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Biomedical subjects

C Tashiro

Publications and source records attributed to C Tashiro.

At least 73 records · Page 4Linked to original sources
PubMed1989

[Synthesis of 2-oxooctahydroimidazo[1,2-alpha]pyridine-3-spiro-4'-piperidine derivatives possessing antiapomorphine activity].

4'-Carbamoyl-1,4'-bipiperidine 1 was dehydrogenated on Pd-C to give 2-oxo-2,3,5,6,7,8-hexahydroimidazo[1,2-alpha]pyridine-3-spiro-4'-p iperidine 2, which was reduced to 2-oxo-1,2,3,5,6,7,8,8a-octahydroimidazo[1,2-alpha]pyridine-3-spiro -4'- piperidine 3 with NaBH4. The iminodibenzyl and similar derivatives of 2 and 3 were synthesized and evaluated by using antiapomorphine test in mice. The derivatives of 3 had more potent antagonistic activity than those of 2 and the order of potency of 3 was: chloriminodibenzyl greater than chlordibenzocycloheptene greater than iminodibenzyl greater than iminostilbene greater than fluorene. Further chemical modification of the most active chloriminodibenzyl derivative 8, such as the substitution of Cl atom to Br atom, N-methylation on amine moiety, the replacement of imidazopyridine ring to imidazopyrrole ring, did not give any positive effect. Therefore, 8 may have potential usefulness as an antipsychotic drug.

Animals↗
PubMed1989

[Changes in the electroretinogram during enflurane anesthesia].

We have investigated a method of intraoperative monitoring of anesthetic depth using the electroretinogram (ERG). The effects of enflurane on ERG were studied in 12 patients undergoing surgical procedures. Recordings were made at 0%, 0.8%, 1.7% end-tidal enflurane concentrations. There were statistically significant increases in the latencies of the a-waves, b-waves and oscillatory potentials (OP) with increasing concentrations of enflurane. The amplitudes of the a-waves were reduced with increasing concentrations of enflurane, but the amplitudes of the b-waves did not change. The latencies of OP were thought to be the most sensitive indicator of the anesthetic depth among these parameters. To apply this technique to clinical practice, there were many problems to be solved. However, this may be one of useful monitors of anesthetic depth in future.

Adult↗
PubMed1989

[Clinical evaluation of buprenorphine suppositories in postoperative patients--plasma concentrations and effects on the respiratory and circulatory system].

The plasma concentrations of buprenorphine were measured and blood gas analysis was done after administration of buprenorphine suppositories (0.2 and 0.4 mg) or its intramuscular injection (0.2mg) in postoperative patients. The C max for 0.4mg suppositories was comparable to that for 0.2mg injection, whereas the T max for suppositories was as large as about 2 hrs in contrast to 1.5 hrs for 0.2mg injection. The size of AUC was in the following order: 0.4mg suppositories greater than 0.2mg injection greater than 0.2mg suppositories. Neither notable increase in PaCO2 nor decrease in respiration rate was observed after administration of the suppositories, indicating that the formulation will not cause clinically significant respiratory depression. No significant changes were observed in blood pressure or pulse rate. Buprenorphine suppositories are considered to be safe for use in postoperative patients. Percent pain relief in the suppository group was smaller than that in the injection group. This appears to be due to a slower rate of increase in the plasma levels of buprenorphine after administration of suppositories than that after intramuscular injection. Therefore, it seems practical to give this drug to postoperative patients before the start of pain.

Administration, Rectal↗
PubMed1989

[Analgesia and anesthesia induced by subanesthetic concentrations of nitrous oxide].

This study was aimed to determine 1) the changes of the anesthetic and analgesic actions of inhalation of subanesthetic concentration of nitrous oxide, and 2) the possible antagonism by naloxone of these actions. Auditory response time (anesthetic action) and pain threshold (analgesic action) were examined before, during and after inhalation of subanesthetic concentration of nitrous oxide in six normal volunteers who were treated with or without intravenous administration of naloxone 1.4 mg. Analgesic action remained at 30 min after nitrous oxide inhalation, while auditory response time returned to control values. Both anesthetic and analgesic effects were unchanged during 100 min inhalation or administration of naloxone. These results indicate that the acute tolerance to these actions of nitrous oxide will not occur, and that naloxone will not show a significant antagonistic action as is observed with morphine.

