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Biomedical subjects

Y Saku

Publications and source records attributed to Y Saku.

26 records · Page 2Linked to original sources
PubMed1992

Effects of angiotensin and atrial natriuretic peptide on the cerebral circulation.

The purpose of the present study was to determine effects of angiotensin (ANG) II on the cerebral circulation. We measured the pial artery pressure (PAP) and CBF in anesthetized rabbits. ANG II (5 micrograms/min) was infused into each carotid artery, and systemic arterial pressure was maintained constant. During infusion of ANG II, there was a significant increase in CBF and fall of PAP, with no change in the large artery resistance (LAR) and a significant decrease in the small vessel resistance (SVR). To investigate whether prostaglandin modulated the ANG II-induced increase in CBF, indomethacin was administered (10 mg/kg i.v.) in another group of animals. Indomethacin itself reduced PAP and increased LAR significantly without changing CBF or SVR. Indomethacin did not attenuate the effects of ANG II on the cerebral circulation. The CMRO2 was assessed during ANG II intracarotid infusion in another group of rabbits. CMRO2 did not change during infusion of ANG II. We also investigated effects of alpha-atrial natriuretic peptide (ANP) on the cerebral circulation. Infusion of ANP (1 microgram/min) decreased LAR by 28% (p less than 0.05) without altering SVR. Administration of ANG II after ANP tended to reduce LAR (p greater than 0.05), with a significant decrease in SVR. The results of the present study suggest that high doses of ANG II can produce cerebral vasodilatation, particularly of small vessels. Blood-borne ANP dilated the large arteries of the cerebral circulation selectively and neither interfered with nor reversed the ANG II-induced increase in CBF.

Angiotensin II↗
PubMed1991

Acquired C1 inhibitor deficiency associated with systemic lupus erythematosus affecting the central nervous system.

A 22 year old woman with systemic lupus erythematosus affecting the central nervous system had acquired C1 inhibitor deficiency. She was admitted for treatment of psychotic behaviour, but showed no signs of angioedema. The serum complement profile of the patient showed normal C3 concentration and a depletion of C4, C2, C1 inhibitor, and C1q. Her parents had normal complement profiles. An extremely reduced C4 concentration may lead to involvement of the central nervous system in systemic lupus erythematosus.

Adult↗
PubMed1990

Hemorrhagic infarct induced by arterial hypertension in cat brain following middle cerebral artery occlusion.

The purpose of this experiment was to determine whether an acute rise in brain perfusion pressure causes hemorrhagic transformation of an infarct without a reopening of the occluded artery. We raised the blood pressure of 22 cats by aortic obstruction 5-24 hours after transorbital middle cerebral artery clipping; hemorrhagic infarcts were induced in 11. Mean arterial blood pressure increased by 57.2 +/- 16.9 mm Hg (mean +/- SD) in the 11 cats with hemorrhagic infarcts and by 40.4 +/- 16.9 mm Hg in the 11 remaining cats with pale brain infarcts (p less than 0.05). Induction of hypertension increased regional cerebral blood flow in the ischemic cortical gray matter more in three cats with hemorrhagic infarcts than in seven with pale infarcts. Our results demonstrate that hemorrhagic transformation of an infarct can be induced by a rapid increase in perfusion pressure to brain tissue already exposed to focal ischemia. We also suggest that the restoration of blood flow through leptomeningeal collaterals plays an important role in the pathogenesis of hemorrhagic infarction in cases without reopening of occluded arteries.

Animals↗
PubMed1990

[A case of left internal capsular infarction with auditory hallucination and peculiar amnesia and dysgraphia].

A 46-year-old businessman suddenly became to behave curiously on the morning, September 1, 1988. He forgot how to go through an automatic ticket gate, which he used every day. In his company, he also forgot how to open the cash box, and he wrote a meaningless report for his business. From the night on that day, he had experienced auditory hallucination in which whispering words of some criticism to his performance for a few days. On the next day, he was admitted to a psychiatric hospital because he was suggested to have schizophrenia. By day 6 after the onset, his curious symptoms completely disappeared. However, slight verbal memory disturbance and cognitive dysfunction still remained. Because the brain CT on day 6 showed a small localized subcortical infarction in the left hemisphere he was transferred to our clinic on day 20 to elucidate the relation between the abnormal behavior and the infarction. His blood pressure was 116/64 mmHg and pulse was regular 63/min. He was clear and did not have any neurological deficit. He kept his episodic memory regarding the events at the onset and could almost recall them precisely. Results of standard blood tests, electrocardiogram, ultrasound cardiogram, electroencephalogram as well as cerebral angiography were normal. Computed tomography and magnetic resonance imaging showed an infarcted lesion in the genu of the left caudate nucleus, adjacent to the anterior part of the thalamus.(ABSTRACT TRUNCATED AT 250 WORDS)

Agraphia↗
PubMed1989

Hemorrhagic infarct of the brain without a reopening of the occluded arteries in cardioembolic stroke.

We examined the brains of 14 patients (four men and 10 women, mean age 68.9 years) who died from brain herniation after cardioembolic stroke with persistent occlusion of the internal carotid-middle cerebral arterial axis. Our examination showed hemorrhagic infarct in seven patients and pale infarct in the other seven, contradicting the commonly proposed pathophysiologic mechanism for the development of hemorrhagic infarct that the opening of previously occluded vessels makes an infarct hemorrhagic. Analysis of blood pressure after stroke revealed one or more surges of arterial hypertension or rapid rise of blood pressure in patients with hemorrhagic infarct without a reopening of the occluded artery. Such arterial hypertension was not always present in patients with pale infarct. Hemorrhage into an infarct with persisting occlusion of the proximal artery is assumed to occur when the involved blood vessels are exposed to the force of arterial blood pressure from the leptomeningeal collaterals. This occurs when arterial blood pressure rises after stroke in the presence of efficient leptomeningeal collaterals and before occlusion of these collaterals by a swollen cerebral hemisphere containing a large infarct.

Adult↗
PubMed1989

[Disturbances of fluid and electrolyte balance in patients with acute stroke].

Serum sodium and potassium concentrations were measured in 196 patients with acute cerebral infarction and 56 with cerebral hemorrhage. All patients were admitted within 7 days of onset and the data within 2 weeks of admission were recorded. The incidences of hypernatremia (serum Na greater than or equal to 149 mEq/l), hyponatremia (less than or equal to 134 mEq/l), hyperkalemia (serum K greater than or equal to 4.8 mEq/l) and hypokalemia (less than or equal to 3.2 mEq/l) were higher in patients with hemorrhage (18, 7, 13 and 14%, respectively) than infarction (4.5, 4.5, 11 and 6%, respectively). The incidences of hypernatremia and hyponatremia in infarction were higher in those who had cortical lesions than in those who had lesions in the basal ganglia or infratentorium. In cerebral hemorrhage, the incidence of hypernatremia was the highest in those with brain stem lesion. Hypernatremia was found in 27% of large sized hematoma, being significantly higher than that of those with medium (16%) or small (1%) hematoma. A similar tendency was also observed in hyponatremia and hyperkalemia. In elderly patients, electrolyte disturbances were more common than in young or middle-aged patients. Renal insufficiency and diabetes mellitus were frequent complications in stroke patients with hypernatremia (42 and 32%, respectively), of which 57% died within one month of admission.

Acute Disease↗