Biomedical subjects

A Nozaki

Publications and source records attributed to A Nozaki.

At least 19 recordsLinked to original sources

PubMed1992

Role of sympathovagal interaction in diurnal variation of QT interval.

To elucidate the role of sympathovagal interaction in diurnal variation of QT interval, 24-hour ambulatory electrocardiographic recordings from 56 subjects (23 control subjects, 18 patients with atherosclerotic coronary artery disease, and 15 patients with diabetes mellitus) were studied. The QT interval at a heart rate of 60 beats/min (QT60) was determined for each of the day and night periods by regression analysis. Sympathetic and parasympathetic activities were assessed by spectral analysis of heart rate variability and represented by the low- and high-frequency components, respectively. The proportion of high-frequency component to the sum of low- and high-frequency components was used as an index of sympathovagal balance. The relative increase in QT60 at night (delta QT60 [%]) was larger in control subjects (4.2 +/- 2.1%) than in patients with coronary artery disease (2.2 +/- 1.8%; p less than 0.01) and diabetes mellitus (-1.5 +/- 4.0%; p less than 0.001). When the data from the 3 subject groups were pooled and analyzed, delta QT60 was correlated with the change in the sympathovagal balance (r = 0.554; p less than 0.001). Low-frequency component in the day alone was also related with delta QT60 (r = 0.554; p less than 0.001), but the ratio or difference of the high-frequency component value between day and night was not. These results indicate that although change in sympathovagal balance was responsible for the diurnal variation in QT interval, the enhanced sympathetic activity in the day was a major determinant of this phenomenon.

Aged↗

PubMed1992

Formation of glycine conjugate and (-)-(R)-enantiomer from (+)-(S)-2-phenylpropionic acid suggesting the formation of the CoA thioester intermediate of (+)-(S)-enantiomer in dogs.

It has been proposed that the chiral inversion of the 2-arylpropionic acids is due to the stereospecific formation of the (-)-R-profenyl-CoA thioesters which are putative intermediates in the inversion. Accordingly, amino acid conjugation, for which the CoA thioesters are obligate intermediates, should be restricted to those optical forms which give rise to the (-)-R-profenyl-CoA, i.e., the racemates and the (-)-(R)-isomers. We have examined this problem in dogs with respect to 2-phenylpropionic acid(2-PPA). Regardless of the optical configuration of 2-phenylpropionic acid administered, the glycine conjugate was the major urinary metabolite and this was shown to be exclusively the (+)-(S)-enantiomer by chiral HPLC. Both (-)-(R)- and (+)-(S)-2-phenylpropionic acid were present in plasma after the administration of either antipode, and further evidence of the chiral inversion of both enantiomers was provided by the presence of some 25% of the opposite enantiomer in the free 2-phenylpropionic acid and its glucuronide excreted in urine after administration of (-)-(R)- and (+)-(S)-2-phenylpropionic acid. The (+)-(S)-enantiomer underwent chiral inversion to the (-)-(R)-antipode when incubated with dog hepatocytes. These data suggests that both enantiomers of 2-phenylpropionic acid are substrates for canine hepatic acyl CoA ligase(s) and thus undergo chiral inversion, but that the CoA thioester of only (+)-(S)-2-phenylpropionic acid is a substrate for the glycine N-acyl transferase. These studies are presently being extended to the structure and species specificity of the reverse inversion and amino acid conjugation of profen NSAIDs.

Animals↗

PubMed1992

Role of anatomic architecture in sustained atrial reentry and double potentials.

To determine the role of anatomic architecture in atrial flutter, electrophysiologic findings were correlated with anatomic features in a modified model of atrial flutter with ligation of the crista terminalis. Crista ligation in the middle right atrium prolonged intraatrial conduction time in a rate-dependent manner in 12 dogs, particularly in the low right atrium. With burst atrial pacing, unidirectional block occurred either in the low right atrium or in the interatrial septal region near the superior vena cava, leading to initiation of atrial flutter. Atrial activation mapping revealed a slow conduction area in the low right atrium where conduction had been delayed by crista ligation. On the intact tissues between the venae cavae, double potentials were recorded, a finding indicative of functional block in the center of the reentrant circuit. The interdeflection time of double potentials changed with the activation sequence of atrial flutter. This change could be explained by assuming that the functional center of the reentrant circuit leaned on the right atrial free wall side. Anatomic study demonstrated that areas of slow conduction, unidirectional block, and functional block in the center of the reentrant circuit were closely related to the location of the intact crista terminalis. In conclusion, the intact portion of the crista terminalis played an important role in the genesis of atrial flutter after blockage of longitudinal conduction through the crista.

