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Biomedical subjects

O Iimura

Publications and source records attributed to O Iimura.

At least 253 records · Page 14Linked to original sources
PubMed1983

The role of L-carnitine in the pathogenesis of cardiomegaly in patients with chronic hemodialysis.

Many reports have suggested that cardiac dysfunction with cardiomegaly is more often observed in patients with chronic hemodialysis. Moreover, cardiac dysfunction has been thought as one of the most important factors affecting the prognosis of these patients. In this study, in order to clarify the role of l-carnitine in the pathogenesis of cardiomegaly, 33 patients with chronic hemodialysis were studied using the multivariate analysis method. Among the factors which may affect cardiac function, the following 10 variables were examined. 1) age, 2) duration of dialysis, 3) plasma carnitine, 4) serum total cholesterol, 5) serum HDL-cholesterol, 6) triglyceride, 7) systolic blood pressure, 8) diastolic blood pressure, 9) left ventricular voltage on a electrocardiogram at rest and 10) hematocrit. The plasma carnitine levels in these patients were markedly reduced and inversely correlated with the cardiothoracic ratio (CTR) on the chest X-ray films (r = 0.38, p less than 0.05). In principal component analysis, the CTR was closely related to hematocrit and plasma carnitine levels. By multiregression analysis, both hypo-carnitinemia and anemia were independently shown to be important causes of cardiomegaly. Thus, it is suggested that the cardiomegaly in patients with chronic hemodialysis may be improved by supplemental therapy with l-carnitine, even in cases with severe anemia.

Adolescent↗
PubMed1983

Plasma antidiuretic hormone levels in patients with normal and low renin essential hypertension, and secondary hypertension.

In order to investigate the antidiuretic hormone (ADH) in essential hypertension and secondary hypertension, plasma ADH levels were measured in normal subjects, in patients with normal and low essential hypertension, and in other patients with various forms of secondary hypertension. Plasma ADH levels were significantly lower in low renin essential hypertension and higher in malignant hypertension than in normal subjects. The plasma ADH levels tended to be lower in renal hypertension and primary aldosteronism, and higher in renovascular hypertension, but these differences were not statistically significant. From these results, it appeared that ADH might play a role in malignant hypertension, but not in the other hypertensive diseases.

Adolescent↗
PubMed1983

A case of 17 alpha-hydroxylase deficiency with special reference to the renal kallikrein-kinin system.

In a 26-year-old male with 17 alpha-hydroxylase deficiency, endocrinological examinations were performed not only after, but also before the onset of clinical signs and symptoms. In addition, the pathophysiological role of the renal kallikrein-kinin system was investigated in this patient. In spite of the fact that this disease is congenital, in the mechanism of its onset, this patient had a period of endocrinological normality before onset; that is, 9 months before onset, both ACTH and cortisol were within the normal range, although the former would be significantly higher and the latter significantly lower than normal values after the onset. In this case, both urinary kallikrein and kininase excretions abnormally increased and then returned to normal after dexamethasone treatment.

Adrenal Cortex Hormones↗
PubMed1983

Generalized epilepsy in a patient with hypokalemic periodic paralysis and cardiac arrhythmia.

A 17-year-old female who had Hypokalemic periodic paralysis with arrhythmia developed syncopal attacks. Although syncope in this rare disorder has been attributed to ventricular tachycardia or ventricular fibrillation, the clinical manifestation, electroencephalogram, serum electrolytes and blood sugar at the attack, and the results of lumbar puncture indicated that idiopathic generalized epilepsy was the cause of the syncopal attacks in the present case. To our knowledge, this is the first case report of the association of epilepsy with periodic paralysis and arrhythmia in the literature.

Adolescent↗
PubMed1983

The excretion of human urinary kallikrein quantity and activity in normal and low renin subgroups of essential hypertension.

In both low and normal renin essential hypertensive groups, urinary excretion of kallikrein quantity by direct radioimmunoassay and activity by kininogenase assay were significantly lower than those in normal subjects. In comparing between normal and low renin groups, no difference was found in kallikrein quantity, while kallikrein activity tended to be lower in the low renin group than in the normal renin group. A significant positive correlation was observed between kallikrein quantity and activity in the normal subjects, the normal renin group and the low renin group. However, the slope of the regression line in the low renin group was significantly more moderate than that in the normal renin group, and tended to be more moderate than that in normal subjects. The addition of kallikrein inhibitors (aprotinin and gabexate mesilate) resulted in a significant suppression of enzymatic activity but not of enzyme quantity. These findings suggest that suppression of the renal kallikrein system in both groups of essential hypertension was confirmed by the decreased excretion of kallikrein both as enzyme quantity and activity, and that in the mechanism of the suppression of urinary kallikrein activity in the low renin group, the renal kallikrein inhibitors may play some role.

Adult↗
PubMed1983

[Case of hepatocellular carcinoma with a marked reduction in the tumor size induced by PSK administration alone].

A 56-year-old man was admitted to our hospital because of right abdominal pain. The edge of the liver was felt 4.5 fingers breadth below the xiphoid process. AFP was 20100 ng/ml and CEA was 5.6 ng/ml. The chest X-ray indicated existence of lymphangitis and some nodular density suggesting lung metastasis in the both lower-lung fields. 99mTc-phytate liver scan showed a large defect along the antero-inferior margin of the right hepatic lobe, which revealed an abnormal uptake of 67Ga-citrate. Ultrasonograms demonstrated a solid mass, 8 X 9 cm, in the right lobe of the liver. A CT-scan of the abdomen also showed a large, rounded, low attenuation mass with central necrosis in the right hepatic lobe: the pancreas and the remaining retroperitoneal structures appeared normal. Following the administration of PSK alone, 3 g daily, for three months, a remarkable regression of both hepatomegaly and lung metastasis was observed. Liver scan, ultrasonograms and CT-scan showed a striking resolution of the intrahepatic mass except central necrosis. AFP decreased to 33.7 ng/ml and CEA was 8.2 ng/ml. After about one year, however, ultrasonogramms showed a newly growing solid mass, 3.5 X 3.5 cm, in the left lobe of the liver. A needle biopsy specimen was taken from the intrahepatic mass, and it was interpreted as hepatoma. He is now healthy.

