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T Ogihara

Publications and source records attributed to T Ogihara.

At least 847 records · Page 47Linked to original sources
PubMed1983

Combination chemotherapy in retroperitoneal poorly differentiated myxoid liposarcoma: a report of a case.

We describe a case of a 47-year-old man with retroperitoneal poorly differentiated myxoid liposarcoma. The retroperitoneal invasion of the sarcoma caused hydroureter-nephrosis, rectal stenosis and also exaggerated steroid induced diabetes mellitus. A remarkable regression was achieved by systemic combination of chemotherapy with prednisolone, cyclophosphamide, vincristine sulfate and actinomycin D. This combination chemotherapy is worth trying if a patient has inoperable liposarcoma. It can also be used to reduce local recurrence rate after surgical or radiation therapy, or both, against liposarcoma.

Antineoplastic Agents↗
PubMed1983

Vascular effects and metabolism of angiotensins and their metabolites in the isolated perfused rat kidney.

The vascular effects of the injection of angiotensin I (AI), des-Asp1-angiotensin I (des-Asp1-AI), angiotensin II (AII), des-Asp1-angiotensin II ( (2-8)AII) and des-Asp1-Arg2-angiotensin II ( (3-8)AII) have been investigated in an isolated perfused rat kidney model, using a closed circuit system. The apparent half-life of these peptides was measured by AI and AII radioimmunoassays. Des-Asp1-AI is less potent than AI and has a shorter duration of action on perfusion pressure and renal flow. Up to 7.6% of circulating AI and 12.4% of circulating des-Asp1-AI are converted by the kidney to AII, (2-8)AII and other AII immunoreactive materials. This intrarenal conversion entirely explains the vasoconstrictor effects of these two peptides. The vasoconstrictor effects of (2-8)AII is similar to that of AII, but (2-8)AII has a shorter duration of action. At the doses injected, renin secretion is completely inhibited by AII and (2-8)AII, it is partially inhibited by AI, an effect which disappears when converting enzyme is inhibited. Des-Asp1-AI is a less potent inhibitor of renin secretion than AI, and (3-8)AII is devoid of any action on renin secretion. The apparent half-life of AI is 24.3 +/- 1.1 minutes, des-Asp1-AI: 20 to 23 minutes, AII: 19.6 +/- 1.8 minutes, (2-8)AII: 12 to 14.5 minutes and (3-8)AII: 12.5 to 13.5 minutes. Differences in the metabolism of these peptides may contribute to the differences of magnitude and duration of their vascular effects.

Angiotensin I↗
PubMed1983

alpha-Adrenergic blocking action of 1-O-hexadecyl-2-O-acetyl-sn-glycero-3-phosphocholine in rats.

The effect of 1-O-hexadecyl-2-O-acetyl-sn-glycero-3-phosphocholine (HAGPC), a major component of antihypertensive polar renomedullary lipid, on the pressor responses to norepinephrine and angiotensin II was investigated in normal Wistar rats. The pressor activity of norepinephrine (1 microgram/kg of body weight (BW)) and angiotensin II (40 ng/kg BW) were markedly suppressed when these substances were injected immediately after intravenous administration of 80 nmol/kg BW of HAGPC. When HAGPC was infused continuously at a rate of 20 nmol/kg BW/min, pressor responses to bolus injection of graded doses (0.5 to 10 micrograms/kg BW) of norepinephrine were significantly lowered, but pressor responses to 10 to 200 ng/kg BW of angiotensin II were not affected. These observations suggest that HAGPC has alpha-adrenergic blocking activity and does not influence angiotensin II receptors.

Adrenergic alpha-Antagonists↗
PubMed1982

Effect of prostacyclin infusion on active and inactive renin release in the isolated perfused kidney.

