in the eye. However, even with interferometry, transverse chromatic aberration of the eye can produce a wavelength-dependent phase shift in the interference fringes, which can be exaggerated by head movements. To reduce the effect of head movements, isoluminant red and green interference fringes of equal spatial frequency and orientation were drifted slowly in opposite directions to guarantee a purely isochromatic (in phase) and a purely isoluminant (out of phase) stimulus during each cycle of stimulus presentation. With this technique we found that observers could resolve red and green stripes at spatial frequencies higher than 20 cycles per degree (c/deg) (20-27 c/deg), substantially higher than has previously been reported. This places a lower bound on the sampling density of neurons that mediate color vision. At all spatial frequencies, even those above the isoluminant resolution limit, a relative phase of the red and the green components could be found that obliterated the appearance of luminance modulation at the fringe frequency. Above the resolution limit, red-green-isoluminant interference fringes are seen as spatial noise, which may be chromatic aliasing caused by spatial sampling at some stage in the chromatic pathway.

Color Perception Tests↗

PubMed1993

Efficiency in detection of isoluminant and isochromatic interference fringes.

We examined the limitations imposed by neural factors on spatial contrast sensitivity for both isochromatic and isoluminant gratings. We used two strategies to isolate these neural factors. First, we eliminated the effect of blurring by the dioptrics of the eye by using interference fringes. Second, we corrected our data for additional sensitivity losses up to and including the site of photon absorption by applying an ideal-observer analysis described by Geisler [J. Opt. Soc. Am. A 1, 775 (1984)]. Our measurements indicate that the neural visual system modifies the shape of the contrast-sensitivity functions for both isochromatic and isoluminant stimuli at high spatial frequencies. If we assume that the high-spatial-frequency performance of the neural visual system is determined by a low-pass spatial filter followed by additive noise, then the visual system has a spatial bandwidth 1.8 times lower for isoluminant red-green than for isochromatic stimuli. On the other hand, we find no difference in bandwidth or sensitivity of the neural visual system for isoluminant red-green and S-cone-isolated stimuli.

Color Perception Tests↗

PubMed1992

Effects of alpha and beta adrenergic blockade on coronary arterial microvessels in the beating canine heart.

OBJECTIVE: The aim was to clarify the effects of alpha and beta adrenergic blockade on coronary arterial microvessels and to assess the role of alpha and beta adrenergic tone in normally beating hearts. METHODS: 47 anaesthetised open chest dogs were studied. The diameters of epicardial arterial microvessels were measured in beating hearts using an incident light fluorescence microscope equipped with a floating objective. Drugs were infused into the left anterior descending coronary artery keeping the heart rate and aortic pressure at control levels. To examine the effect of alpha adrenergic blockade, phentolamine (100 micrograms.kg-1) was given in the absence or presence of beta adrenergic blockade (propranolol 50 micrograms.kg-1). To examine the effect of beta adrenergic blockade, propranolol (50 micrograms.kg-1) or three doses of ICI 118,551 (a selective beta 2 antagonist, 0.1, 0.5, and 1.0 microgram.kg-1.min-1) was given. RESULTS: Coronary arterial microvessels were divided into three groups according to the control diameters (D) of small (D less than 100 microns), medium (100 less than or equal to D less than 200 microns) and large (D greater than or equal to 200 microns) groups. In the absence of beta adrenergic blockade, phentolamine significantly dilated all vessel groups: small +19.6 (SEM 5.6)%, medium +5.8(2.3)%, large +5.3(0.9)%. In the presence of beta adrenergic blockade, the vasodilator effect of phentolamine was completely abolished. Propranolol constricted all vessel groups: small -3.6(1.1)%, medium -4.8(1.0)%, large -3.5(1.0)%. ICI 118,551 significantly constricted the large vessel group [-2.5(0.6)%] at the mid dose, and the medium and large vessel groups [medium -3.1(0.8)%, large -3.5(1.3)%] at the highest dose. CONCLUSIONS: These data indicate that (1) the vasodilator effect of phentolamine is induced by beta adrenergic stimulation; (2) resting alpha adrenergic tone of coronary arterial microvessels is minimal in normally beating hearts, and (3) resting beta adrenergic tone may play a physiological role in coronary arterial microvessels, and beta 2 adrenergic tone predominates in arterial microvessels greater than 100 microns in diameter.

