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Biomedical subjects

S Murabayashi

Publications and source records attributed to S Murabayashi.

At least 37 records · Page 2Linked to original sources

Urinary dopamine, noradrenaline and adrenaline in type 2 diabetic patients with and without nephropathy.

We measured the urinary excretions of dopamine, noradrenaline and adrenaline, their conjugated metabolites, urinary excretion of sodium and creatinine clearance simultaneously in 21 patients with Type 2 (non-insulin-dependent) diabetes and 6 normal subjects. The mean (+/- SEM) value for urinary excretion of dopamine (52.4 +/- 8.8 micrograms/day) in diabetic patients with nephropathy (Group C, n = 12) was significantly lower (P less than 0.01) than in the normal subjects (Group A, 179.7 +/- 15.5 micrograms/day) and in diabetic patients without nephropathy (Group B, n = 9, 131.5 +/- 16.5 micrograms/day). The mean values for the urinary excretions of noradrenaline and adrenaline were also significantly lower (P less than 0.01) in Group C than in Groups A and B. In addition, the mean urinary excretion of conjugated metabolite of dopamine in Group C was significantly lower (P less than 0.05) than in Group A. There was a trend toward the observation that the mean 24-h urinary excretion of sodium in Group C (121.6 less than 12.9 mEq) was lower as compared with that in Group A (140.8 +/- 8.9 mEq) or B (150.7 +/- 17.9 mEq). A multiple regression analysis revealed that the 24-h urinary excretion of dopamine correlated significantly with creatinine clearance, systolic (P less than 0.01) and diastolic (P less than 0.05) blood pressures. The results indicate that synthesis or secretion of renal dopamine might decrease with a progression of diabetic nephropathy.(ABSTRACT TRUNCATED AT 250 WORDS)

Creatinine↗

Effects of dilevalol, an R, R-isomer of labetalol, on blood pressure and renal function in patients with mild-to-moderate essential hypertension.

The effects of oral dilevalol (an R, R-isomer of labetalol), a new beta-adrenoceptor blocker with beta 2-receptor stimulating and alpha-recepter blocking properties on blood pressure, renal function, plasma renin activity (PRA) and plasma aldosterone have been studied in 15 patients with mild-to-moderate essential hypertension treated with it for 6 weeks. Two patients with apparent treatment failure and one patient who developed muscle pain and cramps, and had an elevated creatine phosphokinase level, were excluded from the study. Dilevalol monotherapy 100 mg once daily for 6 weeks significantly lowered both the systolic and diastolic blood pressure compared to placebo. Total renal vascular resistance was significantly reduced, and RBF and GFR remained unchanged. Dilevalol significantly decreased PRA. The results suggest that prolonged daily treatment with dilevalol preserves renal function and produces a concomitant hypotensive action in patients with mild-to-moderate essential hypertension. The ancillary pharmacological properties of dilevalol rather than PRA suppression may be relevant to its renal effects.

Adrenergic beta-Antagonists↗

Spontaneous remission of acromegaly after pituitary apoplexy following head trauma.

A 34-year-old man with acromegaly was observed, and the clinical course and various endocrinological deficiencies occurring before, during and after the development of pituitary apoplexy were evaluated. Following the attack, the patient experienced acute reductions in growth hormone (GH) and other pituitary hormones, adrenohypophyseal insufficiency and transient diabetes insipidus which appeared subsequent to glucocorticoid therapy. The level of growth hormone in serum and cerebrospinal fluid (CSF) was measured synchronously, and the respective regressions of GH levels in serum and CSF were observed. The results demonstrated the utility of measuring hormonal levels in CSF in the clinical evaluation of pituitary apoplexy in a patient with a functioning pituitary tumor.

Acromegaly↗

Effect of cimetidine on the pharmacokinetics and pharmacodynamics of enalapril in normal volunteers.

The possible effects of cimetidine on the pharmacokinetics and pharmacodynamics of enalapril, a pro-drug requiring hepatic de-esterification to an active angiotensin-converting enzyme (ACE) inhibitor enalaprilat, were assessed in a randomized, crossover study. Cimetidine (400 mg) or placebo was administered orally every 12 h for 3 days and on the day of a single oral administration of enalapril maleate (10 mg) to seven healthy male subjects. Serum ACE, plasma renin activity (PRA), plasma aldosterone concentration (PAC), and alpha-human atrial natriuretic peptide (alpha-hANP) were measured before and 4 h after the enalapril dosing. There were no significant differences in any serum- and urine-derived kinetic parameters of enalapril and enalaprilat, nor in hemodynamics, PAC, or alpha-hANP between the two treatment trials. ACE decreased and PRA increased to a similar extent in the two trials. Serum enalaprilat concentration correlated significantly (p less than 0.001) with percentage of inhibition of ACE activity. The results suggest that the pharmacokinetics and pharmacodynamics of enalapril are unaffected by preadministration of cimetidine. Thus, cimetidine does not appear to alter hepatic esterase activity toward enalapril.