The effect of prostacyclin infusion into the renal artery of the isolated perfused hog kidney on the release of active and inactive renin was investigated. Infusion of prostacyclin at a rate of 0.1 microgram/min resulted in a significant increase (p less than 0.01) in active renin and a significant fall (p less than 0.01) in inactive renin. Prostacyclin also increased urinary kallikrein excretion (p less than 0.05). The results indicate that the kidney secretes not only active renin but also inactive renin, and suggest that prostacyclin stimulates the conversion of inactive renin to the active form through the activation of the renal kallikrein system.

Animals↗
PubMed1982

[Urinary epinephrine and norepinephrine excretion in patients with medullary thyroid carcinoma and their relatives].

Medullary thyroid carcinoma can arise as a component of multiple endocrine neoplasia (MEN) syndrome which includes adrenal pheochromocytoma. Familial medullary thyroid carcinoma with no association of other components of MEN syndrome is also reported. Epinephrine and norepinephrine excreted in 24 hour urine and/or randomly voided urine were measured for screening of pheochromocytoma in patients with medullary thyroid carcinoma of either the hereditary or sporadic type and in their relatives. Six patients with clinical symptoms and signs suggesting pheochromocytoma had a markedly increased epinephrine and epinephrine/norepinephrine (E/N) ratio and a less dominant increase of norepinephrine in 24 hour urine. The diagnosis of pheochromocytoma was proved later at surgery. Among 10 patients with hereditary medullary thyroid carcinoma without any clinical symptoms and signs for pheochromocytoma, 6 patients had increased epinephrine and E/N ratio and normal norepinephrine, and the remaining 4 had normal epinephrine, norepinephrine and E/N ratio in 24 hour urine. The six patients with increased epinephrine and E/N ratios were regarded as having latent adrenal medullary hyperfunction. The mean ages of the 6 patients with proved pheochromocytoma, the 6 with latent adrenal medullary hyperfunction and the 4 with normal urinary catecholamine fractions were 51.3, 42.5 and 28.5 years, respectively. At least one patient in each family with hereditary medullary thyroid carcinoma had proved pheochromocytoma or latent adrenal medullary hyperfunction, leaving no family with hereditary medullary thyroid carcinoma only. Urinary epinephrine, norepinephrine and E/N ratios in patients with sporadic medullary thyroid carcinoma and relatives of patients with medullary thyroid carcinoma were not higher than those in normal subjects. Measurements of epinephrine and norepinephrine in randomly voided urine are also a valuable and convenient method for the screening of pheochromocytoma in patients with medullary thyroid carcinoma and their relatives, because they gave results similar to those in 24 hour urine.

Adolescent↗
PubMed1982

[Plasma norepinephrine variation with dietary sodium intake in normotensive subjects and patients with essential hypertension].

Sympathetic nervous system may play an important role in the pathogenesis of essential hypertension. The present study was undertaken to evaluate the interaction between sodium intake and sympathetic nervous activity in the patients with essential hypertension. Plasma and urinary catecholamines (CA) were measured in 38 hypertensive patients (WHO 1-2 stage) and 24 age-matched normal subjects on regular (urinary sodium excretion (UNaV): 133 +/- 8 mEq/day; mean +/- SEM), high (UNaV 317 +/- 90 mEq/day), and low (UNaV 67 +/- 28 mEq/day) sodium diets for each 5 days at random. CA were analyzed by THI methods after HPLC separation. Twenty-four hour urinary norepinephrine (NE), epinephrine (E), and electrolytes (Na+, K+) excretion on the 5th day of each regimen were determined. In the 6th day morning supine and 5 min upright plasma NE(PNE), plasma E (PE), and plasma renin activity were determined after blood pressure and pulse rate measurement. The results were also analyzed according to the difference between salt-sensitive and non-salt-sensitive type of hypertensive patients. Plasma NE was 1.1 +/- 0.4 p mol/ml (supine), 1.5 +/- 0.4 p mol/ml (upright) in normotensive subjects and 1.8 +/- 1.1 p mol/ml (supine), 2.5 +/- 1.1 p mol/ml (upright) in the patients with essential hypertension, 24 hr urinary NE excretion were 116 +/- 54 micrograms/day in normotensive subjects and 138 +/- 88 micrograms/day in the patients with essential hypertension on regular sodium intake. Mean plasma NE levels in patients with essential hypertension were always higher than those in normotensive subjects on any sodium diets. Plasma NE and urinary NE were significantly reduced by high sodium intake and increased by low sodium intake in both normotensive subjects and the patients with essential hypertension. Percentile decrease in PNE when the diet was changed from low sodium to high sodium was much greater in normotensive subjects than the patients with essential hypertension. These tendency was observed in both salt-sensitive and non-salt-sensitive hypertensive patients. However, PNE in non-salt-sensitive hypertensive subjects tended to be higher than those in salt-sensitive hypertensive subjects. These results suggest that abnormal relationship between sodium intake and sympathetic nervous system may play an important role in the pathogenesis of essential hypertension.

