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Biomedical subjects

T Okuno

Publications and source records attributed to T Okuno.

At least 379 records · Page 21Linked to original sources
PubMed1981

Dexamethasone hypertension in rats.

The effects of dexamethasone (DEX) on systolic blood pressure, sodium balance and the renin-angiotensin system were studied in rats. DEX significantly increased systolic blood pressure within three days of its administration, but this effect of DEX on blood pressure was not enhanced by concurrent use of saline solution. In DEX-treated rats, urine volume was significantly increased and urinary sodium excretion showed a tendency toward a slight increase compared to control rats. On the 8th day of DEX administration, plasma renin substrate (PRS) was significantly elevated compared to control rats, whereas plasma aldosterone concentration (PAC) was not significantly different from that of control rats. These results suggest that hypertension induced by DEX may not be dependent on sodium retention or activation of the renin-angiotensin system.

Angiotensinogen↗
PubMed1980

[Studies on the mechanism of secretion of adrenal steroid hormones from adenomas of primary aldosteronism and Cushing's syndrome (author's transl)].

The mechanism of secretion of adrenal steroid hormones from adenomas of primary aldosteronism and Cushing's syndrome was studied in 10 patients with primary aldosteronism and in 3 patients with Cushing's syndrome in in vivo and in vitro experiments. In all of the 10 patients with primary aldosteronism, ACTH stimulated aldosterone secretion from the adenomas more significantly than did angiotensin II and III. DOC and cortisol which were contained in the adenomas were also stimulated more significantly by ACTH than by angiotensin II and III. Responses of the adenomas of Cushing's syndrome to various stimulations were less than those of primary aldosteronism. Secretion of cortisol and aldosterone from the adenomas of Cushing's syndrome was stimulated by ACTH and angiotensin II to a similar degree. From these studies, it seems that secretion of adrenal steroid hormones from adenomas of primary aldosteronism is more sensitive to extradrenal stimulations than that of Cushing's syndrome, and ACTH is the main factor in the control of the secretion of adrenal steroid hormones from the adenomas.

Adenoma↗
PubMed1980

Effects of prostaglandins E2, I2 and F2 alpha, arachidonic acid and indomethacin on pressor responses to norepinephrine in conscious rats.

The effects of prostaglandins E2 (PGE2), I2 (PGI2) and F2 alpha (PGF2 alpha), arachidonic acid and indomethacin on pressor responses to norepinephrine were examined in conscious rats. Intravenously infused PGE2, (0.3, 1.25 micrograms/kg/min), PGI2 (50, 100 ng/kg/min), PGF2 alpha (1.8, 5.4 micrograms/kg/min) and arachidonic acid (0.7, 1.4 mg/kg/min) did not change the basal blood pressure. Both PGE2 and PGI2 significantly attenuated pressor responses to norepinephrine, whereas PGF2 alpha significantly potentiated them. Arachidonic acid, a precursor of the prostaglandings (PGs), significantly attenuated pressor responses to norepinephrine. Since the attenuating effect of arachidonic acid was completely abolished by the pretreatment with indomethacin (5 mg/kg), arachidonic acid is thought to exert an effect through its conversion to PGs. On the contrary, intravenously injected indomethacin (0.2--5.0 mg/kg) facilitated pressor responses to norepinephrine in a dose-related manner without any direct effect on the basal blood pressure. These results suggest that endogenous PGs may participate in the regulation of blood pressure by modulating pressor responses to norepinephrine in conscious rats.

Animals↗
PubMed1980

The effects of prostaglandins E2 and I2, and arachidonic acid on vascular reactivity to norepinephrine in isolated rat mesenteric artery, hind limb and splenic artery.

The effects of prostaglandins E2 (PGE2) and I2 (PGI2), arachidonic acid, and indomethacin on the vascular reactivity to norepinephrine were tested in three different isolated rat vascular beds (mesenteric artery, hind limb and splenic artery) perfused with the Krebs bicarbonate solution. In these vascular beds PGE2 (0.25--16 ng/ml), PGI2 (0.1--100 ng/ml), arachidonic acid (0.1--10 micrograms/ml) or indomethacin (5--25 micrograms/ml) in the perfusate did not change the basal pressure. In the splenic artery, both PGE2 and PGI2 attenuated the vascular response to norepinephrine in a dose-related manner. In the mesenteric vascular bed and the hind limb, however, PGE2 potentiated the vascular response to norepinephrine, while PGI2 attenuated this response. Acahidonic acid, a prostaglandin precursor, potentiated the vasoconstrictor response to norepinephrine in the mesenteric artery and the hind limb, whereas in the splenic artery, attenuation of the response to norepinephrine occurred. In these three vascular beds, indomethacin, a prostaglandin synthetase inhibitor, attenutated the vascular response to norepinephrine. In the mesenteric artery and the hind limb, PGE2 and not PGI2 reversed the effect of indomethacin, while in the splenic artery, neither PGE2 nor PGI2 reversed the inhibitory effect of indomethacin. These results suggest that, at least in the rat mesenteric artery and the hind limb where the modulating effect of arachidonic acid is similar to that of PGE2, PGE2 and not PGI2 is a primary endogenous prostaglandin in determining the vascular reactivity to norepinephrine.

