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Biomedical subjects

C Okuda

Publications and source records attributed to C Okuda.

At least 37 records · Page 2Linked to original sources

Relationship between tissue reactions and morphological changes of the fungi in chromoblastomycosis: morphometry and electron microscopy.

To investigate the histological distribution and the morphology of the fungi and the tissue reactions in chromoblastomycosis, especially in the process of transepidermal elimination, cutaneous lesions of two patients with this disease were studied morphometrically and ultrastructurally. In the dermis, most of the fungal elements appeared as sclerotic cells and their cell wall showed an irregular, worm-eaten leaf-like appearance; they seemed to be continuously attacked by polymorphonuclear neutrophils. The epidermis eliminated 10-20% of all the organisms in the skin lesions, and the hypha-forming activity tended to be higher in the epidermis than in the dermis. Ultrastructurally, basal keratinocytes facing the dermal abscess containing fungal elements frequently appeared as dark cells, suggesting an increased proliferation activity. Spinous keratinocytes facing intraepidermal microabscesses containing fungal elements showed an abnormal accumulation of tonofilaments and further early keratinization in the spinous cell layer. All of the morphological changes of the dermis and epidermis are regarded as defence reactions against the fungi existing in the skin lesions. There is a close relationship between tissue reactions and morphological changes of fungi in chromoblastomycosis.

Aged↗

Clorgyline-induced increases in presynaptic DA: changes in the behavioral and neurochemical effects of amphetamine using in vivo microdialysis.

Microdialysis was used in behaving rats to further characterize the behavioral and regional dopamine (DA) response to the monoamine oxidase (MAO) inhibitor clorgyline and determine how MAO inhibition affects amphetamine (AMPH)-induced changes in behavioral and extracellular DA dynamics. Although clorgyline (4.0 mg/kg) did not significantly alter behavior, it produced prolonged increases in caudate and accumbens extracellular DA and 3MT and corresponding decreases in homovanillic acid (HVA) and dihydroxyphenylacetic acid (DOPAC). Clorgyline pretreatment altered the behavioral response to both low (0.25 mg/kg) and moderate (2.5 mg/kg) doses of AMPH, which was characterized by a shift to more intense forms of stereotype and corresponding decreases in locomotion. The caudate and accumbens DA response to AMPH (0.25 mg/kg) was also significantly augmented, consistent with an increase in AMPH-releasable cytoplasmic DA. Thus, the potentiated DA response in clorgyline-pretreated animals may be responsible for the changes in the stereotypy profile. Possible implications of these observations for the augmented behavioral response observed with repeated AMPH administration are discussed.

3,4-Dihydroxyphenylacetic Acid↗

Deprenyl alters behavior and caudate dopamine through an amphetamine-like action.

In vivo microdialysis was used to concurrently measure the behavioral and caudate dopamine (DA) responses to the alleged irreversible type B monoamine oxidase inhibitor deprenyl. The effects were contrasted to those of the type A monoamine oxidase inhibitor, clorgyline. Consistent with its effects as an irreversible monoamine oxidase inhibitor, clorgyline produced an increase in DA concentration that remained elevated for at least 6 h. In contrast, the deprenyl-induced elevation in DA concentration occurred more rapidly, achieved a higher peak response, and then returned to baseline within 2 h following drug administration. The two drugs also produced distinctive changes in DA metabolite levels. Whereas the pattern of clorgyline-induced effects were consistent with irreversible monoamine oxidase inhibition, deprenyl produced an amphetamine-like response profile. Further, deprenyl but not clorgyline significantly increased locomotor activity. These results suggest that deprenyl does not augment caudate DA levels through monoamine oxidase inhibition. Rather, the pattern of its effects on caudate DA dynamics and behavior supports previous evidence that deprenyl produces its effects through its metabolism to amphetamine-like substances.

3,4-Dihydroxyphenylacetic Acid↗

Cerebral extracellular glucose and lactate concentrations during and after moderate hypoxia in glucose- and saline-infused rats.

