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T Kamibayashi

Publications and source records attributed to T Kamibayashi.

32 records · Page 2Linked to original sources
PubMed1993

Effect of local anaesthetics on the stimulus-secretion coupling in bovine adrenal chromaffin cells.

This study was carried out to determine the relative potencies of local anesthetics to inhibit the cholinergic synaptic transmission using cultured bovine adrenal chromaffin cells, and to clarify if the inhibitory action would correlate with biophysical and pharmacological properties. Local anaesthetics (bupivacaine, etidocaine, tetracaine, lignocaine and procaine; 0.02-2 mM) inhibited carbachol-induced catecholamine release from the cells in a concentration-dependent manner. This inhibition was completely reversible. IC50 (concentration of 50% inhibition) of each anaesthetic showed no correlation with the lipid solubility. The local anaesthetics showed greater inhibitory potency at a higher extracellular pH. The results suggest that clinically relevant concentrations of local anaesthetics inhibit the stimulus-secretion coupling in the chromaffin cells. The un-ionized based form plays a major role, and the inhibitory potency does not depend on the lipid solubility of the anaesthetics.

Adrenal Medulla↗
PubMed1993

Adrenoceptor mechanism involved in thiopental-epinephrine-induced arrhythmias in dogs.

The authors investigated the role of alpha 1- and beta-adrenoceptors on induction of ventricular arrhythmias during thiopental anesthesia in dogs and compared with that during halothane anesthesia. Throughout this study, arrhythmogenic threshold of epinephrine during thiopental anesthesia was designed to be comparable with that during halothane anesthesia. Phenylephrine, an alpha 1-agonist, and isoproterenol, a beta-agonist, consistently failed to provoke arrhythmias during thiopental or halothane anesthesia. The interaction between phenylephrine and isoproterenol in inducing arrhythmias was synergistic and additive during halothane and thiopental anesthesia, respectively, indicating that adrenoceptor mechanism in thiopental-epinephrine arrhythmias is different from that in halothane-epinephrine arrhythmias. During thiopental anesthesia, incidence of arrhythmias with blood pressure elevation by epinephrine, phenylephrine, or angiotensin II was not different, and increasing heart rate by electrical pacing did not replace isoproterenol in the arrhythmogenic interaction between isoproterenol and phenylephrine. The results indicate that blood pressure elevation due to the combined inotropic action of alpha 1- and beta-adrenoceptor agonists is a critical factor in the genesis of thiopental-epinephrine arrhythmias.

Adrenergic alpha-Agonists↗
PubMed1993

Quantitative analysis of pulmonary clearance of exogenous dopamine after cardiopulmonary bypass in humans.

The contribution of the lung to the clearance of exogenous dopamine after cardiopulmonary bypass (CPB) was analyzed quantitatively in humans and compared with the contribution of the lung before CPB. The pulmonary and arterial plasma concentration of dopamine and the pulmonary plasma flow were measured simultaneously during infusion of dopamine. Contribution of the pulmonary circulation was defined as the ratio between clearance through the pulmonary circulation and the total plasma clearance of dopamine. The calculated contribution values after CPB were 12.0, 10.7, 11.4, 16.2, and 16.7% at the doses of 3.0, 4.0, 5.0, 6.0, and 7.0 micrograms.kg-1.min-1, respectively. Those values before CPB were 15.6% and 17.4% at the doses of 1.0 and 2.0 micrograms.kg-1.min-1, respectively. The comparison of the values before and after CPB did not achieve statistical significance. Furthermore, there were no significant correlations between the pulmonary clearance after CPB and mean pulmonary arterial pressure, pulmonary vascular resistance, or CPB time. The results suggest that the pulmonary clearance mechanism for dopamine after CPB is maintained as effectively as that before CPB and is not influenced by pulmonary hypertension or CPB time.

Adult↗
PubMed1992

Selective beta 1 and beta 2 adrenoceptor blockade on epinephrine-induced arrhythmias in halothane anaesthetized dogs.

Beta 2 as well as beta 1 adrenoceptors have been recognized in the heart of vertebrates. They mediate a positive chronotropic action of catecholamines. We compared the effect of selective beta 1 and beta 2 adrenoceptor antagonists on the genesis of halothane-epinephrine arrhythmias in dogs. The arrhythmogenic dose (AD) of epinephrine was increased in the presence of l-metoprolol, a selective beta 1 antagonist (8.40 +/- 1.13 micrograms.kg-1 x min-1; mean +/- SEM), compared with control value (2.62 +/- 0.56) (P < 0.05). In contrast, ICI-118,551, a selective beta 2 antagonist, did not change the AD (2.36 +/- 0.43). Adding ICI-118,551 to l-metoprolol did not affect the AD of epinephrine in the presence of l-metoprolol alone (6.34 +/- 0.74 vs 8.40 +/- 1.13). These results suggest that selective beta 1 blockade is effective in preventing halothane-epinephrine arrhythmias, but selective beta 2 blockade is not.

