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T Shibutani

Publications and source records attributed to T Shibutani.

At least 37 records · Page 2Linked to original sources
PubMed1997

Experimentally induced periodontitis in beagle dogs causes rapid increases in osteoclastic resorption of alveolar bone.

This study was undertaken to observe osteoclast differentiation related to inflammatory progression in aggressive periodontitis induced in beagle dogs by ligature of the gingival sulcus. To monitor osteoclastic activity, we used histochemical methods (staining for tartrate-resistant acid phosphatase [TRAP]) to visualize osteoclasts and their TRAP-positive precursors and biochemical methods (ELISA assay of pyridinium crosslinks) to detect bone matrix degradation products in gingival crevicular fluid (GCF), serum, and urine. For histochemical study, tissue specimens were prepared from 3 adult female beagle dogs induced with experimental periodontitis by silk ligature placement below the gingival margin of mandibular molars ligated for 3, 7, and 21 days. For biochemical study for pyridinoline measurement, the 24 mandibular molars of 4 male beagle dogs were ligated. GCF, urine, and serum were collected at day 0 and at 3, 7, 14, and 21 days after ligation. In the early inflammatory phase of ligature-induced periodontitis (day 3), TRAP+ mononuclear and TRAP+ multinucleated cells were present in the gingival connective tissue, and active bone-resorbing cells were found in excavated lacunae at the alveolar crest, but osteoclasts were not infiltrating the periodontal ligament during this early phase. During later stages of the inflammatory process (7 and 21 days), osteoclasts appeared at both the gingival and ligament side of the alveolar bone. Osteoclastic bone resorption appeared to be more severe on the bone surface at the gingival side than on the bone surface of the periodontal ligament side. Measurement of pyridinoline significantly increased in GCF and urine 3 days after ligation. The results suggested that bone at the crest of the alveolar bone is rapidly resorbed within 3 days of inducing experimental periodontitis.

Acid Phosphatase↗
PubMed1997

[Long-term prognosis in patients with exercise-induced ST-segment elevation after myocardial infarction].

The present study investigated whether the exercise-induced ST-segment elevation can predict the prognosis for patients with myocardial infarction. Among 529 patients with myocardial infarction, 411 underwent treadmill exercise testing about 5 weeks after the onset. All patients were followed up (mean [+/-SD] 54 +/- 41 months) to compare the incidence of cardiac events. One hundred and eighteen patients (22%) could not perform the exercise test due to cardiac or noncardiac limitation. Ineligibility for exercise test was most useful for risk stratification. Multivariate analysis showed that elimination from the stress test with cardiac limitation was the most significant predictor for cardiac death. Excluding the 16 patients with bundle branch block, the 395 patients were classified into four groups of ST-segment elevation (107 cases, 27%), ST-segment elevation combined with depression (22 cases, 6%), ST-segment depression (106 cases, 27%), ST-segment unchanged (160 cases, 40%). Among the various stress test abnormalities, only low exercise duration was a predictor for cardiac death. ST-depression and ST-elevation combined with depression were independent risk predictors for all cardiac events. Most patients with ST-elevation had single-vessel disease with excellent exercise capacity and low incidence of cardiac events. ST-segment elevation during exercise 5 weeks after myocardial infarction is not associated with a poor prognosis.

Aged↗
PubMed1997

[Aortic valve insufficiency caused by nonpenetrating chest trauma difficult to distinguish from infective endocarditis with transesophageal echocardiography: a case report].

A 58-year-old man was involved in an automobile accident and suffered remittent fever, leukocytosis and high C-reactive protein level. He developed a diastolic murmur 2 months after the accident. Transesophageal echocardiography showed severe aortic regurgitation with a vegetation-like echo image attached to the right coronary cusp leaflet, suggesting infective endocarditis. Intensive medical treatment for 11 months did not improve the vegetation-like echo-image, so aortic valve replacement was performed. Disruption of the right coronary cusp leaflet was confirmed surgically. Prolapse had occurred as a result of disruption during diastole. The vegetation-like echo-image was considered to be the tip of this leaflet.

Aortic Valve Insufficiency↗
PubMed1996

Role of reactive oxygen intermediates in cytomegalovirus gene expression and in the response of human smooth muscle cells to viral infection.