To assess the effect of a glucose infusion on brain extracellular fluid (ECF) during systemic hypoxia, changes in glucose and lactate concentrations in cerebral ECF during and after moderate hypoxic hypoxia were measured in adult, conscious, unrestrained rats, with a microdialysis probe in the posterior hippocampus. The rats were given either saline (n = 6) or 50% glucose solution (n = 6) for 3 h, starting 60 min before the onset of hypoxia. Hypoxia was produced by circulating 7% O2 gas in a plastic chamber for 90 min. In saline-infused animals, brain ECF glucose concentrations decreased slightly during hypoxia, although blood glucose concentrations did not change. Blood lactate concentrations increased to 6.28 +/- 0.91 mM, at 60 min after the onset of hypoxia (P less than 0.05). Brain ECF lactate concentrations increased to 3.53 +/- 0.20 mM and remained constant during 60 min of steady-state hypoxia (P less than 0.05) and decreased to the basal level within 60 min after the end of hypoxia. When sodium lactate solution was infused intravenously for 90 min (n = 4), blood lactate concentrations increased to a level as high as those found during hypoxia. However, the brain ECF lactate concentration increased only to 1.86 +/- 0.09 mM. In glucose-infused animals, the blood glucose concentration reached 339.1 +/- 32.3 mg/dl at the end of the glucose infusion, and the brain ECF glucose concentration increased to 54.7 +/- 7.3 mg/dl.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Effects of glucose infusion on cerebral cortical glucose and lactate concentrations during endotoxemia in rats.

Hypoglycemia has been observed in several species before death from endotoxemia. Although several studies have emphasized the importance of maintaining brain glucose at normal concentration during endotoxemia, the effect of glucose infusion on cerebral glucose metabolism has not been studied. Accordingly, the effects of glucose infusion on interstitial glucose and lactate concentrations in the cerebral cortex during endotoxemia were studied in 22 Wistar rats. Cerebral glucose and lactate were measured at 30-min intervals for 4 h using microdialysis. Animals were divided into four groups: 1) saline-infused control (n = 5); 2) saline-infused endotoxemia (n = 7); 3) glucose-infused control (n = 5); and 4) glucose-infused endotoxemia (n = 5). In groups 2 and 4, endotoxemia was induced by intravenous injection with E. coli lipopolysaccharide B (5 mg.100 g-1). One hour after endotoxin administration, saline or 50% glucose was infused at a flow rate of 0.5 ml.100 g-1.h-1 for 3 h. Endotoxin induced a significant increase (P less than 0.05) in blood glucose in the saline-infused rats, which survived for 4 h (n = 5), from 91.6 +/- 15.4 mg.100 ml-1 at baseline to 136.3 +/- 23.3 mg.100 ml-1 (149%) at 1 h, followed by a gradual decrease (to 63% of the basal concentration at 4 h). Similar changes were observed in brain glucose (14.9 +/- 1.9 mg.100 ml-1 baseline, 175% of baseline at 2 h, and 57% of baseline at 4 h).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Lactate in rat skeletal muscle after hemorrhage measured by microdialysis probe calibrated in situ.

The interstitial lactate concentration in rat skeletal muscle was measured in the normal state and after hemorrhage using a microdialysis probe, and the values calculated by in vitro and in vivo calibration were compared. After withdrawal of 30% of the estimated total blood volume, the lactate concentration in the dialysate gradually increased and then maintained an almost constant level. It was found that interstitial lactate levels of skeletal muscle calculated by the in vitro calibration method were not significantly different from those calculated by in vivo calibration in both the normal state and after hemorrhage. These data indicate that the absolute lactate concentration in the muscle interstitium in the normal state and after acute hemorrhage can be practically measured by a microdialysis probe calibrated in vitro. From the comparison of lactate concentrations in blood and in the muscle interstitium, it was suggested that rat skeletal muscle functions as a lactate consumer, rather than as a lactate producer, after acute hemorrhage.

Acute Disease↗

Continuous measurement of lactate concentration in skeletal muscle and liver interstitium using a microdialysis method after acute hemorrhage in anesthetized rats.

Interstitial lactate concentration in rat skeletal muscle was continuously measured using a microdialysis method following an acute hemorrhage. For comparison, similar measurements were also performed for liver. Normal lactate levels of skeletal muscle and liver interstitium were 0.58 +/- 0.10 mM and 1.23 +/- 0.04 mM, respectively. After withdrawal of 30% of the estimated total blood volume within 3 min, a constant high blood lactate level was achieved. The lactate concentrations in muscle and liver interstitium also increased to 270 and 210% of the basal levels, respectively, but they did not exceed the blood level. These findings led us to hypothesize that skeletal muscle as well as liver functions as a lactate consumer rather than a producer after acute hemorrhage.

Animals↗

[Anesthetic management of an infant with a single ventricle (asplenia syndrome) for non-cardiac surgery].