Adrenergic beta-Antagonists↗
PubMed1992

[A hypertensive crisis during surgery in a patient with neuroblastoma].

Neuroblastoma is the most common solid tumour in infancy and childhood. The tumour usually produces large amounts of catecholamines. Few patients with neuroblastoma, however, were reported to have become hypertensive because of catecholamine metabolism within the tumour itself. This is one of the most important differences compared with pheochromocytomas. We experienced a hypertensive crisis accompanied by tachycardia and an increase in the plasma catecholamine concentration during surgery in a patient with neuroblastoma. The plasma catecholamine level was comparable to that of pheochromocytoma. Phentolamine and propranolol were effective to control the hypertension and tachycardia.

Catecholamines↗
PubMed1991

Myocardial epinephrine sensitization with subanesthetic concentrations of halothane in dogs.

The authors investigated myocardial epinephrine sensitization by subanesthetic concentrations of halothane. The dose-response relationship for the action of halothane was examined with etomidate plus varying subanesthetic concentrations of halothane in dogs. The arrhythmogenic threshold of epinephrine was decreased in a dose-dependent manner at end-tidal concentrations of halothane between 0.1 and 0.3%. At end-tidal halothane is greater than 0.3%, and no further reduction of arrhythmogenic threshold of epinephrine occurred. The plasma concentrations of epinephrine producing four or more premature ventricular contractions in 15 s were 201.3 +/- 34.3, 98.1 +/- 13.9, 60.3 +/- 8.63, 57.9 +/- 12.8, 54.5 +/- 8.61, and 53.9 +/- 4.86 ng/ml (mean +/- SEM), at 0, 0.1, 0.3, 0.5, 1.0, and 1.5% of halothane at end-tidal concentrations, respectively. The results suggest that in the presence of etomidate, halothane produces myocardial sensitization to epinephrine at subanesthetic concentrations as low as 0.1%. Increasing halothane to 0.3% produces a further reduction in the arrhythmogenic dose of epinephrine.

Anesthesia↗
PubMed1991

Dexmedetomidine prevents epinephrine-induced arrhythmias through stimulation of central alpha 2 adrenoceptors in halothane-anesthetized dogs.

Since alpha 2-adrenergic agonists have important effects on the adrenergic system that have recently been applied to the anesthetic setting, we investigated the effect of stimulation of alpha 2 adrenoceptors on epinephrine-induced arrhythmias in halothane-anesthetized dogs. The arrhythmogenic threshold for epinephrine was determined during halothane anesthesia in the presence of dexmedetomidine, a selective alpha 2 agonist, and L-medetomidine, a stereoisomer of medetomidine that lacks alpha 2-agonist activity. Dexmedetomidine increased the arrhythmogenic threshold for epinephrine in a dose-dependent manner during halothane anesthesia. At the highest dose of dexmedetomidine, 0.5 microgram.kg-1.min-1, there was a three-fold increase in both the arrhythmogenic dose of epinephrine and the plasma epinephrine concentration that was reached at this dose. On the other hand, L-medetomidine over the same dose range did not effect the arrhythmogenic dose of epinephrine. Atipamezole, a central alpha 2 antagonist that crossed the blood-brain barrier, blocked the antiarrhythmic action of dexmedetomidine. L-659,066 a peripheral alpha 2 antagonist that does not penetrate the blood-brain barrier, did not affect the antiarrhythmic action of dexmedetomidine. Thus, dexmedetomidine's antiarrhythmic effect on epinephrine-induced arrhythmias during halothane anesthesia appears to be mediated at least in part by stimulation of central alpha 2 adrenoceptors.

Adrenergic alpha-Agonists↗
PubMed1991

Enhancement by propofol of epinephrine-induced arrhythmias in dogs.

Although propofol is a widely used intravenous anesthetic, its effect on epinephrine-induced arrhythmias remains unknown. This study examined the possible interaction between propofol and epinephrine that might affect the induction of ventricular arrhythmias in dogs. The arrhythmogenic threshold of epinephrine was determined during anesthesia with halothane alone, propofol alone, etomidate alone, or etomidate plus varying doses of propofol. The arrhythmogenic dose and the corresponding plasma concentration of epinephrine during propofol anesthesia (blood propofol concentration 18.0 +/- 0.98 micrograms/ml) were 2.52 +/- 0.43 micrograms.kg-1.min-1 and 23.6 +/- 8.5 ng/ml, respectively. During halothane anesthesia (end-tidal 1.3 MAC), they were 2.66 +/- 0.21 micrograms.kg-1.min-1 and 35.7 +/- 1.9 ng/ml, respectively. During etomidate anesthesia, they were 9.67 +/- 1.06 micrograms.kg-1.min-1 and 205 +/- 27.5 ng/ml, respectively. The dose-effect relationship for propofol was examined during etomidate plus propofol anesthesia. Propofol reduced the arrhythmogenic plasma concentration of epinephrine in a concentration-dependent manner: at blood propofol concentrations of 2.33 +/- 0.46, 5.46 +/- 0.71, and 11.2 +/- 0.81 micrograms/ml, the corresponding plasma epinephrine concentrations were 182.6 +/- 52.5, 89.0 +/- 28.8, and 26.6 +/- 6.9 ng/ml, respectively. These results suggest that propofol enhances epinephrine-induced arrhythmias in a dose-dependent manner in dogs.