Because cytomegalovirus (CMV) may contribute to restenosis and atherosclerosis and because smooth muscle cells (SMCs) are involved in these disease processes, we examined CMV-SMC interactions. Using confocal microscopy to identify a redox-sensitive fluorescent marker, we found that CMV infection of SMCs generates intracellular reactive oxygen intermediates (ROIs). CMV also activated nuclear factor kappa B (NF kappa B), a cellular transcription factor, as demonstrated by increased NF kappa B binding to DNA (electrophoretic mobility shift assay). Antioxidants inhibited activation, suggesting a role of ROIs in CMV-induced NF kappa B activation. By using antioxidants to assess the role of ROIs in modulating virally mediated effects, we also found that CMV-induced ROIs (1) are critical to the transactivation of the viral major immediate promoter (MIEP) by its immediate-early protein IE72 (determined by cotransfection of an IE72 expression vector and a reporter gene downstream from the MIEP) and (2) are necessary for IE72 expression (determined by immunocytochemistry) and viral replication (determined by viral titer assay on indicator cells) following CMV infection of SMCs. Because ROIs, through activation of NF kappa B, can also induce expression of cellular genes involved in immune and inflammatory responses, the ROI response to CMV infection may also represent a parallel survival mechanism that has evolved in the host cell to protect against viral infection. We conclude that CMV induces intracellular ROI generation within minutes after infection of SMCs and then uses these ROIs to facilitate its own gene expression and replication. Conversely, antioxidants inhibit CMV immediate-early gene expression and viral replication.

Animals↗
PubMed1996

The interaction between pindolol and epinephrine contained in local anesthetic solution to the left ventricular diastolic filling velocity in normal subjects.

To evaluate the interaction between the nonselective beta-blocker, pindolol, and epinephrine contained in a local anesthetic solution, the left ventricular diastolic filling velocity was examined with pulsed Doppler echocardiography. Arterial blood pressure (BP), the R-R interval on the electrocardiogram (RR), and Doppler echo-cardiographic measurements were recorded in seven healthy volunteers after 45 micrograms of epinephrine contained in lidocaine (L-E) was injected in the maxilla after pretreatment with 5 mg of pindolol. The administration of L-E caused the elevation of BP and an increase in RR interval. Peak early (E) and peak atrial (A) filling velocities decreased, whereas isovolumic relaxation time (IVRT) and diastolic filling period (DFP) were prolonged. Although the ratio of E to A (E/A) remained unchanged, E/A/DFP was reduced. In contrast, when L-E was given without pindolol pretreatment, RR interval was shortened and BP was unchanged. The increase of both E and A velocities and the shortening of both IVRT and DFP were observed. E/A remained unchanged but E/A/DFP was increased. These results suggested that L-E caused opposite effects on the left ventricular filling velocity in the presence or absence of pindolol. We conclude that epinephrine activates the left ventricular relaxation rate but impairs it in the presence of pindolol.

Adrenergic beta-Antagonists↗
PubMed1996

Anesthetic considerations of two sisters with Beckwith-Wiedemann syndrome.

Anesthetic considerations of 21-mo-old and 4-yr-old sisters with Beckwith-Wiedemann syndrome during surgical repair of cleft palate and reduction of macroglossia are presented and discussed. This syndrome is characterized by exomphalos, macroglossia, gigantism, hypoglycemia in infancy, and many other clinical features. This syndrome is also known as exomphalos, macroglossia, and gigantism (EMG) syndrome. Principal problems associated with anesthetic management in this syndrome are hypoglycemia and macroglossia. Careful intraoperative plasma glucose monitoring is particularly important to prevent the neurologic sequelae of unrecognized hypoglycemia. It is expected that airway management would be complicated by the macroglossia, which might cause difficult bag/mask ventilation and endotracheal intubation following the induction of anesthesia and muscle paralysis, so preparations for airway difficulty (e.g., awake vocal cord inspection) should be considered before induction. A nasopharyngeal airway is useful in relieving postoperative airway obstruction.

Airway Obstruction↗
PubMed1996

The effects of the hypothalamus on hemodynamic changes elicited by vagal nerve stimulation.

To investigate the means by which neurogenic shock or syncope occur in dentistry, we determined the hemodynamic response to the activation of vagal tone in cats while they were under emotional stress. The hypothalamus and the vagal nerve were electrically stimulated to produce emotional stress and to activate vagal tone, respectively. Hemodynamic changes were recorded during vagal stimulation (Va group) and during vagal stimulation preceded by hypothalamic stimulation (AH + Va group). Although blood pressure decreased in both groups, the degree of hypotensive response in the AH + Va group was greater than the response in the Va group. Total peripheral resistance (TPR) was reduced in the AH + Va group but was increased in the Va group. The blood flow to the skeletal muscles in the AH + Va group was greater than that of the Va group. Reduced TPR, which could be due to vasodilation in the skeletal muscles, was the cause of intensified hypotension in the AH + Va group. Clearly, the hypotension produced by vagal stimulation was worsened when it was preceded by hypothalamic stimulation; this occurrence could be related to the tendency of blood to flow to the skeletal muscles.