Adult↗
PubMed1982

Direct renal action of captopril (SQ 14225): dissociation of natriuretic and vascular actions in isolated perfused rat kidney.

Direct effects of captopril on renal function were examined in isolated perfused rat kidneys. Captopril induced a significant increase in urinary volume and urinary sodium excretion (1.8- and 1.7-fold, respectively; both p less than 0.005), whereas urinary potassium excretion and renovascular resistance were not significantly changed. Because the perfusion medium lacks angiotensinogen, kininogen and aldosterone, the natriuretic action in perfused kidneys may not be related to its inhibitory action on angiotensin I converting enzyme or kininase II. Because the natriuresis was not accompanied by changes in renovascular resistance, it is suggested that captopril possesses a direct natriuretic action and that this property may partly explain the mechanism of captopril-induced natriuresis clinically observed.

Animals↗
PubMed1982

Effect of three angiotensin II antagonists, [Sar1, Thr8]-, [Sar1, Ile8]- and [Sar1, Ala8]angiotensin II on blood pressure and endocrine factors in normal subjects.

The biological effects of 1-Sarcosine, 8-Threonine angiotensin II ([Sar1, Thr8]ANG II) on blood pressure, plasma aldosterone concentration (PAC) and plasma renin activity (PRA) were investigated in six normal subjects on an unrestricted diet, and compared with those of 1-Sarcosine, 8-Isoleucine ANG II ([Sar1, Ile8]ANG II) and 1-Sarcosine, 8-Alanine ANG II ([Sar1, Ala8]ANG II). All three ANG II analogues (AIIA) showed agonistic pressor activity, that of [Sar1, Ile8]ANG II being greater than that of [Sar1, Thr8]ANG II or [Sar1, Ala8]ANG II. The antagonistic effect of [Sar1, Thr8]ANG II on blood pressure was less than [Sar1, I1e8]ANG II or [Sar1, Ala8]ANG II. Both [Sar1, Ile8]ANG II and [Sar1, Ala8]ANG II increased PAC and blocked the steroidogenic action of ANG II, while [Sar1, Thr8]ANG II showed little effect on PAC. All three AIIA caused similar suppression of PRA and showed no inhibitory effect on the decrease in PRA produced by ANG II. These results indicate that [Sar1, Thr8]ANG II is an AIIA with weak agonistic pressor action and that it has vascular selective properties. It is also suggested that ANG II receptors in a variety of target organs are heterogeneous.

1-Sarcosine-8-Isoleucine Angiotensin II↗
PubMed1982

Medullary carcinoma of the thyroid with ectopic ACTH syndrome.

An autopsied patient with medullary carcinoma of the thyroid and ectopic ACTH syndrome is reported. A microadenoma of pancreatic islet coexisted in this case, which is assumed to be of D cell origin. Immunohistochemical study revealed decreased number of pituitary ACTH cells. Some of them showed Crooke's degeneration. Hormone assay study of tumor tissue and plasma disclosed abnormal ACTH, beta-MSH as well as calcitonin. Somatostatin and Substance P were also demonstrated in tissue. Histologically the tumor showed solid alveolar pattern with a minor part consisting of small cell variant and this histologic variation is discussed.

ACTH Syndrome, Ectopic↗