Adrenergic alpha-Antagonists↗

PubMed1992

Microvascular sites and mechanisms responsible for reactive hyperemia in the coronary circulation of the beating canine heart.

Our aim was to elucidate the site and mechanism responsible for reactive hyperemia in coronary circulation. In in vivo beating canine hearts, microvessels of the left anterior descending coronary artery (LAD) were observed through a microscope equipped with a floating objective. Flow velocity of the LAD was measured with a suction-type Doppler probe. The LAD was occluded for 20 or 30 seconds and then released, and reactive hyperemia was observed before and after 8-phenyltheophylline (7.5 mg/kg i.v.) or glibenclamide (200 micrograms/kg into the LAD) infusion. During the occlusion, only arterial microvessels smaller than 100 microns in diameter dilated. Dilation of those vessels was partially attenuated by 8-phenyltheophylline and completely abolished with glibenclamide. In the early phase of reactive hyperemia, all arterial microvessels dilated, and the magnitude of peak dilation was greater in vessels smaller than 100 microns compared with those larger than 100 microns. Vasodilation during reactive hyperemia ceased within 60 seconds in vessels smaller than 100 microns but was sustained for more than 120 seconds in those larger than 100 microns. 8-Phenyltheophylline did not change peak dilation of arterial microvessels but reduced dilation after the peak. Glibenclamide remarkably attenuated dilation of all arterial microvessels in the whole phase of reactive hyperemia. These results indicate that all arterial microvessels are responsible for reactive hyperemia after coronary artery occlusions of 20-30 seconds, but there is greater participation of vessels smaller than 100 microns in the early phase of reactive hyperemia. Dilation of vessels larger than 100 microns assumes an important role in the later phase. ATP-sensitive K+ channels mediate dilation of arterial microvessels both in brief ischemia and reactive hyperemia.

Adenosine↗

PubMed1991

Nonlinear distortion of gratings at the foveal resolution limit.

Aliasing by the foveal cone mosaic causes high frequency interference fringes to look like bright and dark zebra stripes (primary zebra stripes) [Williams, Vision Research, 25, 195 (1985); Vision Research, 28, 433 (1988)]. Some observers report another type of zebra stripes defined by variations in chromaticity as well as brightness, which we call secondary zebra stripes. The conditions required to see the secondary zebra stripes are almost identical to those required to see the primary zebra stripes, except that they are seen at approximately half the spatial frequency. We consider the hypothesis that the secondary zebra stripes arise from aliasing by a particular packing arrangement of the M and L cone submosaics, but present evidence favoring an alternative hypothesis based on a known local nonlinearity in the visual system.

Color Vision Defects↗

PubMed1990

Neuropeptide Y modulates vasoconstriction in coronary microvessels in the beating canine heart.

The purpose of this study was to determine whether neuropeptide Y has a direct vasoconstrictor effect at low doses, mimicking the physiological plasma concentration on the specific site(s) of coronary arterial microvessels in in situ beating canine left ventricles. Coronary microvessels were directly observed by means of an intravital microscope and video system equipped with a floating objective. Epi-illuminated fluorescence coronary microangiography was performed in open-chest anesthetized dogs (n = 14) to examine the changes in internal diameter of epimyocardial arterial microvessels. Flow velocity of fluorescently labeled microshperes in capillaries was also measured (n = 6). To eliminate secondary effects of neuropeptide Y on coronary microvessels via autonomic nervous modulation, experiments were conducted under pharmacological blockade of the regional autonomic nervous system by intracoronary injection of propranolol, 50 micrograms/kg; phentolamine, 100 micrograms/kg; and atropine, 5 micrograms/kg. Aortic pressure and heart rate were kept constant during the experiments. Intracoronary infusion of three different doses of neuropeptide Y (1, 10, and 100 pmol/kg/min) for 5 minutes significantly constricted small microvessels (less than 100 microns in diameter) (-5.2 +/- 1.4%, -8.5 +/- 1.5%, and -14.0 +/- 1.7%; p less than 0.05 versus before neuropeptide Y at each dose), medium microvessels (100-200 microns in diameter) (-5.5 +/- 1.6%, -10.6 +/- 1.8%, and -16.8 +/- 2.1%, p less than 0.05 versus before neuropeptide Y at each dose), and large microvessels (greater than 200 microns in diameter) (-3.6 +/- 0.6%, -5.8 +/- 0.8%, and -10.0 +/- 1.1%; p less than 0.05 versus before neuropeptide Y at each dose) in a dose-dependent manner. Capillary flow velocity was reduced by 17.2 +/- 3.1% by an intracoronary dose of 100 pmol/kg/min of neuropeptide Y (p less than 0.05). The present study indicates that low doses of neuropeptide Y exert a homogeneous direct vasoconstrictor effect on various sizes of coronary arterial microvessels and reduce capillary flow velocity. These results suggest that neuropeptide Y may play a physiological role in modulating coronary microvascular tone.

