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Biomedical subjects

Y Tabuchi

Publications and source records attributed to Y Tabuchi.

At least 127 records · Page 7Linked to original sources
PubMed1985

Renal vein prostaglandins in renovascular hypertensive patients.

To investigate the role of intrarenal prostaglandins in the pathophysiology of renovascular hypertension, we measured bilateral renal vein prostaglandins (PGE2, 6-keto-PGF1 alpha) and plasma renin activity (PRA) of nine patients with renovascular hypertension caused by fibromuscular dysplasia. Both PGE2 and PRA on the stenotic side were significantly higher than those on the non-stenotic side. The difference in 6-keto-PGF1 alpha levels between the stenotic and the non-stenotic sides was not significant. PGE2 ratio of the stenotic and the non-stenotic sides was significantly correlated with PRA ratio of the stenotic and contralateral sides. These results suggest that renal PGE2 plays an important role in the maintenance of renal blood flow through modulation against vasoconstriction in the renal vasculature and that renal PGE2 may be closely associated with renal renin secretion in the renovascular hypertension.

6-Ketoprostaglandin F1 alpha↗
PubMed1985

Hypotensive mechanism of acetyl glyceryl ether phosphorylcholine (AGEPC) in dogs. Effects on hemodynamics and humoral factors.

One-O-hexadecyl-2-O-acetyl-sn-glycero-3-phosphorylcholine (AGEPC) was intravenously administered to anesthetized dogs to study the effects on hemodynamics and several endocrine factors. The effect of AGEPC on local blood flow was also studied by direct intra-arterial injection. Following intravenous injection, blood pressure and cardiac output decreased significantly (p less than 0.001). Changes in total peripheral resistance (TPR) and heart rate were biphasic. TPR increased significantly (p less than 0.01) after an initial slight reduction. Heart rate decreased significantly (p less than 0.01) with only a transient slight elevation. Femoral blood flow was increased (p less than 0.001) by intraarterial injection and decreased (p less than 0.05) by intravenous administration. Plasma norepinephrine (p less than 0.001), epinephrine (p less than 0.01), thromboxane B2 (p less than 0.001), 6-0-PGF1 alpha (p less than 0.01), aldosterone (p less than 0.001) and cortisol (p less than 0.001) were elevated, but plasma renin activity did not change. These results suggest that the hypotensive mechanism of AGEPC is due to both cardiosuppression and vasodilation. AGEPC increased plasma catecholamines, thromboxane A2, PGI2, aldosterone and cortisol which, in turn, may modify hemodynamics.

Aldosterone↗
PubMed1985

Sensitive assay and kinetic property of urinary inhibitor of Na+, K+-ATPase in sodium-loaded patients with essential hypertension.

A sensitive assay method to evaluate the inhibitor of Na+, K+-ATPase in human urine was developed by measuring the inorganic phosphate liberated from ATP in vitro using Na+, K+-ATPase from porcine cerebral cortex. Ouabain inhibited the Na+, K+-ATPase by competing with the potassium ion (an apparent Ki = 2.6 +/- 0.89 X 10(-8) M, n = 8) under the condition of 100 mM NaCl, 4.5 mM MgSO4 and 0.56 mM ATP. The apparent Km value of KCl was 0.4 mM. Factors inhibiting Na+, K+-ATPase were detected in the post-salt fraction on Sephadex G-15 chromatography following the ethanol extraction of lyophilized fresh urine of sodium loaded human subjects (300 meq Na+/day, for 4 days) with essential hypertension. Two active fractions around the 400 daltons following salt were eluted on Sephadex G-15 chromatography. The slower eluted factor competed kinetically with potassium ion, but the inhibitory activity was lost within two days during storage at 4 degrees C. The faster-eluted inhibitor lost its activity within a day. These results indicate that the unstable inhibiting factors of Na+, K+-ATPase exist in human urine and one of these factors inhibits ouabain sensitive Na+, K+-ATPase by binding to the potassium binding site (or very close to it), which exists at the outer surface of the cell membrane of this enzyme.

Binding Sites↗
PubMed1985

Involvement of endogenous prostaglandins in salt-induced hypertension.

Insufficient production of prostaglandins, which are possible antihypertensive agents, may be a pathogenetic factor in hypertensive patients on salt loading. We compared the levels of plasma PGE2, plasma renin activity (PRA) and urinary 6-keto-PGF1 alpha (6-O-PGF1 alpha), a major stable metabolite of PGI2, on day 5 of salt deprivation and also on day 5 of subsequent salt loading in 17 patients with essential hypertension. Salt loading decreased plasma PGE2, and slightly increased urinary 6-O-PGF1 alpha. On salt loading, a positive correlation was found between the levels of plasma PGE2 and urinary sodium excretion. On salt deprivation, PRA was significantly correlated with plasma PGE2. The per cent change in mean blood pressure on changing from salt restriction to salt loading was inversely correlated with the per cent change in PGE2, and positively correlated with the per cent change in 6-O-PGF1 alpha excretion. These findings suggest that on salt restriction, PGE2 is involved in the renin-angiotension system and that on salt loading, PGE2 is produced to compensate for the excessive sodium. The finding that PGE2 production was attenuated progressively as the mean blood pressure increased on salt loading in patients with essential hypertension suggests that insufficient compensatory PGE2 production is a pathogenetic factor in salt-induced hypertensive patients. In contrast, PGI2 may be produced adaptively to regulate blood pressure during changes in salt balance.

