Search PubMed⌕ Search

Biomedical subjects

T Omae

Publications and source records attributed to T Omae.

At least 127 records · Page 7Linked to original sources

Enhanced blood pressure response to regular daily stress in urban hypertensive men.

Twenty-eight urban untreated hypertensive men (mean age: 54 years; systolic (SBP)/diastolic (DBP) blood pressure at clinic: 148/96 mmHg] and 26 age- and sex-matched normal controls (54 years, 118/78 mmHg) were examined during normal daily activities by ambulatory blood pressure monitoring. When compared with home blood pressures, clinic blood pressures were 8/10% (SBP/DBP) higher in the hypertensives, but 1/3% lower in the normotensives. The values were significantly different for both groups (P less than 0.01 for SBP; P less than 0.001 for DBP). In contrast, the blood pressures fell in a similar manner in both groups during sleep. On working days, the blood pressures during work were 10/9% higher than the corresponding home blood pressures in the hypertensives and only 3/3% higher in the normotensives. These differences were significant (P less than 0.01 for both SBP and DBP). The results show that the blood pressures of hypertensives were hyperreactive to casual daily stress. In the normotensives, left ventricular wall thickness determined by echocardiography was correlated significantly with the blood pressures during work (r = 0.5, P less than 0.05 for SBP and DBP) and at home (r = 0.4, P less than 0.05 for SBP).

Adult↗

Causes of death in the elderly and their changing pattern in Hisayama, a Japanese community. Results from a long-term and autopsy-based study.

The causes of death for the elderly were prospectively studied in Hisayama, Japan, a rural community. We compared 1,621 subjects, aged 40 years or over, recruited in 1961, and 2,053 subjects recruited in 1974. Each cohort was studied in a follow-up that lasted 10 years; they had autopsy rates of 82.1% and 86.1% during each 10-year period, respectively. The most common causes of death for those aged 70 years or over were cerebrovascular disease, malignant neoplasms, and pneumonia. Deaths due to cerebrovascular disease tended to decrease in the recent cohort, but the proportion of decline was more prominent in cases aged 40 to 69 years. There was a sex difference in the changing pattern of mortality from heart diseases including ischemic heart disease. Deaths by both heart diseases and ischemic heart disease increased in the more recent cohort of aged women, whereas they decreased in the aged men. Pneumonia was an important cause of death for the elderly in both cohorts. Deaths due to "senility" were rare, being only 1% of the deceased aged 70 or over. With prolonged lifespan, especially for women, the impact of atherosclerosis and its related disorders on the recent Japanese aged population appears to have increased.

Adult↗

Circadian variations of urinary dopamine, norepinephrine, epinephrine and sodium in normotensive and hypertensive subjects.

Under standardized conditions, we determined circadian urinary excretion of sodium (Na) and free dopamine (DA), norepinephrine (NE) and epinephrine (E) in 20 normotensive, 20 borderline hypertensive and 10 mild hypertensive middle-aged men. The 24-hour excretions of water, Na, DA, NE and E were comparable between the normotensives and the hypertensives. In the total study population, these parameters showed significant time-related changes: high excretion during the daytime and low excretion in the night. The circadian variations of urinary DA, NE and E were similar among the 3 groups. The circadian curve of urinary DA was similar to those of Na and water excretion. In the total study population, 24-hour water and Na excretion correlated positively with urinary DA, but not with NE or E. These results suggest that endogenous DA may play a role in the circadian variation of water and sodium metabolism. The circadian excretion of urinary catecholamines may not be altered in middle-aged subjects with borderline or mild hypertension.

Age Factors↗

Predisposing factors of recurrent embolization in cardiogenic cerebral embolism.