Analysis of Variance↗
PubMed1995

Effects of chronic treatment with carvedilol on abnormalities of endothelium-dependent relaxation and structure of endothelium in resistance arteries of SHRSP.

1. This study investigated the effects of chronic treatment with carvedilol, a beta-blocking agent with an alpha-blocking activity, on blood pressure, endothelium-dependent relaxation and the endothelial structure of the mesenteric resistance artery in stroke-prone spontaneously hypertensive rats (SHRSP). 2. Chronic treatment with carvedilol at a dose range of 30-120 mg/kg per day lowered systolic blood pressure of SHRSP from 234.9 +/- 3.3 to 198.7 +/- 3.1 mmHg at 16 weeks of age. 3. Acetylcholine-induced endothelium-dependent relaxation was impaired in the mesenteric artery from SHRSP and high concentrations of acetylcholine produced contractions. The impairment of the relaxation was abolished in the presence of indomethacin. Carvedilol treatment improved the impairment in the preparation from SHRSP. The structural abnormality of endothelium was observed in the preparation from SHRSP. The abnormality could be prevented by the antihypertensive treatment. 4. These results suggest that the impairment of endothelium-dependent relaxation in the preparation from SHRSP is due to the corelease of an endothelium-derived contracting factor which is considered to be a product of cyclo-oxygenase pathway of arachidonic acid cascade and that the impairment can be prevented by the antihypertensive treatment with carvedilol.

Acetylcholine↗
PubMed1995

Beta-adrenergic stimulation induces ST-segment elevation in dogs with healing myocardial infarction.

There is controversy with regard to the mechanism of the exercise-induced ST-segment elevation in myocardial infarction. The purpose of the present study was to investigate the mechanism of ST-segment elevation through pharmacologic interventions. Transmural anterior myocardial infarction was produced by gelatin sponge embolization of the left anterior descending artery in seven closed-chest dogs. One and four weeks after myocardial infarction, the dogs underwent the following three interventions: right atrial pacing, norepinephrine infusion (3.75, 7.5, and 15 micrograms/min) with the pacing, and methoxamine injection (2.5 and 5.0 mg) with the pacing. All dogs had transmural infarction with a mean infarct size of 12.0 +/- 4.2% of the left ventricular weight. Right atrial pacing did not induce significant changes in ST-segment. Norepinephrine induced a marked elevation of ST-segment at leads V1 to V4, while methoxamine did not. Norepinephrine induced a significant increase in left ventricular ejection fraction, while methoxamine produced a marked decrease in the ejection fraction and an increase in ventricular volume. The mean percent radial shortening of the non-infarct ventricular wall showed a significant increase with norepinephrine, but a decrease with methoxamine. In conclusion, myocardial ischemia and wall motion abnormality may be excluded as possible mechanisms of ST-segment elevation and an enhanced beta-adrenergic mechanism in the non-infarct myocardium is suggested to be responsible for ST-segment elevation.

Adrenergic beta-Agonists↗
PubMed1995

Failure of aspirin and diltiazem to prevent the formation of acute coronary thrombi in dogs.

The aim of the present study was to determine the efficacy of aspirin and diltiazem in preventing the formation of coronary thrombi in dogs. Canine coronary thrombi were produced by inserting a small catheter filled with collagen powder into the endothelial-injured, partially occluded left anterior descending coronary artery. Neither aspirin (bolus of 30 mg/kg, followed by 100 mg/kg/h by infusion), nor diltiazem (0.1 mg/kg, followed by 0.3 mg/kg/h by infusion) prevented the formation of coronary thrombi. The mortality in aspirin group was significantly higher than that in control and diltiazem groups. These results indicate that aspirin and diltiazem do not inhibit thrombus formation in the canine model of coronary thrombosis.

Animals↗
PubMed1995

An echocardiographic study of interactions between pindolol and epinephrine contained in a local anesthetic solution.

