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Biomedical subjects

Y Sakurai

Publications and source records attributed to Y Sakurai.

At least 685 records · Page 38Linked to original sources
PubMed1978

Implication of renal prostaglandin E in urinary sodium excretion.

To investigate the role of renal prostaglandin in the regulation of sodium metabolism, ruinary prostaglandin E excretion, an indicator of renal prostaglandin synthesis, urinary sodium excretion, plasma renin activity and urinary aldosterone excretion were measured in 84 normal subjects and 55 patients with essential hypertension on ad lib intake of sodium. The excretion rates of urinary prostaglandin E were 736.8 +/- 32.2 ng/day in normal subjects and 394.3 +/- 28.7 ng/day in essential hypertensives. The excretion rate was significantly decreased in essential hypertensives (P less than 0.001). A significant positive correlation was found between urinary sodium excretion and urinary prostaglandin E excretion in normal subjects (r = 0.39, P less than 0.001), and in essential hypertensives (r = 0.62, P less than 0.001). There was no correlation between the renin-angiotensin-aldosterone system and urinary prostaglandin E excretion in normal subjects as well as in essential hypertensives. The present data show that renal prostaglandin might be involved in the renal handling of sodium, and prove the possibility that the decrease of renal prostaglandin synthesis is one of the etiological factors in essential hypertension.

Adolescent↗
PubMed1978

[Studies on circadian susceptibility rhythm to haloperidol (author's transl)].

Rats were given haloperidol in a variety of doses and time combinations and the sedation period were then measured. A clear-cut daily fluctuation in the sedative effect was observed, and the pattern of fluctuation differed depending on the dosage. In an attempt to elucidate the mechanism of this phenomenon, haloperidol was administered at two different times between which there was a significant difference in the sedation period. No difference was found. Thus it is presumed that daily fluctuation in the sedative effect of haloperidol may be ascribed not to the daily fluctuation in the levels of absorption, excretion, metabolism, or distribution of this drug, but rather to the daily fluctuation at the level of catecholamine receptors in the brain. There was a daily fluctuation in the antiapomorphine effect of haloperidol in a variety of doses and time combinations, and the pattern of fluctuation almost equaled that of the sedative effects of haloperidol. The daily fluctuation of the sedative effect is probably due to effects of circadian rhythm in brain dopamine receptors.

Animals↗
PubMed1978

Effect of furosemide on urinary kallikrein excretion in patients with essential hypertension.

The effect of furosemide on urinary kallikrein excretion was studied in 10 patients with essential hypertension and 9 normal volunteer subjects. After intravenous administration of furosemide and 2 hours of upright posture, urine volume (UV), urinary sodium (UNaV) and potassium (UKV) excretion, plasma renin activity (PRA), plasma aldosterone concentration (PAC) and urinary kallikrein markedly increased. However, the augmentation of urinary kallikrein in patients with essential hypertension (1.50 +/- 0.19 EU/2 hr) was less remarkable than that in normal subjects (2.33 +/- 0.24 EU/2 hr), although the same degrees of response were observed in PRA and PAC. The increments of UV, UNaV and UKV in patients with essential hypertension were also significantly lower than in normal subjects. Significant positive relations were found between urinary kallikrein and UV or UNaV in both hypertensive and normotensive groups, but there was no such correlation before fursemide administration. It is likely that diuresis and natriuresis induced by furosemide are somehow associated with an increase in urinary kallikrein excretion. Blunted response of urinary kallikrein in essential hypertension may suggest an abnormality in the renal kallikrein-kinin system in this disease.

Adult↗
PubMed1978

Urinary prostaglandin and sodium metabolism in patients with essential hypertension.