Adult↗
PubMed1985

Hypotensive mechanism of potassium supplementation in salt-loaded patients with essential hypertension.

To investigate the hypotensive mechanism of potassium supplementation, blood pressure responses and hormonal changes were measured during KCl supplementation in salt-loaded patients with essential hypertension. Ten patients with essential hypertension were placed on low sodium intake, high sodium intake, and high sodium intake with KCl supplementation. Blood pressure increased during NaCl loading and decreased during KCl supplementation. The levels of urinary sodium and fractional sodium excretion increased after KCl supplementation. Reduction in blood pressure after KCl supplementation was correlated with an increase in blood pressure after NaCl supplementation, i.e., potassium sensitivity and sodium sensitivity were correlated. Plasma PGE2 and norepinephrine increased after KCl loading. Increases in plasma PGE2 were correlated with a reduction of blood pressure by KCl. These results indicate that natriuresis and hypotensive action of KCl are associated with increased PGE2 production, and the sympathetic nerve activity suggests a compensatory increase for the decrease in blood pressure.

Blood Pressure↗
PubMed1984

Synergic effects of kallikrein-kinin and prostaglandins on renin release on infusion of isolated hog kidney with aldosterone.

The effects of infusion of a large amount of aldosterone into the renal artery of isolated perfused hog kidney on the release of renin, prostaglandins (PG) and kinin and the excretion of urinary kallikrein were investigated. Infusion of aldosterone at a rate of 100 ng/min (100 to 800 ng/ml of perfusate) resulted in significant releases of renin, PG (PGE2 , 6-0-PGF1 alpha), and kinin and increase in urinary kallikrein. Infusion of aldosterone and an inhibitor of kallikrein, aprotinin, decreased the releases of renin, PG and kinin and infusion of aldosterone with indomethacin decreased the release of PG but increased that of kinin and urinary kallikrein without significant change in renin releases. These findings suggest that the release of renin by aldosterone may result from synergic effects of renal PG and the kallikrein -kinin system.

Aldosterone↗
PubMed1984

Familial amyotrophic lateral sclerosis: features of multisystem degeneration.

Two sibling cases of familial amyotrophic lateral sclerosis (ALS) revealed degeneration usually associated with other systemic degenerative disorders. The changes in the 41-year-old sister were compatible with those reported in other familial ALS cases affecting the upper and lower motor neurons, posterior columns, and spinocerebellar tracts. The 45-year-old sister revealed more wide-spread degenerative changes involving not only motor neuron systems, but also proprioceptive, general somatic afferent and spinocerebellar afferent systems. Intracytoplasmic hyaline inclusions were observed in the oculomotor nuclei. Clinical manifestations of urinary disturbance and oculomotor impairment seldom seen in sporadic ALS were interpreted to be due to the unusual distribution of the morbid process. These pathologic findings suggest that familial ALS may be a multisystemic degenerative disorder, frequently involving the spinocerebellar tracts, but occasionally involving other systems as well.

Adult↗
PubMed1984

PGE2, 6-O-PGF1 alpha and sodium balance in essential hypertensive patients.

Insufficient production of PGE2 has been thought to be a pathogenic factor in hypertensive patients on salt loading. However, the inter-relationship between PGE2 and sodium is still uncertain. Essential hypertensive patients participated in a salt balance study for two consecutive 5-day periods of restriction and repletion. Urinary PGE2 increased on the second or the third day of salt balance, but subsequently declined and remained stable. On the fifth day, PGE2 excretion on salt loading was lower than on salt deprivation. Changes in urinary PGE2 during salt loading paralleled those in urinary sodium excretion. Urinary 6-O-PGF1 alpha did not show any significant change. On salt deprivation PGE2 excretion was correlated with plasma renin activity (PRA). These results suggest the possibility that PGE2 is involved in sodium excretion on salt loading and that on salt depletion PGE2 excretion increases in association with activation of the renin-angiotensin axis.

6-Ketoprostaglandin F1 alpha↗
PubMed1984

[A clinicopathological study on hematogenous recurrence of colo-rectal cancer--with special reference to prediction and prevention of the recurrence].