Animals↗

PubMed1992

Role of anisotropy in determining the selective action of antiarrhythmics in atrial flutter in the dog.

OBJECTIVE: The aim was to clarify the electrophysiological and anatomical features of the preferential site of action of antiarrhythmic drugs in the re-entrant circuit of canine atrial flutter. METHODS: Electrophysiological and anatomical findings were correlated in 17 anaesthetised adult mongrel dogs with atrial flutter associated with an intercaval anatomical obstacle, before and after intravenous administration of disopyramide (2 mg.kg-1) and flecainide (2 mg.kg-1). RESULTS: Before drug injection, a rate dependent prolongation of conduction time occurred in the low right atrium where the conduction was slow during atrial flutter. Disopyramide (n = 8 dogs) and flecainide (n = 9 dogs) terminated atrial flutter, with conduction block occurring in this slow conduction area in the low right atrium. Although the degree of drug induced prolongation of refractoriness in this particular area was similar to those in other areas of the right atrium, conduction was depressed to a greater extent in this region. Anatomical study revealed that a thick pectinate muscle that branched from the crista or crista terminalis itself ran perpendicular to the wavefront of the pacing impulse and atrial flutter in this slow conduction area. CONCLUSIONS: These data indicated that slow conduction might be attributed, at least in part, to anisotropic conduction over the thick muscle bundle in the low right atrium, and that antiarrhythmic drugs preferentially produced conduction block in this area. Anisotropic conduction in the low right arium is an anatomical substrate for slow conduction in the re-entrant circuit and for the site preference of antiarrhythmic drugs in the present canine model.

Animals↗

PubMed1992

Reappraisal of the coupling interval of ventricular extrasystoles as an index of ectopic mechanisms.

OBJECTIVE: A mathematical model of modulated ventricular parasystole based on the relation between the coupling interval and the preceding RR interval was developed in an attempt to distinguish between parasystolic automaticity and other mechanisms. MATHEMATICAL MODEL: The relation between the coupling interval and the preceding RR interval was examined by plotting the coupling interval of each extrasystole against the preceding RR interval (coupling interval/RR diagram). The coupling interval/RR diagrams obtained from simulations with various modulation modes suggested that the parasystolic mechanism was likely when the dots representing extrasystoles appeared as discrete clusters. In contrast, a linear horizontal accumulation of dots indicated a non-parasystolic mechanism. CLINICAL OBSERVATION: To verify the validity of the simulations, 24 hour electrocardiographic recordings from 60 patients with frequent ventricular extrasystoles (> 1000/day) were analysed to determine whether the extrasystoles showed intrinsic periodicity. Intrinsic periodicity indicative of a parasystolic mechanism was seen in 14 (93%) of 15 patients in whom the coupling interval/RR diagram was characteristic of a parasystolic mechanism. When the coupling interval did not change (variability < 200 ms) over a wide range of RR intervals (> 700 ms) intrinsic periodicity was never identified (0/17). Parasystolic automaticity was the likely mechanism in 11 of the remaining 28 patients (39.3%) in whom coupling interval/RR diagrams were not definitive. CONCLUSION: These data indicate that definite patterns of coupling interval/RR diagrams can be used to distinguish between parasystolic and non-parasystolic mechanisms.

Adolescent↗

PubMed1992

[Primary ureteral tumor in the residual ureter: a report of two cases].

Two cases of primary ureteral tumor in the residual ureter are reported. One was in a 40-year-old woman who had undergone simple nephrectomy for renal tuberculosis 6 years earlier. The other was in a 59-year-old man 11 years after ureterostomy for hydronephrosis. They presented with hematuria. Cystoscopic examination revealed a ureteral tumor out of the residual ureteral orifice. Computed tomographic scan showed a perivesical mass attached to the urinary bladder. It is useful for examination of ureteral stump's condition. We performed ureterectomy. The pathological study revealed the former high grade transitional cell carcinoma with squamous cell carcinoma and lymph nodes metastasis and the latter low grade transitional cell carcinoma. They have been free of disease for 5.5 years and 1.75 years, respectively. These cases are the nine and tenth reports of primary ureteral tumor of the ureteral stump in the Japanese literature.

