Search PubMed⌕ Search

Biomedical subjects

T Okuno

Publications and source records attributed to T Okuno.

At least 397 records · Page 22Linked to original sources
PubMed1979

Central and peripheral effects of bradykinin and prostaglandin E2 on blood pressure in conscious rats.

Bradykinin or prostaglandin E2 (PGE2), when injected intravenously, decreased blood pressure of conscious rats in a dose-dependent manner, while intracerebroventricular injections of bradykinin or PGE2 caused a dose-dependent increase in blood pressure. SQ 14,225, an inhibitor of angiotensin converting enzyme, potentiated the central pressor or peripheral depressor effect of bradykinin. Indomethacin, an inhibitor of prostaglandin synthesis, almost completely inhibited the central pressor effect of bradykinin when injected intraventricularly. Indomenthacin, when injected intravenously, failed to inhibit the peripheral depressor effect of bradykinin, whereas it significantly attenuated the peripheral depressor effect of bradykinin when the angiotensin converting enzyme was inhibited with SQ 14,225. These results suggest that the central pressor effect of bradykinin is mainly mediated by the synthesis of prostaglandins in the central nervous system, while only a small fraction of peripheral depressor effect of bradykinin is, at least in conscious rats, mediated by the synthesis of prostaglandins in the systemic circulation.

Animals↗
PubMed1979

Effects of intracerebroventricular administration of prostaglandins I2, E2, F2 alpha and indomethacin on blood pressure in the rat.

The effects of intraventricularly administered prostaglandins I2 (PGI2), E2 (PGE2), F2alpha (PGF2 alpha) and indomethacin on systemic blood pressure were investigated in conscious rats. PGI2 (1.25--10 micrograms/kg) decreased blood pressure in a dose-related manner, whereas PGE2 (100--1000 mg/kg) dose-dependently increased blood pressure. Both PGF2 alpha (0.31--20 micrograms/kg) and indomethacin (0.625--40 micrograms/kg) had no effects on blood pressure. These results indicate that intraventricular injection of PGI2 or PGE2 can induce significant changes in blood pressure, while endogenous prostaglandins synthesized in the brain seem to play a minor role in direct regulation of systemic blood pressure in the rat.

Animals↗
PubMed1979

Effect of prostaglandin E2 on vascular reactivity to norepinephrine in isolated rat mesenteric artery, hind limb and splenic artery.

The effects of prostaglandin E2 (PGE2) 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 (0.1-64 ng/ml) or indomethacin (09.1-96 microgram/ml) in the perfusate did not change the basal pressure. In the mesenteric vascular bed and the hind limb, PGE2 dose-dependently potentiated the vascular response to norephinephrine, whereas PGE2 dose-dependently inhibited the vascular response to norepinephrine in the splenic artery. In these three vascular beds indomethacin in the perfusate dose-dependently attenuated the vascular response to norepinephrine. In the mesenteric artery and the hind limb PGE2 restored the effect of indomethacin, but in the splenic artery PGE2 did not restore the inhibitory effect of indomethacin. These results indicate that the modulating effect of exogenously administrated PGE2 on the vascular action to norepinephrine varies in different vascular beds. It is also suggested that the contribution of endogenous PGE2 synthesized in the vascular wall to the vascular reactivity to norepinephrine is, as well as the effect of exogenous PGE2, different in different vascular beds.

Animals↗
PubMed1979

Carbamazepine as a sole anticonvulsant for partial seizures.