Adult↗

Titanium-nickel intravascular endoprosthesis: a 2-year study in dogs.

Twelve 5-mm-internal-diameter intravascular endoprostheses of noncorrosive, shape-memory titanium-nickel (TiNi) alloy were delivered transluminally by catheter and implanted in the iliac (n = 10) and femoral (n = 2) arteries of six normal dogs for either 1 or 2 years in order to evaluate the implantation technique and long-term effects. The patency rates were as follows: at 1 month, 92% (11/12); at 1 year, 100% 11/12 widely patent; 1/12 recanalized); and at 2 years, 100% (3/4 without stenosis; 1/4 with 20% stenosis). No migration, erosion, inflammation, surface thrombus, or stenosis of the side branches was seen; an absence of untoward angiographic and histopathologic effects was detected at 1 and 2 years. The neointima was completely endothelialized, without changes in thickness over time, 229.3 +/- 127.6 microns after 1 year and 223.3 +/- 216.7 microns after 2 years (p = not significant). The neointimal layer became thicker toward its distal aspect (p less than or equal to .05). Satisfactory delivery, long-term patency, and biocompatibility (manifested as a thin, stable neointima) were observed for the TiNi intravascular endoprosthesis at 1 and 2 years.

Animals↗

Biological performance of TiNi shape memory alloy vascular ring prostheses: a two year study.

A method was developed for the noninvasive insertion of a vascular ring prostheses aimed at preserving arterial patency and preventing restenosis following angioplasty. Using a specially designed 7F catheter 22 nitinol (TiNi) wire prostheses (I.D. 5 mm; 0.25 mm thickness) were torsion reduced in diameter and inserted under fluoroscopy into both carotid (n = 2) and iliac-femoral arteries (n = 20) of dogs. Aspirin (650 mg BID) and Persantin (200 mg BID) were given for only 30 days postoperatively. Angiography of all rings at 1, 6, 12 months exhibited excellent biocompatibility and long term patency 91% (20/22) as reported in Trans ASAIO 32:30, 1986. Four rings inserted in the right and left common iliac arteries and femoral artery were followed for up to 2 years and exhibited 100% patency. Angiography demonstrated that the anchorage of the prostheses was stable and the lumen was uniformly covered by a thin neointimal layer of endothelial like cells. The prostheses were patent with no evidence of thrombosis or inflammation. In view of the problem of recurrent stenosis occurring during the healing period after balloon angioplasty (PTA or PTCA), this approach may lead to a new means of clinical intervention in atherosclerosis.

Alloys↗

Multiple oral doses of nicardipine, a calcium-entry blocker: effects on renal function, plasma renin activity, and aldosterone concentration in mild-to-moderate essential hypertension.

We studied the effects of nicardipine administered in a 4-week fixed oral maintenance dosage (20 or 40 mg t.i.d.) on renal function, plasma renin activity (PRA), and plasma aldosterone concentration in seven patients with mild-to-moderate essential hypertension. Glomerular filtration rate and renal blood flow were measured by means of sodium thiosulfate and para-aminohippurate, respectively. Nicardipine increased renal blood flow by 11.5% +/- 4.3% (mean +/- SE; P less than 0.05) and glomerular filtration rate by 16.3% +/- 6.4% (P less than 0.05) and decreased total renal vascular resistance by 30.0% +/- 2.7% (P less than 0.05), with a significant (P less than 0.05) reduction in systolic and diastolic blood pressure as compared with placebo values. Nicardipine increased PRA significantly (P less than 0.05), whereas plasma aldosterone concentration remained unchanged. Our results indicate that nicardipine given in a multiple oral dosage has some favorable renal effects with a concomitant hypotensive action in patients with mild-to-moderate essential hypertension. Nicardipine appears to blunt the secretion of aldosterone responding to an increased PRA possibly through its calcium-antagonizing action.

Adult↗

Renal kallikrein in diabetic patients with hypertension accompanied by nephropathy.