Ketamine and fentanyl were used for surgery of esophageal hiatus hernia in a 9 month old boy with single ventricle (asplenia syndrome). The patient was orally premedicated with diazepam 2.5 mg, and intravenously with atropine 0.04 mg. General anesthesia was induced with ketamine-fentanyl-pancuronium-100% oxygen, and maintained with fentanyl-pancuronium-100% oxygen. The total dose of ketamine or fentanyl was 0.8 mg.kg-1 or 15 micrograms.kg-1, respectively. Systolic blood pressure and heart rate of the patient were stable during ketamine-fentanyl anesthesia. Arterial oxygen saturation measured by pulse oximetry was over 90% and arterial oxygen tension was above 60 mmHg during the operation. Ketamine-fentanyl anesthesia might be useful for non-cardiac surgery of a child with cyanotic congenital heart disease.

Anesthesia, General↗

[Anesthetic management of a patient with norepinephrine-secreting neuroblastoma by using prostaglandin E1].

The anesthetic management of a 5-month-old male with norepinephrine-secreting neuroblastoma was described. Partial excision of the tumor was carried out under general anesthesia induced with enflurane, fentanyl and succinylcholine, and maintained with enflurane, nitrous oxide and oxygen. In this case, hypertension was observed intraoperatively and prostaglandin E1 was continuously infused at a rate of 0.1-0.5 micrograms.kg-1.min-1 to control blood pressure. Severe hypotension after removal of the tumor was not observed. Continuous administration of prostaglandin E1 was useful in this patient with norepinephrine-secreting neuroblastoma.

Alprostadil↗

Trichophyton rubrum invasion of human hair apparatus in tinea capitis and tinea barbae: light- and electron microscopic study.

We have previously reported morphological changes of Trichophyton violaceum and Microsporum canis in hair apparatuses in tinea capitis. To investigate the morphology of Trichophyton rubrum in the human hair apparatus, two cases of tinea capitis and one case of tinea barbae were examined by light- and electron microscopy. The fungal elements, which were located in the lower keratogenous zone, showed non-septate hyphae in the outer part of the hair cortex. With the upward development of the hair layers, some hyphae invaded the keratinized hair cuticle and keratinized inner root sheath and were transformed into arthrospores. Some hyphae remaining in the hair cortex were also transformed into arthrospores, while other hyphae in the hair cortex did not survive, but degenerated. In T. rubrum hair infection, there is a distinct relationship between the morphological changes of the fungi and the hair cell differentiation as seen in T. violaceum and M. canis infections. However, T. rubrum displays unique morphological changes, which are different from those of T. violaceum and M. canis, in hair apparatuses.

Adult↗

Epidermolysis bullosa simplex (Koebner) is a keratin disorder. Ultrastructural and immunohistochemical study.

A skin biopsy specimen was obtained from a 1-month-old female with epidermolysis bullosa simplex (Koebner). Histologically, an intraepidermal separation was seen and considered to be formed by cytolysis of the epidermal basal cells. Ultrastructurally, the basal cells were lacking in cytoplasmic tonofilaments, and the initial change of the cytolysis seemed to be cleavages of the cytoplasm. Immunohistochemically, a basal cell keratin was expressed in a suprabasal cell layer but not in the basal cell layer, and a panepithelial keratin was not detected in the basal cell layer. These findings suggest that keratin production of the epidermal cells may be delayed, resulting in a weakness of the basal cells against minor trauma to the skin.

Biopsy↗

[Effects of hypoxia on the brain cholinergic system in the rat].

Effects of mild hypoxic hypoxia on brain cholinergic system in the rat were investigated with choline acetyltransferase (CAT), acetylcholinesterase (AChE) and muscarinic acetylcholine receptor (MR) as indicators of cholinergic system. Hypoxic exposure of 10% oxygen concentration was undertaken for one week. The activity of CAT and AChE was reduced, while MR increased. CAT is known as the specific enzyme of cholinergic neuron, but AChE is contained also in postsynaptic neuron of the cholinergic neuron. Reduction in the activity of both enzymes may mean reduction in the activity of cholinergic system. MR is contained in postsynaptic membrane. The increase in MR may indicate recovery from agonist-dependent desensitized receptor.

Animals↗

Changes in brain monoamines and their metabolites during and after hemorrhagic shock in the rat.

The alteration of monoamines and their metabolites in the brain during and after hemorrhagic shock in the conscious state was measured in rats. Blood pressure was maintained at 40-70 mmHg (5.3-9.3 kPa) for 60 min by withdrawing 8 ml of blood intermittently. The content of monoamines, as well as their metabolites, increased in various brain regions during hemorrhage, compared with the content in the control rats. Sixty min after the end of the bleeding period, almost no significant change in the contents of brain monoamines nor of their metabolites was observed. These results may indicate not only an increased release of monoamines from nerve terminals, but also an increased synthesis of them during hemorrhagic shock. Soon after the bleeding was stopped, the increased monoamine turnover rate returned to almost normal levels.