The efficacy, serum concentration and side effects of CBZ for partial seizures in children were evaluated. The study was undertaken on 27 patients with partial seizures ranging from 5 to 17 years of age. Further 15 patients with various types of epilepsy taking CBZ with other anticonvulsants were selected as controls to compare the serum levels of CBZ. In nineteen of the 27 patients seizures were controlled completely, in whom serum CBZ levels varied fro trace to 15.6 mcg/ml, average being 8.18 +/- 3.40 mcg/ml, while those of uncontrolled ones ranged from 3.5 to 11.3 mcg/ml, average being 7.50 +/- 2.97 mcg/ml. There was no significant difference between both groups of the above. EEG was improved in the seven of 19 seizure-free cases, serum levels of which ranged from 5.9 to 13.2 mcg/ml. With regard to the side effects, transient leucopenia was observed in four patients and serum GOT and GPT slightly elevated in two. Correlation between dose and serum level in the monotherapy group was not significant as well as in the combined therapy group. Serum DBZ levels in the monotherapy group were significantly higher than those in combined therapy group.

Adolescent↗
PubMed1979

Tuberous sclerosis: early neurologic manifestations and CT features in 18 patients.

Early clinical manifestations and radiologic features of tuberous sclerosis were studied in 18 consecutive patients encountered in the past two years, including two patients harboring an associated intraventricular tumor (giant-cell astrocytoma). Depigmented naevi rather than adenoma sebaceum, infantile spasms and intracranial calcifications were the cardinal early features in this present series, and CT scanning proved to be the single most useful diagnostic technique in the early detection of intracranial calcifications and therefore for the early diagnosis of this disorder. CT scanning was also useful in detecting the intraventricular tumors in the early stage before they became clinically manifest.

Adolescent↗
PubMed1979

Computed tomography of cerebral palsy: evaluation of brain damage by volume index of CSF space.

Between 1976 and 1978, we examined 110 Japanese children with cerebral palsy using a CT 1000 and a CT 1010 (EMI). In 92% of all patients, there were abnormal findings. Cortical atrophy was seen in 51%, ventricular dilatation in 86%, localized low density areas in 22%, brain anomalies in 10% and asymmetry of cerebral hemisphere in 31%. In spastic hemiplegia, the characteristic CT revealed asymmetrical ventricular dilatation without cortical atrophy and localized low density areas in the cerebral hemisphere contralateral to the palsy. In spastic tetraplegia, CT revealed moderate to marked diffuse cerebral atrophy or brain anomalies. In athetosis, CT revealed normal or slight cerebral atrophy. In 60 cases where a CT 1010 was used, we calculated the volume index of CSF space by computer, Eclipse S/200, and analyzed the relationship between the clinical features of cerebral palsy and the volume index of CSF space.

Adolescent↗
PubMed1979

Central hypertensive actions of angiotensin I, II and III in conscious rats.

The effects of intracerebroventricular administrations of three natural angiotensins, angiotensin I (ANG I 3.8 X 10-11-9.4 X10-10 mol/kg body weight), II (9.6 X 10-12-2.4 X 10-10 mol/kg body weight) and III (2.7 X 10-10 2.5 X 10-9 mol/kg body weight) on systemic blood pressure were investigated in conscious rats. Angiotensin II (ANG II), ANG I and angiotensin III (ANG III), increased blood pressure in a dose-related manner. The order of potency of angiotensins was ANG II greater than ANG I greater than ANG III. The intraventricular administration of a converting enzyme inhibitor (SQ 14225, 6.9 X10-8 mol/kg) abolished the central effect of ANG I, while an angiotensin II analogue ([Sar1-Ala8]ANG II, 1.1 X 10-8 mol/kg) administered intraventricularly inhibited the central pressor effects of these three angiotensins. These results suggest that ANG II is a main mediator of the renin-angiotensin system in the central nervous system.

Angiotensin I↗
PubMed1979

Responses of aldosterone-producing adenomas to ACTH and angiotensins.