Adult↗

PubMed1991

A new method for estimating preexcitation index without extrastimulus technique and its usefulness in determining the mechanism of supraventricular tachycardia.

The preexcitation index has been shown to be useful in determining the mechanism of paroxysmal supraventricular tachycardia (SVT) and the site of the accessory pathway in atrioventricular (AV) reentrant tachycardia. To test whether a preexcitation index could be computed analytically instead of by scanning the whole SVT cycle with extrastimuli, 19 patients with SVT were studied. The new index was computed using the following formula: (AV conduction time during SVT) + (ventriculoatrial conduction time during ventricular pacing at the SVT cycle length) - (SVT cycle length). There was a strong correlation between the preexcitation index determined by the extrastimulus technique and the new index in 15 patients in whom the preexcitation index could be determined (r = 0.99, p less than 0.01). The value on the new index was greater than 90 ms only in patients with dual AV nodal pathways. In the 4 patients in whom the preexcitation index could not be determined by the extrastimulus technique, the new index could differentiate AV reentrant tachycardia (index for 2 patients, 60 and 60 ms, respectively) from AV nodal reentrant tachycardia (index for 2 patients, 100 and 105 ms, respectively). In conclusion, the new index provided help in determining the mechanism of SVT, even when retrograde atrial preexcitation by a ventricular extrastimulus did not occur.

Adolescent↗

PubMed1991

Acute effect of percutaneous transluminal mitral commissurotomy on QT interval: possible role of afterload in contraction-excitation feedback.

Percutaneous balloon valvuloplasty for pulmonary or aortic stenosis results in QT prolongation, a finding supporting the presence of contraction-excitation feedback in man. Though afterload reduction alters the QT interval, the effect of changes in preload on ventricular repolarization is yet unknown. To test whether diastolic stretch modified ventricular repolarization, the change in the QT interval was determined in 15 patients who underwent percutaneous transluminal mitral commissurotomy (PTMC) for mitral stenosis. After successful PTMC, the QT interval was prolonged in five, shortened in two, and was unchanged in eight patients, but the mean QT interval in 15 patients did not change (406 +/- 31 msec versus 412 +/- 40 msec, p = NS). However, linear regression analysis revealed a strong correlation between changes in the QT interval and those in systemic vascular resistance (r = -0.83, p less than 0.01). These data indicated that changes in the QT interval after PTMC were small compared with those seen with valvuloplasty for pulmonary or aortic stenosis, and were dependent on afterload but not on preload.

Adult↗

PubMed1991

Effects of antiarrhythmic drugs on canine atrial flutter due to reentry: role of prolongation of refractory period and depression of conduction to excitable gap.

Antiarrhythmic drugs prolong the effective refractory period and depress conduction. To determine the exact role played by these two electrophysiologic effects in the termination of reentry, the effects of disopyramide, flecainide, propafenone and E-4031, a new class III drug, were examined in a canine model of atrial flutter (cycle length 120 +/- 4 to 131 +/- 3 ms) caused by reentry. Atrial flutter was induced in 32 anesthetized open chest dogs after placement of an intercaval crush. The excitable gap ranged from 9 +/- 2% to 11 +/- 4% of the basic flutter cycle length. The effective refractory period in the reentrant circuit during atrial flutter was estimated by subtracting the excitable gap from the basic flutter cycle length. Prolongation of flutter cycle length by the test drugs was proportional to the interatrial conduction time (r = 0.87, p less than 0.001). Atrial flutter was terminated by each test drug in all dogs except for flecainide and propafenone in one dog each. E-4031 prolonged the refractory period during atrial flutter to 129 +/- 6 ms, which did not differ significantly from the flutter cycle length immediately before termination (134 +/- 4 ms). The refractory period during atrial flutter after injection of the other drugs was shorter than the flutter cycle length before termination of atrial flutter (for example, flecainide 126 +/- 5 vs. 179 +/- 11 ms, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1991

Onset of induced atrial flutter in the canine pericarditis model.