Journal Article↗

Hemorrhage-induced regional brain thyrotropin-releasing hormone release in conscious rats measured by microdialysis.

The septum, nucleus accumbens and preoptic area in the brains of conscious, freely moving rats were perfused using microdialysis probes. The TRH concentration significantly increased in the septum after withdrawal of 30% of the total blood volume but remained at constant levels in the other brain areas. Also, high potassium dose-dependently stimulated TRH release in vivo. These results suggest that blood loss stimulates septal TRH release, probably by membrane depolarization of TRH-containing nerve terminals.

Animals↗

The interaction of neuromuscular relaxants with rabbit lung muscarinic receptors.

The interaction of muscle relaxants with airway muscarinic receptors of rabbit lung was investigated in vitro by the [3H]QNB binding technique. Pancuronium, vecuronium, alcuronium and succinyl choline chloride (SCC) inhibited the binding of [3H]QNB to rabbit lung muscarinic receptors in a dose-dependent manner. The values of IC50 (the concentration giving 50% inhibition) of pancuronium, vecuronium, alcuronium and SCC were 1.54 x 10(-5), 2.52 x 10(-5), 8.40 x 10(-5), and 4.00 x 10(-3) mol/l respectively. As the values of Kd increased with minimal change in the value of Bmax, while not influencing the number of receptors, these muscle relaxants had an inhibitory action on the affinity of muscarinic receptors to [3H]QNB in the order: pancuronium greater than or equal to vecuronium greater than alcuronium greater than SCC. Applying IC50 values to human conditions, clinical doses of these muscarinic relaxants are unlikely to exhibit any significant vagolytic action in lung tissue.

Alcuronium↗

[The effect of xanthine oxidase inhibitor on hindlimb ischemia-induced thromboxane A2 release].

Our previous studies demonstrated that the bilateral hindlimb ischemia/reperfusion stimulates thromboxane A2 (TXA2) production. The present study tests the role of xanthine oxidase-derived oxygen free radicals in mediating this event. In twelve anesthetized dogs, the abdominal aorta and the inferior vena cava were clamped for 150 min, declamped and reperfused for 30 min. Two groups were studied: untreated control group and pretreated group with xanthine oxidase inhibitor, allopurinol 100 mg.kg-1 orally 24 hr before clamping plus 25 mg.kg-1 intravenously 15 min before clamping. In the control group, plasma TXB2 levels increased markedly after reperfusion. On the other hand, prior treatment with allopurinol attenuated the increase in plasma TXB2 levels at 30 min after reperfusion. This model revealed partial ischemia, because the femoral arterial blood flow was approximately 15% of baseline during clamping. However, the present study suggests that ischemia/reperfusion stimulates TXA2 production, which may be partly affected by hypoxanthine-xanthine oxidase-derived oxygen free radicals and may be an important mechanism responsible for reperfusion injury.

Allopurinol↗

[The effectiveness of angiotensin II antagonist on experimental pulmonary embolism--comparison of propranolol with prostaglandin F2 alpha].

We studied the effects of angiotensin II (A-II) antagonist, propranolol and prostaglandin F2 alpha (PGF2 alpha) on arterial hypoxemia after injecting autologous muscle to induce massive pulmonary embolism. Twenty-four anesthetized paralyzed dogs were divided into four groups; control, intravenous A-II antagonist (1-sarcosine, 8-isoleucine A-II) infusion at 5 micrograms.kg-1.min-1, intravenous propranolol injection at 1.5-2.0 mg, and intravenous PGF2 alpha infusion at 1 microgram.kg-1.min-1. With FIO2 of 0.33, the administration of A-II antagonist produced an increase in arterial PO2 from 134 +/- 16 (mean +/- SE) to 155 +/- 11 mmHg during infusion, and to 160 +/- 9 mmHg 30 min after infusion. Simultaneous hemodynamic measurements demonstrated no significant changes in arterial blood pressure and heart rate, but a slight increase in cardiac output was observed. On the other hand, propranolol and PGF2 alpha did not reverse the pulmonary oxygenation. Cardiac output decreased after propranolol, and alveolar dead space and pulmonary artery pressure increased further after PGF2 alpha. We conclude that A-II antagonist may be effective in the treatment of massive pulmonary embolism, possibly by improving the ventilation-perfusion relationship. The exact mechanism of the effect of A-II antagonist has not been clarified.

Angiotensin II↗