To elucidate the control mechanism of aldosterone production in primary aldosteronism, in vivo and in vitro studies were done in 7 patients with aldosterone-producing adenomas. In the in vivo study, plasma aldosterone was stimulated more significantly by (Formula: see text), synthetic ACTH than by angiotensin II or furosemide. Diurnal variations of plasma aldosterone, which were studied in 4 patients, were similar to those seen in normal controls. In agreement with the results in the in vivo study, the in vitro study also revealed ACTH stimulated aldosterone and deoxycorticosterone (DOC) from the adenoma more markedly than angiotensin II or III. There was no adenoma which was more sensitivie to angiotenion II or III than to ACTH. From these results it is considered that changes in plasma aldosterone induced by the exogenous administration of angiotensin II or ACTH in patients with aldosterone-producing adenoma are mainly based on changes in aldosterone production in the adenoma. Furthermore, in patients with an aldosterone-producing adenoma in whom diurnal variations of plasma aldosterone similar to those in normal subjects are observed, responses of aldosterone to angiotensin II are supposed to be less than those to ACTH.

Adenoma↗
PubMed1978

Localization of cytochrome P-450-linked mixed function oxidase and steroid hydroxylations within zones of bovine adrenocortices.

The localization of contents and activities of components of cytochrome P-450-linked mixed function oxidase system and the hydroxylation of steroids in mitochondria and microsomes within zones of adrenocortices was investigated. NADPH-adrenodoxin reductase activity was higher in the zona glomerulosa than in the other zones. Adrenodoxin content was present at high concentration in the zona fasciculata. The localization of cytochrome P-450 within zones of adrenocortices has already been reported (Ichikawa, Y., Kuroda, M. and Yamano, T. (1970) J. Cell Biol 45, 640--653). The zona fasciculata contained more mitochondrial and microsomal cytochromes P-450 than the zona glomerulosa or zona reticularis. Cleavage activity of the side chain of cholesterol was found in three zones. However, particularly high activity was observed in the zona fasciculata and zona reticularis. 11beta-Hydroxylation was found in the zona glomerulosa. 21-Hydroxylation activity was especially higher in the zona fasciculata than in the other zones.

Adrenal Cortex↗
PubMed1978

Evaluation of dithiothreitol (DTT) for inactivation of IgM antibodies.

A newly introduced sulphydryl compound, dithiothreitol (DTT), is evaluated for its optimal conditions of inactivation of IgM antibodies. The maximal effects of DTT reagent are observed when its final concentrations are between 0.0025 M and 0.005 M, pH between 7.0 and 8.0, and incubation at 37 degrees C. Concentrations over 0.01 M, pH values greater than 8.0, and an incubation temperature over 40 degrees C resulted in a gel formation of the specimen. Examination of both 'cold' and 'warm' type antibodies demonstrated that the results obtained by the DTT reagent are in close agreement with those obtained by 2-mercaptoethanol reagents and DEAE Sephadex treatment. Since the procedure is simple and rapid and lacks offensive odour, DTT is recommended for routine use in blood banking for the inactivation of IgM antibodies.

Dithiothreitol↗
PubMed1978

Detection and properties of TSH-binding inhibitor immunoglobulins in patients with Graves' disease and Hashimoto's thyroiditis.

TSH-binding inhibitor immunoglobulins (TBII) have been detected in patients with Graves' disease and Hashimoto's thyroiditis by using the radioreceptor assay of TSH. In untreated Graves' patients, TBII levels correlated well with thyroidal 99mTc uptake at 30 min and the grade of epithelial hyperplasia of thyroid follicles. There were many Graves' patients whose sera contained high TBII levels but no detectable bioassayable thyroid-stimulating activity (LATS), and in these patients, close correlation was observed between serum levels of TBII and bioassayable LATS-protector activity. TBII were detectable in 2 (10%) of 20 patients with Hashimoto's thyroiditis, both of whom were clinically hypothyroid. The serum or IgG fraction from one of them, however, did not contain any significant LATS, LATS-protector, or human thyroid adenylate cyclase-stimulating activity and caused inhibition of adenylate cyclase stimulation by TSH. In that patient, TBII may be acting to block TSH binding to TSH receptors, thus causing TSH unresponsiveness and hypothyroidism.

Adolescent↗