To test the hypothesis that induced atrial flutter evolves from a transitional rhythm, the onset of 99 episodes of induced atrial flutter (mean cycle length 135 +/- 18 ms) lasting greater than 5 min in 40 dogs with sterile pericarditis was first characterized. In 85 (86%) of the 99 episodes, atrial flutter was preceded by a brief period (mean 1.4 +/- 0.9 s, range 0.4 to 42) of atrial fibrillation. Then, in 11 open chest studies, atrial electrograms were recorded simultaneously from 95 pairs of right atrial electrodes during the onset of 18 episodes of induced atrial flutter (mean cycle length 136 +/- 16 ms). Atrial flutter was induced by a train of eight paced atrial beats, followed by one or two premature atrial beats (7 episodes) or rapid atrial pacing (11 episodes). A short period of atrial fibrillation (mean cycle length 110 +/- 7 ms) induced by atrial pacing activated the right atrium through wave fronts, which produced a localized area of slow conduction. Then unidirectional conduction block of the wave front occurred for one beat in all or a portion of the area of slow conduction. This permitted the unblocked wave front to turn around an area of functional block and return through the area of slow conduction that had developed the unidirectional conduction block, thereby initiating the reentrant circuit. The location of the unidirectional block relative to the direction of the circulating wave fronts determined whether the circus movement was clockwise or counterclockwise. The area of slow conduction and unidirectional conduction block occurred where the wave front crossed perpendicular to the orientation of the atrial muscle fibers, suggesting a role for anisotropic conduction. These areas included the high right atrial portion of the sulcus terminalis (10 episodes), the low right atrial portion of the sulcus terminalis (4 episodes) and the pectinate muscle region (4 episodes). It is concluded that the development of a localized area of slow conduction in the right atrium followed by unidirectional conduction block in this area produced during a short period of atrial fibrillation or rapid atrial pacing is necessary for atrial flutter to occur in this model.

Animals↗

PubMed1991

Antiarrhythmic drugs preferentially produce conduction block at the area of slow conduction in the re-entrant circuit of canine atrial flutter: comparative study of disopyramide, flecainide, and E-4031.

STUDY OBJECTIVE: The aim was to test whether antiarrhythmic drugs preferentially suppressed conduction in the area of slow conduction in the re-entrant circuit. DESIGN: Intravenous disopyramide [n = 8, plasma concentrations: 1.4 (SEM 0.2) micrograms.ml-1], flecainide [n = 8, 0.6(0.1) micrograms.ml-1], and E-4031, a new class III antiarrhythmic drug [n = 8, 5.6(1.0) ng.ml-1], were investigated for their effects on atrial flutter due to re-entry in dogs with intercaval crush. In three dogs, detailed atrial activation sequence during atrial flutter was determined with a hand held bipolar electrode and an epicardial isochronal map was drawn. EXPERIMENTAL MATERIAL: 24 anaesthetised adult mongrel dogs were used. MEASUREMENTS AND MAIN RESULTS: There was an area of slow conduction during atrial flutter in the low right atrium. Atrial flutter was terminated in all dogs except for one treated with flecainide. In 92% of the dogs, conduction block occurred in the low right atrium in which the area of slow conduction was located. Increase in local conduction time was greater in the area of slow conduction than other parts of the atria (percent ratio to the increase in cycle length of atrial flutter: 63% with disopyramide, 52% with flecainide, and 99% with E-4031). CONCLUSION: These data suggested antiarrhythmic drugs preferentially suppressed conduction at the area of slow conduction in the re-entrant circuit leading to termination of atrial flutter in this canine model, irrespective of electrophysiological effects of antiarrhythmic drugs.

Animals↗

PubMed1991

Effects of pentisomide and E-4031 on canine atrial flutter due to reentry: a comparative study with disopyramide and propafenone.