Administration, Inhalation↗
PubMed1988

Depression of phase-transition temperature by anesthetics: nonzero solid membrane binding.

The anesthetic-induced depression of the main phase-transition temperature of phospholipid membranes is often analyzed according to the van't Hoff model on the freezing point depression. In this procedure, zero interaction between anesthetics and solid-gel membranes is assumed. Nevertheless, anesthetics bind to solid-gel membranes to a significant degree. It is necessary to analyze the difference in the anesthetic binding between the liquid-crystal and solid-gel membranes to probe the anesthetic action on the lipid membranes. This article describes a theory to estimate the anesthetic binding to each state at the phase-transition temperature. The equations derived here reveal the relation between the partition coefficients of anesthetics and the anesthetic effects on the transition characters: the change in the transition temperature, and the broadening of transition. The theory revealed that the width of transition temperature is determined primarily by the membrane/buffer partition coefficients of anesthetics. Our previous data on the local anesthetic action on the transition temperature of the dipalmitoylphosphatidylcholine vesicle membrane (Ueda, I., Tashiro, C. and Arakawa, K. (1977) Anesthesiology 46, 327-332) are analyzed by this method. The numerical values for the partition of local anesthetics into the liquid-crystal and solid-gel dipalmitoyl-phosphatidylcholine vesicle membranes at the phase-transition temperature are: procaine 8.0 x 10(3) and 4.7 x 10(3), lidocaine, 3.7 x 10(3) and 2.3 x 10(3), bupivacaine 4.1 x 10(4), and 2.6 x 10(4), and tetracaine 7.3 x 10(4) and 4.7 x 10(4), respectively.

1,2-Dipalmitoylphosphatidylcholine↗
PubMed1988

Effects of carboxyhemoglobin on pulse oximetry in humans.

Carboxyhemoglobin (HbCO)-induced reading errors of the Biox 3700 (version J, Ohmeda) pulse oximeter were determined in 6 healthy volunteers rendered hypoxic (Sa(O)(2) from 65-100%) by breathing mixtures of air in nitrogen. The oximeter reading (Sp(O)(2)) before and after cigarette smoking was compared with oxyhemoglobin percentage (%HbO(2)). Mean HbCO levels were; 3.0 +/- 1.0 (SD) % before cigarette smoking and 5.2 +/- 1.7% after smoking, whereas mean methemoglobin was unchanged as 0.5 +/- 0.1%. The correlations of the Sp(O)(2) (y) with %HbO(2) (x) were; y = 1.01x - 0.30 (r = 0.990, n = 21, P < 0.001) when %HbCO was less than 2.5, and y = 1.01x + + 3.21 (r = 0.964, n = 33, P < 0.001) when %HbCO was above 5.0%. The reading error, (Sp(O)(2) - %HbO(2)), could be expressed as a function of %HbCO; 1.06 x %HbCO(2) - 2.49 (r = 0.669, n = 83, P < 0.05). Thus, the Sp(O)(2) is approximately the sum of %HbCO(2) and (%HbCO - 2.5), and overestimates %HbO(2) in the high levels of HbCO. The pulse oximeter should be used with caution in patients with the elevated level of %HbCO.

Journal Article↗
PubMed1988

Synergistic interaction of alpha 1- and beta-adrenoceptor agonists on induction arrhythmias during halothane anesthesia in dogs.