Anesthesia↗
PubMed1991

Phenytoin prevents epinephrine-induced arrhythmias through central nervous system in halothane-anesthetized dogs.

The authors investigated the effect of phenytoin through the central nervous system on epinephrine-induced arrhythmias in halothane-anesthetized dogs. The arrhythmogenic dose (AD) of epinephrine during halothane anesthesia was determined in the presence of phenytoin (1 mg/kg), vehicle, and saline, which were administered directly into the cisterna magna. Phenytoin increased the AD of epinephrine as compared with vehicle or saline. The cerebrospinal and plasma concentration of phenytoin during the arrhythmias were 23.6 and less than 0.5 micrograms/ml, respectively. There was no significant difference in AD between the vehicle and saline groups. The same dose of phenytoin (1 mg/kg) administered intravenously did not affect the AD of epinephrine, and the plasma concentration of phenytoin during the arrhythmias was 1.2 micrograms/ml. These findings suggested that phenytoin exerts a protective effect against halothane-epinephrine arrhythmias through a central mechanism and that the central nervous system may be involved, at least in part, in the myocardial sensitization by halothane.

Anesthesia↗
PubMed1990

[Experimental study on a mechanical root canal enlargement].

It is difficult for us to enlarge a root canal by using hand-instruments in a molar tooth, so we experimented by using mechanical equipment. We examined the human extracted premolar which we had preserved in physiological saline solution by using a speculative root canal enlarging machine. Then we observed the time and condition of enlarging root canal by X-ray. After slicing off, we examined with our eyes and with an electronic microscope. Afterward, we compared hand-instruments with the enlarging machine. As the results of this experiment; 1. Time by hand filing instruments took three or four times to make a root canal enlargement by a speculative enlarging machine. 2. After enlarging a root canal, we made a root canal filling. Observing them by X-ray and ground specimen, we recognized a good result in the root canal enlargement and in the condition of the root canal filling. 3. Observing the figure by electronic microscope, in the case of using a speculative machine, we found that the slicing aspects of dentin which had been enlarged by root canal were thoroughly smoothed in the center part of the root canal, but it was not smoothed in the root apex region. 4. It had a tendency to remain part of the cutting dentin near the apical area both by using hand cutting instruments and by using a speculative machine.

Bicuspid↗
PubMed1989

[Electron microscopic study on the tissue reaction after root canal filling following artificial periapical lesions--about periapical lesions induced by carrageenin].

Although a number of reports on the formation of periapical lesions have been down, little study on the healing stage of this one is seen. Therefore, the aim of this study was to investigate the changes of the fine structure of the healing stage of the artificial periapical lesions after root canal filling and to make an experimental model for the further screening test of various kinds of medicaments and materials for root canal treatment and root canal filling. In this study, the first mandibular molars of male Wistar strain rats were used. Periapical lesions were induced by 0.5% carrageenin and after three weeks, the root canals of the first molars were filled with gutta-percha points and sealers. Then, the healing stage of the periapical lesion was observed light microscopically, electron-microscopically and enzyme (alkaline phosphatase, ALP, and acid phosphatase, ACP)-histochemically. The results were as follows after the root canal filling with carrageenins: 1. At 1 to 7 days, a great number of neutrophils and histiocytes were observed and expansion of periapical lesions caused by the irritation followed by root canal filling was observed. 2. At 2 to 3 weeks, a great number of leukocytes, histiocytes and fibroblasts were observed in the vicinity of the root apex. 3. At 4 to 5 weeks, a great number of histiocytes and mast cells were observed and granulated tissues of the periapical lesions had a tendency to become fibrosis and new calcified cement increased at the root apex. 4. At 7 to 10 weeks, the fibroblast granulation tissue around the periapical lesions synthesized active collagen fibers and the deposition of new alveolar bone was seen within the resorbed alveolar bone. 5. At 15 to 20 weeks, the periapical lesions could be thought to be healing histopathologically although some of inflammatory cells were seen 20 weeks after treatment. 6. At 10 weeks, strong positive responses of ALP were recognized. At 20 weeks, the general appearance of both the ALP and ACP staining showed almost the same response as that of normal periodontium. 7. As for the prognosis, "over filling" showed better healing than that of "under filling". 8. In the case which the root apex was fractured, inflammation lasted for a long period.

Animals↗