Effects of new antiarrhythmic drugs, pentisomide [3.5 +/- 0.5 mg/kg intravenously (i.v.) n = 8], and E-4031 (5.6 +/- 1.0 micrograms/kg, n = 8), a class III drug, on atrial flutter (AF) caused by reentry were compared with those of disopyramide (1.6 +/- 0.2 mg/kg, n = 8) and propafenone (2.2 +/- 0.2 mg/kg, n = 8). AF was induced with burst atrial pacing after we made an intercaval crush in anesthetized, open-chest dogs. Termination of AF did not differ among test drugs (8 of 8 with disopyramide, 7 of 8 with propafenone, 6 of 8 with pentisomide, and 8 of 8 with E-4031). Cycle length (CL) of AF was prolonged more with propafenone (57 +/- 10%) and pentisomide (41 +/- 5%) than with E-4031 (12 +/- 3%, p less than 0.05). This was also true for increase in interatrial conduction time determined at a pacing CL of 150 ms. Increase in atrial effective refractory period (ERP) determined at a basic pacing CL of 300 ms did not differ among test drugs. Changes in CL of AF correlated significantly with those in interatrial conduction time (r = 0.84, p less than 0.001), but not with those of ERP (r = 0.10, NS). Reinitiation of AF was significantly greater in propafenone (7 of 7) and pentisomide (5 of 6) groups than in disopyramide (1 of 8) and E-4031 (0 of 8) groups (p less than 0.001). Pentisomide and E-4031 were effective in terminating canine AF due to reentry, as were disopyramide and propafenone. Reinitiation of AF was greater in dogs treated with antiarrhythmic drugs that had more prominent effects on conduction time than on ERP.

Animals↗

PubMed1991

Multiplexing studies of effects of rapid atrial pacing on the area of slow conduction during atrial flutter in canine pericarditis model.

BACKGROUND: We report that rapid atrial pacing interrupts atrial flutter when the orthodromic wave front from the pacing impulse is blocked in an area of slow conduction in the reentry circuit. To characterize the area of slow conduction during atrial flutter and rapid pacing, we studied 11 episodes of induced atrial flutter, mean cycle length 157 +/- 20 msec, in eight dogs with sterile pericarditis. METHODS AND RESULTS: Atrial electrograms were recorded simultaneously from 95 pairs of right atrial electrodes during the interruption of atrial flutter by rapid atrial pacing, mean cycle length 139 +/- 21 msec. Areas of slow conduction during atrial flutter were demonstrated at one to three sites in the reentry circuit. After rapid pacing captured the reentry circuit, one area of slow conduction either disappeared (10 episodes) or the degree of slow conduction in an area of slow conduction decreased (one episode). Both changes were in association with activation of the region by a wave front from the pacing impulse that arrived from a direction different than that during the induced atrial flutter. Interruption of atrial flutter during rapid pacing occurred when the orthodromic wave front from the pacing impulse blocked in an area of slow conduction that had either newly evolved during rapid pacing (seven episodes) or that was previously present (four episodes). CONCLUSIONS: Areas of slow conduction present during atrial flutter and rapid pacing of atrial flutter are functional and depend on both the atrial rate and the direction of the circulating wave fronts. Interruption of atrial flutter by rapid pacing results from block of the orthodromic wave front of the pacing impulse in an area of slow conduction in the reentry circuit.

Animals↗

PubMed1990

Effects of a thromboxane A2 synthetase inhibitor on ventricular fibrillation threshold during coronary artery occlusion and reperfusion.

The effects of a new thromboxane A2 synthetase inhibitor (DP-1904) on electrical stability of the heart were tested in anesthetized, open chest dogs. The incidence of spontaneous ventricular arrhythmias, ventricular refractory period and ventricular fibrillation threshold (VFT) during ligation of the left anterior descending coronary artery (LAD) for 180 min and after reperfusion were measured as indices of stability. Ventricular fibrillation and ventricular tachycardia occurred spontaneously after ligation of LAD in 56% of 9 control dogs and 29% of 7 dogs which received intravenous DP-1904 (100 mg) before ligation of LAD (n.s.). In the control group, the ventricular refractory period decreased in the ischemic region; consequently, the difference in refractory period duration between the ischemic and non-ischemic regions (i.e., dispersion) increased 30 min after coronary ligation (7 +/- 9 ms vs 32 +/- 17 ms, p less than 0.05). The dispersion at 30 min after coronary ligation, though, was not affected in the DP-1904 treated group (2 +/- 4 ms vs 10 +/- 9 ms, n.s.). The VFT (determined with pulse trains) decreased from 28 +/- 5 mA to 15 +/- 11 mA (p less than 0.05) 30 min after coronary ligation in the control group, but was not affected (30 +/- 0 mA vs 27 +/- 4 mA) in the DP-1904 group. The plasma concentration of thromboxane B2 decreased after DP-1904 administration (baseline vs 30 min after coronary ligation: 475 +/- 165 pg/ml vs 165 +/- 74 pg/ml, n = 3, p less than 0.05), while the concentration of 6-keto-prostaglandin F1 alpha increased gradually. In conclusion, DP-1904 prevents a decline in electrical stability in the ischemic region of the canine heart during coronary occlusion.