An increasing number of dental patients are taking beta-adrenergic blockers for the treatment of hypertension or angina pectoris. If epinephrine-containing local anesthetics are administered to such patients, interactions between epinephrine and the beta-blocking agent may induce cardiovascular complications. We assessed in volunteers the effects of intraoral injection with 2% lidocaine containing 1:80,000 epinephrine (L-E) on cardiac function after pretreatment with the beta-blocking agent pindolol. M-Mode echocardiography was used for the assessment. The injection of L-E after administration of pindolol did not alter cardiac preload, whereas it reduced the stroke volume, due to an increase in afterload and a decrease in myocardial contractility. Reductions in stroke volume and heart rate led to a decrease in cardiac output. Because total peripheral vascular resistance increased markedly, blood pressure was elevated despite the reduced cardiac output. These results suggest that cardiac function of dental patients on beta-blocker therapy can be adversely affected by epinephrine-containing local anesthetics. Therefore, when such an anesthetic solution has to be used in patients on beta-blocker therapy, careful systemic monitoring is needed.

Adrenergic beta-Antagonists↗
PubMed1995

The incidence of arrhythmias during induction of general anesthesia.

In this study, our induction methods of endotracheal anesthesia was evaluated with reference to electrocardiogram, hemodynamic status and arterial blood gas analysis on 153 patients. From the beginning of induction, electrocardiogram was recorded continuously to the completion of intubation. The blood pressure and heart rate were also measured. Arterial blood samples were taken at 40 seconds of apneic period after the mask was removed from the patient's face (CONT group), at 40 seconds of apnea with intratracheal spray (LIDO group), and after intubation following intratracheal spray (INT group). In the electrocardiographic survey, arrhythmias during intubation were rare (1/113, 0.9%). PaCO2 values in INT group showed a significant elevation (+ 14.0 mmHg; p < 0.01) compared to these in CONT group. As a result of careful and gentle induction techniques, the incidence of arrhythmias during intubation was very low. However, an elevation of PaCO2 was not avoidable, even in smooth and successful intubation. In conclusion, the importance of more adequate ventilation coupled with skillful intubation in a shorter period to avoid hypercapnia and arrhythmias is appreciated again in the endotracheal anesthesia for the maxillofacial surgical patients with anatomical airway problems.

Adult↗
PubMed1994

Inhibitory effect of perindopril, a novel angiotensin-converting enzyme inhibitor, on neointima formation after balloon injury in rats and cholesterol-fed rabbits.

We investigated the effect of perindopril, a novel angiotensin-converting enzyme (ACE) inhibitor, on neointima formation in vessel walls after balloon injury in rats (carotid artery) and cholesterol-fed rabbits (thoracic aorta). Continuous treatment with perindopril significantly reduced neointima formation in both species, as compared with the control group: intima/media (I/M) ratio (rats -62%; p < 0.001; rabbits -25%, p < 0.05); neointima area (rats -65%, p < 0.01; rabbits -24%, p < 0.05). These changes involved reduction of intimal smooth muscle cells (SMC) in rats and of macrophages in rabbits. Furthermore, perindopril also significantly decreased ACE activity in both aortic tissue and serum [11.38 +/- 0.87 vs. 34.93 +/- 6.44 pmol His-Leu (HL)/mg/min (p < 0.01) and 2.79 +/- 0.28 vs. 38.50 +/- 5.41 pmol HL/mg/min (p < 0.001), respectively], aortic contraction evoked by angiotensin I (AI) and mean blood pressure (BP, 84.9 +/- 3.5 vs. 109.3 +/- 3.8 mm Hg, p < 0.001) as compared with control values. These results indicate that perindopril may reduce neointima formation by suppressing the aortic renin-angiotensin system (RAS). These findings indicate that perindopril may be capable of preventing restenotic lesions after angioplasty in humans [corrected].

Angioplasty, Balloon↗
PubMed1994

Exercise-induced ST-segment elevation and hemodynamic responses one month after myocardial infarction.

Changes in hemodynamics and plasma norepinephrine levels during supine bicycle exercise after myocardial infarction were measured to investigate the mechanism of exercise-induced ST-segment elevation. Seventy-eight patients were divided into groups which showed either ST elevation (STE), ST depression (STD), or no ST changes (STU). Most of the STE group had anterior myocardial infarction (90.6%) and single-vessel disease (76.7%). The STE group achieved a significantly higher workload (119.5 +/- 4.0 watts, mean +/- SEM) than the STD group (82.3 +/- 2.8, p < 0.01). Heart rate and cardiac output at maximal workload were significantly higher in the STE group (136.6 +/- 3.4 beats/min, 7.44 +/- 0.28 l/min/m2) than in the STD group (110.0 +/- 3.9, 4.83 +/- 0.36, p < 0.01). Pulmonary artery pressures were less elevated in STE than STD patients. Plasma norepinephrine levels increased significantly at maximal workload in STE patients, as compared to the other groups. In conclusion, the STE group achieved a higher exercise level associated with augmented sympathetic activity, which may be a possible mechanism of exercise-induced ST elevation after myocardial infarction.