Carcinoma, Hepatocellular↗
PubMed1982

Hemodynamic and natriuretic responses to intravenous infusion of dopamine in patients with essential hypertension.

In order to clarify the role of dopamine on the pathophysiology of essential hypertension, mean arterial pressure (MAP), heart rate (HR), urine volume (UV), urinary sodium excretion (UNaV), endogenous creatinine clearance (Ccr), fractional excretions of sodium (FENa), inorganic phosphorus (FEP) and potassium (FEK), plasma renin activity (PRA), plasma aldosterone concentration (PAC) and plasma noradrenaline concentration (PNA) were measured before and after intravenous infusion of dopamine (3 micrograms/kg/min, 60 min) in normotensive (NT) and essential hypertensive subjects (EHT). Following dopamine infusion, a significant decrease of MAP and an increase of HR were observed in EHT but not in NT. UV, UNaV, Ccr, FENa, FEP and FEK increased significantly in both NT and EHT, and changes in these except for Ccr were significantly greater in EHT than in NT. In EHT, following dopamine infusion, PNA was clearly elevated, but no remarkable change was found in PRA and PAC. A significantly positive correlation was found between delta UNaV and delta FENa or delta FEP, and between delta FENa and delta FEP, while no significant relation was observed between delta UNaV and delta Ccr, delta MAP or MAP before dopamine infusion. A significant inverse correlation between supine PRA before dopamine infusion and delta FENa or delta FEP and a positive correlation between age and delta FENa or delta FEP were also observed in these patients. The changes in UNaV positively correlated with delta FENa and delta FEP in both low renin (group L) and normal renin EHT (group N) and with delta Ccr i group N but not in group L. The mean values of delta FENa, delta FEP and delta FEK were significantly higher in group L as compared with those in age-matched group N. These results suggest that, since the enhanced response to infused dopamine may reflect reduced dopaminergic activity, attenuation of renal dopaminergic activity might exist and be involved through a distribution of water-sodium metabolism, at least in part, in the pathophysiological mechanism in EHT, particularly in group L.

Adult↗
PubMed1982

An improved method for the determination of human blood kinin levels by sensitive kinin radioimmunoassay.

A highly sensitive and specific radioimmunoassay for kinin (minimal detectable amount, 0.5 pg/tube) was applied to measure the blood kinin level. A five ml blood sample was collected with a siliconized needle and plastic syringe which contained 2.5 ml of 0.8 N-HCl. The blood kinin was extracted with butanol, following reextraction with water. According to this procedure, the mean recovery (mean +/- SE) calculated from added 125I-bradykinin (500 CPM) and the known amounts of cold bradykinin were 50.4 +/- 0.8% and 51.1 +/- 2.2%, respectively. In comparison with other sampling methods in 6 normal subjects, the blood samples taken without HCl in syringes showed a higher level (24.4 +/- 10.1 pg/ml) than the samples with HCl (5.3 +/- 1.3 pg/ml). And very high levels were obtained in the plasma samples collected by the method of Talamo or Vinci (0.53 +/- 0.24 ng/ml and 3.5 +/- 1.3 ng/ml, respectively). The kinin content in blood samples taken with HCl was stable at -20 degrees C for at least one month, but increased significantly at room temperature or 4 degrees C for 48 hours. Blood samples were obtained from 17 normal subjects, and 3 patients with acute myocardial infarction. Blood kinin levels in the patient with acute myocardial infarction, 121 +/- 20.9 pg/ml, were significantly higher than those in normal subjects (3.8 +/- 0.5 pg/ml). From these results, it was concluded that high levels of blood kinin reported previously may have resulted from inadequate sampling procedures. Thus, in order to measure blood kinin accurately, inactivation of the kinin generating and destroying enzymes must be done immediately after the sampling. In addition, this radioimmunoassay method should be very useful in investigating the pathophysiological role of blood kinin in various diseases.

Blood Specimen Collection↗
PubMed1982

[Kallikrein].

Explore the source record for details and available documents.

Animals↗
PubMed1981

Excretion of human urinary kallikrein quantity measured by a direct radioimmunoassay of human urinary kallikrein in patients with essential hypertension and secondary hypertensive diseases.

Recently, we established a very sensitive, specific and simple direct radioimmunoassay method for human urinary kallikrein. In this study, in order to clarify whether or not the low or high excretion rate of urinary kallikrein activity in patients with essential hypertension, primary aldosteronism, pheochromocytoma and Bartter's syndrome is caused by changes in enzyme quantity, urinary kallikrein excretion was measured with this direct radioimmunoassay method in normal subjects and in patients with these diseases. Urinary kallikrein excretion measured as enzyme quantity was significantly lower in patients with essential hypertension, and higher in patients with primary aldosteronism and Bartter's syndrome. These results are consistent with other previously reported data and our data measured by means of esterase assay or kininogenase assay. The results also suggest that lowered or elevated excretion of urinary kallikrein activity in these diseases is caused, in part at least, by the lowered or elevated excretion of enzyme quantity.

Bartter Syndrome↗