The authors investigated the role of alpha 1- and beta-adrenoceptors on the induction of arrhythmias during halothane anesthesia in the dog. The arrhythmogenic doses (ADs) of various combinations of alpha 1- and beta-adrenoceptor agonists were determined in dogs (N = 105) during halothane anesthesia. Isoproterenol (ISP) and phenylephrine (PHE) administered separately failed to induce arrhythmias in doses up to 4 micrograms/kg and 200 micrograms/kg, respectively. The interaction between ISP and PHE in inducing arrhythmias showed typical hyperbolic isoboles. At a systolic pressure of 140 mmHg, the AD of ISP in the presence of PHE was significantly lower than that in the presence of angiotensin II (ANG II). At a systolic pressure of 150, 160, 170, or 180 mmHg, there was no significant difference between the AD of ISP in the presence of PHE and that in the presence of ANG II. Increasing heart rate by electrical pacing did not replace ISP in the arrhythmogenic interaction between ISP and PHE. The results indicate that both alpha 1- and beta-adrenoceptor agonists are important for producing arrhythmias during halothane anesthesia, and that these agonists synergistically interact on the heart by different mechanisms.

Adrenergic alpha-Agonists↗
PubMed1987

Postoperative paraplegia associated with epidural narcotic administration.

Epidural injections of buprenorphine were given for postoperative pain relief to a patient with pulmonary carcinoma who underwent a right upper lobectomy. Paraplegia occurred postoperatively and the patient's neurological status deteriorated after each injection of epidural narcotic. Laminectomies on the third postoperative day revealed an expanded oxidized cellulose (Oxycel) pledget in the epidural space. Neurologic dysfunction after epidural narcotic administration was caused by the oxidized cellulose which had migrated into the epidural space following use for surgical haemostasis and subsequently expanded with the narcotic solution and blood.

Aged↗
PubMed1986

Electroretinogram as a possible monitor of anesthetic depth.

The effects of volatile anesthetics, i.e., methoxyflurane, halothane and enflurane, on the electroretinogram (ERG) were studied in 15 albino rabbits. The ERG was analyzed in terms of the a-wave, and the first oscillatory component (01) in the b-wave. The 01 peak latency showed a significant dose-related prolongation when anesthetic end-tidal concentrations were in excess of 0.8 minimum alveolar concentration (MAC). One MAC, a measure of anesthetic potency, is the end-tidal concentration of an anesthetic at 1 atmosphere that induces immobility in 50% of animals against a noxious stimulus. The amplitudes of the a-wave and the 01 decreased in dose-dependent manners, but their changes were less striking than those of the 01 latency. The peak latency of the a-wave remained unchanged. We conclude that the 01 peak latency is a useful monitor of the depth of inhalational anesthesia.

Anesthesia↗
PubMed1984

Anaesthetic management with morphine in phaeochromocytoma.

Morphine was used as the principal anaesthetic agent for five patients undergoing resection of phaeochromocytoma, and changes in plasma catecholamines were monitored. Phenoxygenzamine (0.5 mg X kg-1 X day-1) was orally given one week before operation. After premedication with hyoscine (0.4 mg) and diazepam (20 mg) of meperidine (50 mg), anaesthesia was induced with an infusion of morphine (1 mg X kg-1) over 30 min and maintained with diazepam, nitrous oxide and oxygen. Pancuronium was used as the muscle relaxant. In three of the five patients, blood pressure transiently rose (ranging from 15 to 60 mg) following orotracheal intubation, but vasodilators were not required. In two of the three, plasma norepinephrine increases were 1.1 and 1.3 ng X ml-1. In the other two patients, whose blood pressure was stable, the change in plasma norepinephrine was 0.1 and 0.7 ng X ml-1. After reaching a peak at the time of ligation of drainage vein from the tumour, plasma catecholamines rapidly decreased to the preoperative levels, but the blood pressure was well maintained in all cases. Ventricular arrhythmias did not occur despite the increased levels of endogenous catecholamines. These findings suggest that morphine can be used as an alternative anaesthetic agent during operation for phaeochromocytoma and that exaggerated pressor responses to morphine (when given slowly) seem not to occur in phaeochromocytoma.

Adrenal Gland Neoplasms↗