Animals↗
PubMed1980

Cerebral atrophy following ACTH therapy.

In a study of 15 patients with infantile spasms and Lennox syndrome 4 (26.7%) showed no cerebral atrophy and 11 (73.3%) showed mild ventricular and sulcal enlargement before ACTH therapy. Ventricular and sulcal enlargement increased soon after ACTH therapy in most patients. Cerebral atrophy was reversible at over 1 month after ACTH therapy. However, in three instances, cerebral atrophy was not reversible, and one patient with infantile spasms had chronic subdural effusion, which appeared to be a complication of treatment with ACTH. Patients on ACTH therapy should be carefully monitored.

Adrenocorticotropic Hormone↗
PubMed1980

Benign subdural effusion in infants.

Twenty cases of infants with computed tomographic low density areas over the frontal lobes that mimicked cortical atrophy are reported. Almost all cases presented with a slight increase in intracranial pressure associated with delayed developmental milestones. Peripheral hypodensity over the frontal lobes disappeared, and the infants' development was essentially normal, in many cases without surgery. The lesion might be called "infantile benign subdural effusion" and should be treated conservatively.

Atrophy↗
PubMed1980

Pituitary hyperplasia due to hypothyroidism.

Two cases of hypothyroidism with computed tomographic evidence of enlargement of the pituitary gland are reported; in both the enlargement disappeared after treatment. These findings are in agreement with the previously reported observation that an increase of TSH production in primary hypothyroidism may lead to pituitary hyperplasia.

Child↗
PubMed1980

Infarction of the internal capsule in children.

The computed tomographic findings in seven boys and two girls with infarction of the internal capsule are reported. Ages at the time of examination ranged from 8 months to 14 years. The etiology was head injury (concussion) in six and unknown in three. Cerebral angiography carried out in four cases showed narrowing of main arteries in two patients.

Adolescent↗
PubMed1980

Elevated homovanillic acid in cerebrospinal fluid of children with infantile spasms.

To determine the role of noradrenaline, dopamine, and serotonin in the brain of patients with infantile spasms, levels of respective major metabolites in cerebrospinal fluid were examined. Homovanillic acid levels were significantly increased in these patients, while 3-methoxy-4-hydroxyphenylethylene glycol and 5-hydroxyindoleacetic acid were not significantly altered, as compared with controls. In patients with febrile convulsion and status epilepticus who were examined during or within a few hours after convulsions the same phenomenon was evident. The increased level of dopamine metabolite was closely related to the occurrrence of convulsions and is considered to be a secondary phenomenon.

Adrenocorticotropic Hormone↗
PubMed1980

Central nervous system involvement in progressive muscular dystrophy.

Several abnormalities in the central nervous system were shown in patients with progressive muscular dystrophy using computerised tomography (CT) scans, electroencephalograms, psychometry, and ophthalmological methods. In congenital muscular dystrophy, the most characteristic finding in the CT scan was a low density area in the white matter, seen in 14 (56%) out of 25 cases. In Duchenne dystrophy, slight cerebral atrophy was observed in 20 (67%) out of 30 cases. It was interesting that in the case of Duchenne dystrophy the older the patient, the more severe were the CT findings. In congenital muscular dystrophy half the patients with a low density area showed a spike or a spike-and-wave complex in the electroencephalogram, and optic atrophy was evident in several cases. It is concluded that progressive muscular dystrophy is not only a myogenic disorder but also one which affects the central nervous system.

Adolescent↗
PubMed1980

Vascular action of high dose estrogen in rats.

Effects of estradiol hemisuccinate and diethylstilbestrol diphosphate on the cardiovascular system in male rats were examined in vivo and in vitro. In conscious rats, intravenously administered estradiol or diethylstilbestrol inhibited vascular responses to norepinephrine in a dose-dependent manner. Diethylstilbestrol in high doses significantly lowered the blood pressure of conscious rats. In the isolated mesenteric arteries perfused with Krebs bicarbonate solution, estradiol or diethylstilbestrol in the perfusate similarly inhibited vascular reactivity to norepinephrine in a dose-dependent manner. As in the in vivo experiments, a decrease in the basal pressure of the mesenteric vascular bed was observed when diethylstilbestrol was added to the perfusate at high concentrations. The results of these in vivo and in vitro studies strongly suggest that estradiol and diethylstilbestrol act directly on the vascular beds and attenuate vascular response to norepinephrine. It is also suggested that diethylstilbestrol by itself causes vasodilatation and a reduction in blood pressure when present at high concentrations.

Animals↗