Hematogenous recurrence was investigated in 325 cases of colo-rectal cancer. Hematogenous recurrence was confirmed in 34 cases including 25 liver, 5 lung, 2 bone, one brain and one skin recurrence. Most of the cases (28 cases, 82.4%) revealed a single or multiple hematogenous recurrences without showing additional other types of recurrence. Histological examination of cancer lesions indicated that patients with the findings consisting of moderate and/or high grade of vein invasion (v2-3), subserosal and extramural vein invasion with node metastasis showed high recurrent rate. One and two year survival rate of the patients treated with MF-MF' adjuvant chemotherapy was greater those the patients with F-F' chemotherapy or those without chemotherapy. However, 3-, 4- and 5- year survival rate did not show significant difference among 3 therapeutic groups. The analysis of survival curves also indicated no significant difference among 3 therapeutic groups. These results may suggest that hematogenous recurrence is derived from pre- and/or intra-operative micrometastasis or transplantation of cancer cells, that patients with the above mentioned histological evidence must be clinically treated as a high risk group for recurrence and that MF-MF' adjuvant chemotherapy can be effective in lowering the recurrence rate during the first one or two years after operation.

Antineoplastic Agents↗
PubMed1984

[A clinicopathological study on carcinoma of the gastric stump, with special reference to mucosal change].

Ten carcinomas of the gastric stump reconstructed by Billroth I (one case) and Billroth II (9 cases) methods were treated an average of 20 (range: 7-46) years after partial gastrectomy. Because of highly advanced carcinoma, total gastrectomy with resection of invaded organs was performed. The 5-year survival rate was 33%, and was not different from that in patients with carcinoma of the cardia. Thus, the prognosis of gastric stump carcinoma was not poor if extended radical operation was carried out. The mucosa showed severe atrophic gastritis with intestinal metaplasia or atrophic and hypertrophic gastritis in patients with carcinoma. However, the mucosa was hyperplasia of the glands in almost all patients with stomal ulcer. Thus, our findings suggest that atrophic change with intestinalization plays a role in gastric carcinogenesis.

Adenocarcinoma↗
PubMed1983

Effect of captopril on renal vascular resistance, renin, prostaglandins and kinin in the isolated perfused kidney.

Vasodilatory and natriuretic effects of captopril were studied in the isolated hog kidney perfused with modified Krebs-Ringer solution. Renal arterial infusion of captopril caused increases in releases of renin, prostaglandins (PGE2, 6-keto-PGF1 alpha and PGF2 alpha) and kinin, and was accompanied by a decrease in the renal vascular resistance and an increase in urinary sodium excretion. Indomethacin administered with captopril diminished the saluretic effect of captopril and evoked an increase in kinin, but was associated with a marked decrease in prostaglandin and renin releases, while renal vascular resistance remained decreased. Indomethacin alone did not alter vascular resistance and kinin; however, renin and prostaglandin releases were decreased. Aprotinin administered with captopril showed a decrease in releases of prostaglandins, renin and kinin without any change in vascular resistance. These results suggest that increased release of kinin induced by captopril contributes to a reduction in renal vascular resistance. Increased prostaglandin release after captopril administration may be caused by an increase in kinin without direct involvement of captopril in prostaglandin synthesis. Renal prostaglandins may enhance sodium excretion and mediate renin secretion in captopril perfusion.

Animals↗
PubMed1983

The diagnostic significance of large action potentials in myopathy.

Electromyographic and histopathological studies were performed on 112 skeletal muscles in 101 subjects with myopathy. The diagnostic significance of large action potentials (LAPs) in myopathy was studied. LAPs were defined as those action potentials with a duration of over 13 ms and an amplitude of over 3 mV (peak to peak). The following results were obtained: Most muscles with LAPs showed the grouped atrophy of small fibers of neuropathic change in addition to myopathic findings. Even in myopathy most LAPs reflected neuropathic change, except in thyrotoxic myopathy. LAPs were not related to an increase of connective tissue increasing the impedance in volume conduction of the action potentials. LAPs were frequently seen in: progressive muscular dystrophy of limb-girdle type; scapuloperoneal dystrophy; distal myopathy; oculopharyngeal dystrophy; myotonic dystrophy; polymyositis; and thyrotoxic myopathy. Other types of myopathy had few LAPs. There were two types of progressive muscular dystrophy. One had LAPs frequently and the other, rarely. In myotonic dystrophy the muscles with LAPs showed scattered small angular fibers, possibly indicating neurogenic changes. Interstitial myositis had LAPs more frequently than parenchymatous polymyositis. The chronic phase of polymyositis had LAPs more frequently than the acute or subacute phases. In thyrotoxic myopathy the muscles with LAPs rarely showed definite neuropathic change histopathologically. Therefore, LAPs in thyrotoxic myopathy may not indicate denervation.

Action Potentials↗