Cardiac Output↗
PubMed1993

Effect of medium pH on osteoclast activity and osteoclast formation in cultures of dispersed rabbit osteoclasts.

We investigated the effect of medium pH on activity of isolated osteoclasts and have also looked at the possibility that medium pH affects osteoclast numbers during culture. Osteoclast-containing cell suspensions prepared from neonatal rabbits were cultured on bovine bone slices at pH 6.5, 7.0, or 7.5. After 24 or 48 h of culture, the cells and bone slices were fixed and stained for tartrate-resistant acid phosphatase (TRAP). After counting the osteoclasts, the cells were removed and the resorption lacunae stained by immunostaining using anticollagen type I antibody and then quantitated. We found that the resorptive activity of isolated rabbit osteoclasts was sharply increased at pH 6.5-7. Osteoclast differentiation and proliferation, on the other hand, were optimal at pH 7.0-7.5 but decreased at pH 6.5. The results thus imply that pH regulation of the bone surface environment can dramatically alter both the number of osteoclasts and their resorptive activity.

Animals↗
PubMed1993

Nucleic acids induce the formation of a carcinogen, 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) in a model system.

Effects of nucleic acids on the formation of 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) were studied in a model system. When a mixture of a certain amount of DNA or RNA, creatinine (1 mmol) and phenylalanine (1 mmol) in 10 ml of 50 mM phosphate buffer, pH 7.4, was heated at 60 degrees C for 4 weeks in a screw-capped vial, PhIP was produced, and the yield of PhIP was dependent on the heating time as well as the dose of nucleic acid added to the mixture. However, PhIP was not detectable in the mixtures without the presence of nucleic acids. Both deoxyribonucleotides and ribonucleotides tested induced the formation of PhIP under the presence of phenylalanine and creatinine, although bases of nucleic acids such as adenine and guanine did not induce PhIP formation. Moreover, we confirmed that 2-deoxy-D-ribose as well as D-ribose induced the formation of PhIP in the presence of creatinine and phenylalanine. These results indicate that nucleic acids can induce the formation of PhIP in the presence of creatinine and phenylalanine in the model system. Our data also suggest that pentose in nucleic acids may participate in PhIP forming reactions.

Carcinogens↗
PubMed1993

Combined effect of the 5-HT2 receptor antagonist DV-7028 and aspirin or heparin on coronary cyclic flow reductions in dogs.

OBJECTIVE: The aim was to study the combined effect of DV-7028, a selective 5-hydroxytryptamine2 receptor antagonist, and aspirin or heparin on cyclic flow reductions in the canine coronary artery. METHODS: Anaesthetised open chest beagle dogs under artificial respiration were used. Cyclic flow reductions were induced by partial occlusion of the left anterior descending coronary artery at the site of endothelial injury. After induction of cyclic flow reductions, test drugs were given to the animals intravenously. RESULTS: DV-7028 (0.1 mg.kg-1) reduced the frequency of cyclic flow reductions by 77% and improved the nadir of coronary blood flow velocity that indicated the severity of cyclic flow reductions. Also, aspirin (1 or 3 mg.kg-1) or heparin (200 U.kg-1) attenuated the cyclic flow reductions. In experiments with drug combinations, DV-7028 was given to animals that had already received aspirin (1 mg.kg-1) or heparin (200 U.kg-1). DV-7028 (0.1 mg.kg-1) completely abolished the cyclic flow reductions remaining after aspirin treatment in three of four animals. Heparin inhibited the cyclic flow reductions in one of five animals and the addition of DV-7028 abolished the remaining cyclic flow reductions in the other four animals. After combined injection of DV-7028 with aspirin or heparin, the coronary blood flow with cyclical reductions returned to the baseline. CONCLUSIONS: The 5-HT2 receptor antagonist DV-7028 can inhibit the cyclic flow reductions that are resistant to aspirin or heparin. The combined regimen of DV-7028 and aspirin or heparin in treatment of acute coronary stenosis is more effective than that of aspirin or heparin alone.

Animals↗