To elucidate the pathophysiology of intracardiac thrombus formation, serial two-dimensional echocardiographic examinations were performed on 30 consecutive patients with acute cardiogenic cerebral embolism in parallel with measurement of hematocrit and plasma levels of antithrombin III. The data from groups of patients with and without newly formed or enlarged thrombi were compared. Intracardiac thrombi were detected in eight of the 30 patients (27%), four at admission and four after admission. Enlargement of the thrombus was observed in four, and systemic embolization recurred in three of the eight. Antithrombin III levels already were low at admission in patients who later developed thrombi or had enlarged thrombi on serial examinations. When the development or enlargement of an intracardiac thrombus was detected by echocardiography, the diameter of the inferior vena cava was found to be reduced. At the same time, a decrease in antithrombin III and an increase in hematocrit were demonstrated. Intracardiac thrombi are frequently detected by repeated echocardiographic examination in patients with cerebral embolism. Dehydration seems to accelerate thrombus formation that is reflected by a decrease in antithrombin III. A low antithrombin III level at admission and/or a decrease in antithrombin III after admission may indicate the possible recurrence of embolism.

Antithrombin III↗

A comparison of lisinopril with enalapril by monitoring plasma angiotensin II levels in humans.

The present study was designed to examine and compare the acute effects of lisinopril (20 mg) and enalapril (10 mg) after a single oral administration on the inhibition of the renin-angiotensin system (RAS) in eight normal subjects. Serum concentration of lisinopril and enalaprilat, an active metabolite of enalapril, reached the respective maximal levels at 6 and 4 hr after administration of the drugs. At 24 hr, the serum concentration of lisinopril was higher than that of enalapril; thus the rate of disappearance of lisinopril was retarded, in comparison to that of enalapril. The reduction of serum angiotensin I converting enzyme (ACE) activity was consistent with the pattern of increase of concentration of the drugs in the serum. However, with these two drugs, the concentration of plasma ANG II was decreased in a similar manner, and it returned to the pretreatment level within 24 hr. Thus, there was no significant difference in ANG II levels throughout the 24 hr-study between the lisinopril and enalapril treatment. The results indicate that a single administration of 20 mg lisinopril and 10 mg enalapril show similar potency for lowering the circulating ANG II level, although lisinopril exerts a more sustained inhibition of serum ACE activity. The measurement of ANG II provides useful informations for evaluating the efficacy of ACE inhibitors for the inhibition of circulatory RAS.

Administration, Oral↗

[Electromyographic study on motor skill in chewing movement. A new concept on relating electromyographic analysis to chewing movements].

This article was aimed to propose a new concept on evaluating electromyographic activities of masticatory muscles during chewing movements viewed from the standpoint of motor skill. Correlation coefficients between the ratio of lateral distance to ten vertical level set at 0.5 mm to 5.0 mm with 0.5 mm step from the end of closing phase and activities of bilateral masseter, anterior and posterior temporalis in each chewing stroke were evaluated using raisin, peanut, soft and hard testing gum in five subjects. Habitual chewing side always demonstrated less numbers of subjects who showed high correlation coefficients especially in the case of soft testing gum.

Chewing Gum↗

Changing pattern of cardiovascular disease in the Japanese population in relation to hypertension control programs.

The changing pattern of cardiovascular disease during the last 30 years in Japan is described. The most striking change was a reduction in deaths caused by hypertensive cerebral hemorrhage. There was no increase in ischemic heart disease in the rural area studied but such a trend was shown in the urban area. A change in risk factors for cardiovascular disease, reduction in blood pressure, and increase in serum cholesterol were more marked in the rural than the urban area. Institution of a hypertension control program and marked changes in lifestyle, including diet, could explain the relatively rapid change in the frequency and the type of cardiovascular disease, particularly cerebral stroke. The prevention of atherosclerotic complications such as cerebral infarction and ischemic heart disease is becoming a more important task in preventive cardiology.

Cardiovascular Diseases↗

Accuracy of diagnosis on death certificates for underlying causes of death in a long-term autopsy-based population study in Hisayama, Japan; with special reference to cardiovascular diseases.

Major categorical diagnosis by International Classification of Diseases and type-specific diagnosis for cardiovascular diseases in death certificates were compared to the diagnosis made at autopsy in 864 consecutive autopsy cases aged 20 or over, among the Japanese residents in Hisayama town. Cerebral stroke was correctly diagnosed in 84%, malignant neoplasms in 78% and cardiac disease in 66%. Cerebral stroke and cardiac disease tended to be overdiagnosed, while malignant neoplasms were underdiagnosed. The validation of certified diagnosis was less reliable in the aged population, and in type-specific diagnosis of cardiovascular diseases. Cerebral hemorrhage with false negative or false positive diagnoses was usually classified into type unspecified stroke or different categories of cerebral stroke, while those misdiagnosed as cases of cerebral infarction frequently had no significant lesions in the autopsied brain. Finally, the relationship between the validation of diagnosis on the death certificates and the secular trend in cardiovascular disease in the Japanese vital statistics was discussed.