Animals↗

PubMed1990

Enhancing effects of myristyl lactate and lauryl lactate on percutaneous absorption of indomethacin in rats.

The enhancing effects of myristyl lactate (ML) and lauryl lactate (LL) on the percutaneous absorption of indomethacin (ID) from test solutions in propylene glycol (PG) were investigated in rats. ID absorption was observed to be markedly enhanced by the addition of ML or LL to PG as compared with the control (PG alone). The marked enhancing effects were observed at concentrations greater than 3% ML and 3% LL in PG. In particular, the maximal enhancement of percutaneous absorption of ID was achieved at 5% ML and LL. To elucidate the mode of action of ML as an enhancer, the percutaneous absorption of ID through the skin pretreated with ML alone was investigated. It was suggested that ML acts on the stratum corneum to produce its effect.

Administration, Topical↗

PubMed1990

[Statistical studies of student clinical practice. 1. Clinical practice of operative dentistry from 1983 to 1989].

Clinical practice has been assigned as a final and very important aspect of study and practice of dental education. In our university, the students are exposed the clinical practice from the latter term of fifth year. This report investigated the protocols of clinical cases from the first to the seventh class of graduates. The results obtained were as follows: 1) The graduates of first class averaged 9 clinical cases. This decreased with the years and the fourth class averaged 5.5 cases. From the sixth class simulator training and mutual practice among the students was introduced and the total average of seventh class was 5.1 cases. 2) The dental practice centers on restoration and 20 percent of all cases were amalgam fillings from the first to four the class. However this decreased from the fifth class and does not take place at present. Composite resin restorations increased. Cast restorations occupied 20 percent of all cases and the proportion hasn't changed. 3) Clinical cases of graduates of fifth class who were first to include treatment between students averaged 7 cases. Mutual treatment practice is useful because of the increase exposure to clinical practice.

Clinical Clerkship↗

PubMed1989

Effects of N-(2,6-dimethylphenyl)-8-pyrrolizidineacetamide hydrochloride hemihydrate on the ventriculo-atrial conductivity of accessory pathways.

The purpose of this study was to examine the effects of N-(2,6-dimethylphenyl)-8-pyrrolizidineacetamide hydrochloride hemihydrate (SUN 1165), a newly developed antiarrhythmic agent belonging to class Ic, on the ventriculoatrial (VA) conductivity of accessory pathways and paroxysmal supra-ventricular tachycardia (PSVT). Twelve patients with accessory pathways were examined by standard electrophysiologic technique before and after a single oral dose of SUN 1165 (100 mg). 1 h after administration, SUN 1165 blocked VA conduction of the accessory pathway in six of twelve patients and prevented the induction of PSVT in six of seven cases. In the cases in which VA block did not occur, the VA interval prolonged (from 178 +/- 7 to 190 +/- 11 ms, p less than 0.05), and the effective refractory period of VA conduction was also increased (from 273 +/- 10 to 318 +/- 15 ms. p less than 0.05). SUN 1165 also prolonged the conduction time in normal conduction systems (AH and HV intervals and QRS duration), but the degree of the prolongation was moderate and not dangerous. There was no adverse effect. These results indicate that SUN 1165 is a potent and safe antiarrhythmic agent, and useful for preventing or stopping PSVT by blocking or depressing VA conduction through accessory pathways.

Administration, Oral↗