6-Ketoprostaglandin F1 alpha↗

PubMed1989

Electrophysiological study of young patients with exercise related paroxysms of palpitation: role of atropine and isoprenaline for initiation of supraventricular tachycardia.

Electrophysiological studies were performed in eight patients (four men and four women, mean (SD) age 24 (5) years with paroxysmal attacks of palpitation during or immediately after exercise. Five patients were competitive athletes at college. In two patients spontaneous supraventricular tachycardia during exercise was recorded by ambulatory electrocardiographic monitoring and in another it was induced by treadmill exercise testing. Two had dual atrioventricular nodal pathways, three had manifest atrioventricular accessory pathways, and three had concealed atrioventricular pathways. Programmed stimulation induced sustained supraventricular tachycardia in six patients--in two after intravenous injection of atropine sulphate (1 mg) and in four during infusion of isoprenaline (0.01 microgram/kg/min). In one patient, non-sustained atrioventricular nodal reentrant tachycardia was induced during isoprenaline infusion. In the remaining patient, who had dual atrioventricular nodal pathways, tachycardia was not inducible. AH block prevented maintenance of reentry in five patients. In five patients shortening of the effective refractory period of the atrioventricular node with atropine (one patient) and isoprenaline (four patients) caused sustained supraventricular tachycardia. The present study indicates that treatment with atropine and isoprenaline may be an important factor in the initiation of supraventricular tachycardia in patients with exercise related paroxysms of palpitation.

Adult↗

PubMed1989

Effects of antiarrhythmic drugs on the repetitive extrasystole threshold and the ventricular fibrillation threshold.

The effects of class 1 antiarrhythmic drugs on the repetitive extrasystole threshold (RET) and the ventricular fibrillation threshold (VFT) were studied in 32 anesthetized dogs with localized transmural necrosis. All four drugs significantly increased VFT. Although lidocaine and mexiletine increased RET, procainamide and disopyramide did not. We conclude that class 1b antiarrhythmic agents prevent ventricular fibrillation by suppressing the initiation of reentry, and that class 1a drugs decrease the vulnerability by preventing the reentrant repetitive excitation from degenerating into chaotic multiple reentries.

Animals↗

PubMed1989

Improved technique of tubeless cutaneous ureterostomy and results of permanent urinary diversion.

An improved technique of tubeless cutaneous ureterostomy through a single stoma was devised by modifing the traditional cutaneous ureterostomy. Using this method, urinary diversions were performed on 12 cases with malignancies: 6 had radical cystectomy and the other 6 had pelvic exenteration. Normal bilateral ureters were observed in 11 cases in preoperative intravenous pyelography. Stomal stenosis was found in 1 case (8.3%) requiring operative stomal revision. Generally satisfactory results were obtained. This method could lower the incidence of complications. A long-term follow-up is needed, but 2 cases who have survived for more than 4 years since the operation have shown excellent results. It was thought that it would be difficult to perform tubeless cutaneous ureterostomy on normal-sized ureters, but our clinical results indicate that this method may be able to provide permanent urinary diversion.

Adult↗

PubMed1989

[Study on fatigue toughness of dental materials. 1. Compressive strength on various luting cements and composite resin cores].

In this study, we investigated compressive strength of various luting cements and composite resin cores in both dry and wet condition, and then influences of repeating load on compressive strength in wet condition of distilled water at 37 degrees C. As frequency of repeating load increased, compressive strength of all materials decreased. It means that the repeated load cycling test used in this study is adequate for evaluating durability of various dental materials. The results were as follows: 1. In the condition of no loading in both dry and wet condition, resin cement indicated the highest compressive strength of all cements examined and was followed by glass ionomer cement, zinc phosphate cement and polycarboxylate cement. Glass ionomer cement was notably influenced in wet condition. 2. After 10,000 cycles of loading in wet condition, resin cement indicated the highest compressive strength again and was followed by glass ionomer cement, polycarboxylate cement and zinc phosphate cement. In particular, compressive strength of zinc phosphate cement decreased remarkably. 3. In the condition of no loading, visible light-cured composite resin core was superior to chemical one. Visible light one was notably influenced in wet condition. 4. After 10,000 cycles of loading, visible light-cured composite resin core was superior to chemical one.

Composite Resins↗