Adult↗

Removal of intracellular waste products by hemofiltration.

Because the total amount of waste products removed by hemofiltration can be measured exactly, it was divided into two components, that removed from the extracellular compartment and that removed from the intracellular compartment, using inulin as a marker for extracellular fluid in five uremic patients treated with hemofiltration in the postdilution mode. The amount removed from the extracellular compartment as a proportion to the total amount removed from the whole body by hemofiltration was 86.5% +/- 10.6% for guanidinosuccinic acid, 69.1% +/- 15.6% for sodium, 59.4% +/- 3.3% for uric acid, 56.4% +/- 2.1% for inorganic phosphate, 45.6% +/- 5.3% for creatinine, 43.1% +/- 7.2% for potassium, 42.9% +/- 3.1% for guanidinoacetic acid, 42.5% +/- 7.5% for methylguanidine, 37.2% +/- 8.4% for chloride, 36.3% +/- 2.8% for urea, and 6.9% +/- 2.9% for glucose. These results show that extracellular substances such as sodium and guanidinosuccinic acid were removed mainly from the extracellular compartment. On the other hand, glucose was removed only from the intracellular compartment, since blood glucose level is regulated. Although uric acid, inorganic phosphate, creatinine, potassium, guanidinoacetic acid, and methylguanidine are intracellular substances, they accumulated also in the extracellular fluid in renal failure, and were removed from both compartments, intracellular as well as extracellular, by hemofiltration.

Body Fluids↗

Alterations in cerebrospinal fluid angiotensin II by sodium intake in patients with essential hypertension.

1. Angiotensin (ANG) levels were measured in the cerebrospinal fluid of 15 patients with essential hypertension on a high sodium diet for 1 week and on a low sodium diet for a further week. ANGs were determined using a system of extraction by Sep-Pak cartridges followed by h.p.l.c. combined with radioimmunoassay. 2. Sodium depletion resulted in increases of ANG II in the cerebrospinal fluid from 1.16 +/- 0.38 (SEM) to 1.83 +/- 0.43 fmol/ml (P less than 0.01) and of ANG III from 0.65 +/- 0.11 to 0.86 +/- 0.15 fmol/ml (P less than 0.01). 3. The ANG II level in the cerebrospinal fluid was found to be unchanged and recovery of added ANG II was approximately 90%, even after incubation for 3 h, on both diets. Thus, it is unlikely that ANG II is produced or degraded in the cerebrospinal fluid in vitro. 4. There was no significant correlation between the cerebrospinal fluid and the plasma ANG II concentration on the low sodium diet. 5. These results suggest that the cerebrospinal fluid ANG II level increases with sodium depletion, and that the effect of the level of ANG II on the activity of the angiotensin-forming system in the central nervous system may be assessed by determination of ANG II in the cerebrospinal fluid in patients with essential hypertension.

Adult↗

The cardiovascular effect of intracerebroventricular endothelin in rats.

To investigate the cardiovascular action of endothelin within the central nervous system, we studied the effect of intracerebroventricular endothelin in conscious Wistar rats. The endothelin increased blood pressure and the heart rate in a dose-related way. The increase in mean blood pressure produced by 100 ng/kg of endothelin (45 +/- 6 mmHg, mean +/- s.e.m., n = 10) was much greater than that produced by the same amount of intravenous endothelin (4 +/- 1 mmHg, n = 7). Pretreatment with intravenous hexamethonium significantly attenuated the rise in blood pressure elicited by intracerebroventricular endothelin. Combined administration of hexamethonium and a vasopressin antagonist abolished the pressor response. These results indicate that centrally administered endothelin raises blood pressure through activation of the sympathetic nervous system and vasopressin. It is suggested that endothelin may play a role in the central regulation of cardiovascular function.

