Search PubMed⌕ Search

Biomedical subjects

C Okuda

Publications and source records attributed to C Okuda.

At least 73 records · Page 4Linked to original sources
PubMed1986

Alteration of the turnover of dopamine and 5-hydroxytryptamine in rat brain associated with hypothermia.

The alteration of monoamines and their metabolites in the brain in response to hypothermia was studied using rats subjected to a cold and immobilization stress. The experiments were designed to compare the responses in the "hypothermal" rats with those in the "normothermal" ones which received the same stress except for the change in body temperature. It has been found that the contents of norepinephrine (NE) and 5-hydroxytryptamine (5-HT) in various cerebral regions were significantly decreased during hypothermia. These decreases were readily reversed by the rewarming of animals. Moreover, the increase in the content of 5-hydroxyindole-3-acetic acid (5-HIAA), the metabolite of 5-HT, was also detected in some cerebral regions where the decrease of 5-HT was observed. Although the dopamine (DA) contents in all cerebral regions examined were found to be unaltered, its metabolites, 3,4-dihydroxyphenylacetic acid (DOPAC) and/or homovanillic acid (HVA) contents in most regions in the brain showed a significant elevation during and/or after the occurrence of hypothermia. These results suggest that the metabolic turnovers of 5-HT and DA in various cerebral regions may be accelerated during hypothermia.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1986

Hypothalamic control of pituitary and adrenal hormones during hypothermia.

In order to investigate neuroendocrinological mechanisms of hypothermia, we determined the changes in plasma concentrations of corticosterone (CS), prolactin (PRL), and thyrotropin (TSH), and their correlations with alterations in hypothalamic dopamine (DA) and thyrotropin releasing hormone (TRH), in rats restrained and immersed in a water bath at various temperatures. A graded decrease of body temperature induced a progressive increase in the plasma level of CS, whereas that of PRL showed a drastic decrease. The plasma level of TSH also showed an increase during mild hypothermia (about 35 degrees C), but this increase was not evident during profound hypothermia (below 24 degrees C). The changes in these hormones were readily reversed by rewarming animals. Although DA content in the hypothalamus was not affected, its metabolites, 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA), showed an increase following the decrease of body temperature. Pretreatment of the animals with sulpiride, a D2-antagonist, prevented the hypothermia-induced inhibition of PRL release. Hypothalamic TRH was significantly decreased during mild hypothermia, and it returned to control levels after rewarming. These results suggest that the decrease in plasma PRL induced by hypothermia may be associated with the activation of hypothalamic DA neurons, whereas the increase in plasma TSH during mild hypothermia seems to be caused by the increased release of TRH in the hypothalamus.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1983

Effect of acebutolol on plasma catecholamine concentrations in anesthetized dogs with ouabain-induced arrhythmias and its direct actions in vitro on the adrenal medulla.

We have performed studies on blood hormone dynamics following intravenous administration of acebutolol, a newly synthesized beta-blocker, and its direct action on the adrenal medulla in vitro. Intravenous injection of acebutolol into anesthetized dogs almost doubled the plasma adrenaline and noradrenaline concentrations within 5 to 15 minutes, while renin activity was reduced to approximately two-thirds of the pre-administration level. When arrhythmia was induced in dogs with ouabain, the plasma adrenaline and noradrenaline levels increased to 220 +/- 109 and 392 +/- 84 pg/ml, respectively, from the basal levels of 44 +/- 24 and 140 +/- 43 pg/ml. The restoration of sinus rhythm following the administration of acebutolol was accompanied by a further increase in the plasma adrenaline and noradrenaline levels to 797 +/- 364 and 1226 +/- 263 pg/ml, respectively. A perifusion experiment indicated that acebutolol directly accelerated catecholamine release from the adrenal medulla in pigs.

Acebutolol↗
PubMed1982

The effects of volatile anesthetics on the binding of 1-anilino-8-naphthalene sulphonate to biological membranes and lipid vesicles: the role of cholesterol.

The effects of volatile anesthetics on the properties of membrane surfaces were studied using the negatively charged fluorescent probe 1-anilino-8-naphthalene sulphonate (ANS). Although the addition of the anesthetics caused no change of the fluorescence quantum yield of ANS bound to the biological membranes, there was a significant increase of the number of binding sites (n) for ANS to the membranes. This increase was also found after treating the membranes with either trypsin or neuraminidase and with vesicles of total lipids extracted from erythrocytes. With phosphatidylcholine (PC) vesicles, the fluorescence increase by the addition of anesthetics was observed only when the vesicle contained cholesterol. The greater increase of the n value was seen in vesicles containing a higher concentration of cholesterol. When the neutral probe, N-phenyl-1-naphthylamine (NPN) was used instead of ANS, this fluorescence increase was not seen. These results were interpreted in terms of the electrostatical change of the membrane lipid region. That is, a change of the surface potential of the membrane is possibly caused by the anesthetics through the interaction with lipid components. Cholesterol plays a critical role in this interaction.

Anesthetics↗