Urinary prostaglandin E (PGE) excretion as an indicator of renal PGE, urinary aldosterone excretion, plasma renin activity, urinary sodium excretion, and urinary potassium excretion were measured after sodium depletion in 15 patients with essential hypertension to investigate the interaction between renal PGE and sodium metabolism. Following sodium depletion, urinary PGE excretion decreased, whereas urinary aldosterone excretion and plasma renin activity increased. Significant positive correlations were found between urinary PGE excretion and urinary sodium excretion (r=0.41, p less than 0.01) or urinary sodium excretion-urinary potassium excretion ratio (r = 0.43, p less than 0.005). These results support the hypothesis that the renal PGE may play an important role in the regulation of sodium metabolism and this action of PGE is independent of the renin-aldosterone system.

Adolescent↗
PubMed1978

Effect of spironolactone on urinary excretion of immunoreactive prostaglandin E in essential hypertension and primary aldosteronism.

To determine the effect of aldosterone antagonist on renal prostaglandin E synthesis, the rate of urinary excretion of immunoreactive prostaglandin E was measured radioimmunologically before and during the oral administration of an aldosterone antagonist, spironolactone, in 5 patients with essential hypertension, 3 with primary aldosteronism and 2 with postoperative primary aldosteronism. Spironolactone was administered at an oral dose of 25 mg 4 times daily for about 1 week. In the control state, the rates of urinary prostaglandin E excretion ranged from 151 ng/day to 4,527 ng/day in essential hypertension. The rates were not augmented in primary aldosteronism but decreased after the removal of an aldosterone producing adenoma. No obvious relationship was observed between plasma aldosterone concentration and the rate of urinary prostaglandin E excretion. On the first day of spironolactone administration, the excretion rates of urinary prostaglandin E were markedly increased independently of basal plasma aldosterone level in all cases except one case of essential hypertension. Urinary prostaglandin E excretion was increased with the concominant increase of urinary Na/K ratio in essential hypertension and primary aldosteronism. After the second day, the augmented urinary prostaglandin E excretion was decreased and the changes of urinary prostaglandin E excretion varied from case to case. These results suggest that synthesis of renal prostaglandin E is not mainly regulated by aldosterone in essential hypertension and primary aldosteronism.

Adult↗
PubMed1978

[Postmortem examination of patients with non-surgically treated ruptured aneurysms (author's transl)].

The is no doubt that radical surgery has been successful in preserving the lives of patients with ruptured aneurysms. On the other hand, no matter how successful we have been we cannot and must not forget the patients who died without undergoing surgery. Therefore, we investigated from clinical course, laboratory work, including angiography and autopsy, 38 cases who died during hospitalization in order to elucidate the causes of death in the natural course and to find the possibilities of minnimizing the number of non-operative fatalies. We classified the causes of death into 3 groups: intracranial hemmatomas, brain ischemia due to vasospasm, and aggravation of the general condition. From the study, it was concluded that most of the lives could have been saved, if appropriate diagnosis and treatment had been made as soon as possible after the initial hemorrhage.

Adult↗
PubMed1978

[Oculomotor palsy caused by aneurysms at the internal carotid-posterior communicating artery junction and its prognosis following intracranial surgery (author's transl)].

Sixty-three cases of an aneurysm at the internal carotid-posterior communicating artery junction with aneurysm-induced unilateral eye-lid ptosis, a symptom of the third nerve palsy, were described. 1) The incidence of this palsy in 189 cases of the aneurysm was thirty-three percent. 2) The palsy before the aneurysm rupture was recognized in three cases (5 percent). The onset of this palsy following an aneurysm rupture was most frequent in the first day and in almost half of the patients within two days, but in four cases the palsy appeared three or four weeks after the aneurysm rupture. 3) The size and direction of the growth of the aneurysms in carotid angiograms were compared between palsy and non-palsy groups and there were no significant differences between them. 4) Thirty-one patients who had had a palsy before direct aneurysm surgery were followed one to ten years post-operatively. In twenty-three (74 percent), the unilateral eye-lid ptosis was recovered by the follow-up. In eleven of the twelve cases operated within two weeks after the onset, the palsy was recovered. On the other hand, in seven of eight not-recovered cases there was a delay of more than two weeks before operation.

Blepharoptosis↗