Animals↗

Effects of intracerebroventricular atrial natriuretic factor on angiotensin II- or sodium-induced blood pressure elevation and natriuresis.

We examined the effects of intracerebroventricular (i.c.v.) administration of atrial natriuretic factor (ANF) on pressor and natriuretic responses induced by i.c.v. angiotensin II (Ang II) or hypertonic NaCl. Conscious male Wistar rats were given one of the following solutions into the lateral ventricle: artificial cerebrospinal fluid (CSF); rat ANF (99-126) 1.0 microgram/kg per min; Ang II 100 ng/kg per min; 0.6 mol/l NaCl; Ang II plus ANF, and 0.6 mol/l NaCl plus ANF. The i.c.v. infusion of artificial CSF or ANF alone did not cause significant changes in mean blood pressure, urinary volume or sodium excretion (UNaV). The i.c.v. infusion of Ang II or 0.6 mol/l NaCl raised mean blood pressure, decreased urinary volume and increased UNaV. When ANF was administered with Ang II, the Ang II-induced responses were diminished significantly (delta mean blood pressure, +10 +/- 3 versus +20 +/- 4 mmHg; delta urinary volume, -38 +/- 9 versus -78 +/- 5 microliters/min; delta UNaV, +0.49 +/- 0.51 versus +2.28 +/- 0.58 mumol/min). The centrally administered ANF opposed the effects of 0.6 mol/l NaCl, though the effect was significant only in respect of blood pressure. Our results indicate that the brain ANF may have an antinatriuretic role in some conditions.

Angiotensin II↗

Increased sodium-calcium exchange in arterial smooth muscle of spontaneously hypertensive rats.

We compared sodium-calcium (Na-Ca) exchange in vascular smooth muscle between spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats. Aortic rings of 11 SHR and 11 WKY rats aged 11-12 weeks were superfused with physiological saline, and isometric tension was measured. Systolic blood pressure was higher in SHR (174 +/- 12 mm Hg) than in WKY rats (132 +/- 4 mm Hg): 1) In the presence of 10 microM phentolamine, 10 microM verapamil, and 5 mM caffeine, reduction of ionized extracellular sodium concentration [( Na+]o) from normal (139.2 mM) to 1.2 mM (replaced by N-methyl-D-glucamine) caused an external Ca2+-dependent increase in tonic tension (calcium entry by Na-Ca exchange). The rate of increase was higher in SHR (35.4 +/- 3.9 mg/min) than in WKY rats (17.9 +/- 1.3 mg/min) (p less than 0.01). 2) In the presence of phentolamine, verapamil, and caffeine, relaxation from low-Na+ contraction was promoted by external calcium removal. The rate of relaxation was directly related to [Na+]o. The rates of relaxation at normal (139.2 mM) [Na+]o were higher in SHR than in WKY rats (p less than 0.05). The rates of relaxation at 1.2 mM [Na+]o (calcium extrusion by adenosine triphosphate-driven calcium pump) were not different between SHR (11.6 +/- 2.8 mg/min) and WKY rats (8.9 +/- 2.5 mg/min). The increase in the rates of relaxation from 1.2 mM to normal (139.2 mM) [Na+]o (calcium extrusion by Na-Ca exchange) was greater in SHR (34.9 +/- 6.6 mg/min) than in WKY rats (17.1 +/- 4.5 mg/min) (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Aspirin lowers blood pressure in patients with renovascular hypertension.

To clarify the role of renal prostanoid in hyperreninemia and high blood pressure in human renovascular hypertension, we measured prostaglandin E2 and renin activity in renal venous and abdominal aortic plasma before and after the intravenous administration of the cyclooxygenase inhibitor, aspirin DL-lysine. Subjects were six patients with unilateral renovascular hypertension and six with essential hypertension. In patients with renovascular hypertension, prostaglandin E2 concentration in renal venous plasma from the stenotic kidney was 9.25 +/- 1.48 pg/ml, which was significantly higher (p less than 0.01) than the concentration in the renal venous plasma from the normal kidney (4.97 +/- 1.02 pg/ml) or in the aortic plasma (2.59 +/- 0.15 pg/ml). Plasma renin activity was also higher in the renal vein of the stenotic kidney than in the other two sites. The stenotic side/normal side ratio of the renal venous prostaglandin E2 correlated significantly with a renin ratio greater than 1.5 (r = 0.8211, p less than 0.05). Intravenous injection of aspirin DL-lysine (18 mg/kg) 30 minutes later markedly suppressed prostaglandin E2 and renin levels at all sites and clearly lowered arterial blood pressure (mean: from 120 +/- 6 to 110 +/- 5 mm Hg, p less than 0.01). The reduction in blood pressure correlated significantly with the suppression of plasma renin activity in the aorta (p less than 0.05) and in the renal vein of the stenotic kidney (p less than 0.01). Conversely, in patients with essential hypertension, aspirin had little effect on renin levels and increased mean blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Brain damage after open heart surgery in patients with acute cardioembolic stroke.

We evaluated 14 patients with acute cardiogenic embolism who underwent open heart surgery soon after the onset to determine the cerebral and cardiac factors that influence neurologic outcome. The mean interval from onset of cerebral embolism to surgery was 5.3 (range 1-16) days. Five of the 14 patients had vegetations from infective endocarditis (including prosthetic valve endocarditis) as embolic sources, eight had intracardiac thrombi, and one had atrial myxoma. The diagnosed site of infarction before surgery was based on computed tomographic and/or angiographic findings. Of the 14 patients, four had infarcts due to major artery occlusion, seven due to cortical branch occlusion, and two due to perforating artery occlusion; one patient presented with a transient ischemic attack without computed tomographic abnormalities. Ten patients (71%) showed no clinical aggravation after open heart surgery; however, two patients died of massive cerebral hemorrhage, one died of deterioration of brain edema, and another became comatose from midbrain hemorrhage immediately after surgery. The four patients with clinical aggravation comprised three with septic embolism and one with aseptic occlusion of a major artery. From these results, infective endocarditis and a large infarct appear to be possible aggravating factors when patients with recent cerebral embolism undergo open heart surgery.

Adult↗

Hemorrhagic transformation in cerebral embolism.

We studied the mechanism of hemorrhagic infarction after acute cerebral embolism in 160 patients by brain computed tomography and angiography. Hemorrhagic infarction during the month after the embolic event was evident in 65 patients (40.6%). Initial angiography a median of 1.5 (range 1-60) days after the event revealed occlusion of the cerebral arteries in 117 of 142 patients (82.4%), and reopening of the vessels was observed in 56 (94.9%) of 59 patients who had follow-up angiography a median of 20 (range 3-47) days after the event. The incidence of hemorrhagic infarction was higher in patients greater than or equal to 70 years old (31 of 61, 50.8%) than in those aged 50-69 years (27 of 72, 37.5%) or less than 50 years (seven of 27, 25.9%) (greater than or equal to 70 vs. less than 50, p less than 0.05). In patients with moderate or large infarcts, hemorrhagic infarction developed in 50.0% or 51.5%, respectively, while in those with small infarcts it developed in only 2.9% (p less than 0.05). No correlation was found between hemorrhagic infarction and history of hypertension or blood pressure during the acute stage of stroke. Thrombolytic and/or anticoagulant therapy did not affect the incidence of hemorrhagic infarction (40.0% with vs. 40.7% without therapy) but tended to cause massive hematoma. Our results indicate that hemorrhagic transformation in cerebral embolism is caused not only by reopening of the occluded vessels but also by other factors such as age and size of the infarct. Hypertension per se seems to be less important for hemorrhagic infarction.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

Positive platelet scintigram of a vertebral aneurysm presenting thromboembolic transient ischemic attacks.

We describe a patient with transient ischemic attacks secondary to a giant aneurysm who showed increased activity on platelet scintigrams at the origin of the left vertebral artery. This is assumed to be the first report of a presumed embolizing aneurysm with positive activity of labeled platelets. Platelet scintigraphy is useful for diagnosing transient ischemic attacks as being secondary to an aneurysm and was proved to provide direct evidence of a thromboembolic source in vivo.

Adult↗