We measured the 24-h excretion of urinary kallikrein in 27 patients with Type 2 (non-insulin-dependent) diabetes and in 10 normal control subjects. Mean (+/- SD) kallikrein excretion in diabetic patients with nephropathy (6.2 +/- 2.4 naphthyl units (NU)/day, n = 13) was significantly lower than in control subjects (12.8 +/- 3.4 NU/day, p less than 0.01) and in diabetic patients without nephropathy (9.4 +/- 3.4 NU/day, n = 14, p less than 0.05). Kallikrein excretion in hypertensive diabetic patients with nephropathy (5.1 +/- 1.6 NU/day, n = 8) was significantly lower (p less than 0.05) than in normotensive patients with nephropathy (8.3 +/- 2.1 NU/day, n = 5). There were no significant differences in kallikrein excretion rate (24-h excretion of urinary kallikrein/24-h creatinine clearance) among control subjects (9.9 +/- 4.3 NU/ml), diabetic patients with (9.0 +/- 3.2 NU/ml) and without (9.3 +/- 3.5 NU/ml) nephropathy. However, kallikrein excretion rate in hypertensive diabetic patients with nephropathy (7.7 +/- 3.3 NU/ml) was significantly lower (p less than 0.05) than in normotensive diabetic patients with nephropathy (11.8 +/- 2.0 NU/ml, n = 10). Respective basal and post-stimulated (with intravenous furosemide 40 mg plus 60 min ambulation) plasma aldosterone concentrations measured in control subjects and in hypertensive diabetic patients with nephropathy were similar and increased to the same extent in the 2 groups (5.5 +/- 3.2 versus 5.3 +/- 3.2 and 9.3 +/- 2.6 versus 10.5 +/- 3.4 ng/ml), although the respective plasma renin activity tended to be lower in diabetic patients than in control subjects (0.7 +/- 0.6 versus 1.3 +/- 0.9 and 1.8 +/- 1.8 versus 3.0 +/- 2.6 ng-1 . ml-1 . h-1).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Plasma renin activity, active and inactive renin concentrations, and their responses to beta 1-adrenoceptor blockade with metoprolol in hyperthyroidism.

Plasma renin activity (PRA), plasma renin concentration (PRC), inactive renin concentration (IRC) and total renin concentration (TRC) were measured in 31 normal controls and in 8 patients with hyperthyroidism. TRC was determined as angiotensin I generated with sheep renin substrate after an acid activation of plasma. The angiotensin I of non-acidified plasma was expressed as PRC. IRC was calculated as TRC minus PRC. The mean values for PRA, PRC, IRC and TRC were significantly (P less than 0.05 to P less than 0.01) higher in the hyperthyroid patients than in the normal or euthyroid controls. The administration of a beta 1-adrenergic blocker, metoprolol (120 mg/day for 14 days), produced a significant (P less than 0.05 to P less than 0.01) fall in levels of T4, PRA and TRC, and reduced the active renin ratio calculated from PRC/TRC significantly (P less than 0.025), as compared to the pretreatment values. Our observations support the idea that the higher PRA in hyperthyroidism is due to an increased secretion of renin. Furthermore, the results may indicate that the conversion of inactive to active renin is accelerated in hyperthyroidism, possibly by an increased sympathetic activity.

Adult↗

Biocompatibility: bioengineering aspects.

Bioengineers have contributed to biocompatibility research. Many materials have been designed, synthesized, and characterized by use of various analytical instruments. The blood compatibility of materials has been studied by focusing on the blood-material interfacial reactions. Although much information has been accumulated regarding such local reactions, understanding of biocompatibility is still limited. A more global approach to study is needed. A new approach to understanding biocompatibility is proposed and discussed. Three points are stressed: interaction within body's defense system and its effect on blood-material reactions; induction of a systemic reaction by a local reaction, which then affects the blood-material interaction; the time sequence of such interactions between local and systemic reactions. To establish a logical approach to study biocompatibility is most important at this moment for the future progress in biocompatibility research.

Biocompatible Materials↗

Renal effects of nicardipine, a calcium entry blocker, in hypertensive type II diabetic patients with nephropathy.

We studied the renal effects of nicardipine, a calcium entry blocker, in eight patients with essential hypertension (group A, WHO I or II), six hypertensive type II diabetics with mild-to-moderate nephropathy (group B, urinary albumin 200-789 mg/day), and six hypertensive type II diabetics with severe or advanced nephropathy (group C, urinary albumin 1,596-4,300 mg/day). The patients received an intravenous dose of nicardipine hydrochloride (0.5 mg) or saline placebo in a random order. Glomerular filtration rate (GFR) and renal blood flow (RBF) were measured by means of thiosulfate sodium and p-aminohippurate, respectively, during the 30 min after the nicardipine or saline injection. Blood pressures were serially monitored during the study. Nicardipine reduced both systolic and diastolic blood pressures significantly (P less than .05 to .01) at all measurement periods in all study groups compared with the respective placebo. Nicardipine increased RBF (P less than .01), GFR (P less than .05), and urinary Na+ excretion (P less than .01) and decreased total renal vascular resistance (P less than .01) in groups A and B, but these parameters remain unchanged in group C. The filtration fraction remained unaltered in all groups. The results indicate that nicardipine has several favorable renal effects with a concomitant hypotensive action in hypertensive type II diabetics with mild-to-moderate nephropathy, as observed in patients with uncomplicated essential hypertension, and the renal pharmacological responsiveness appears to be related to the severity of nephropathy.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

A malignant pheochromocytoma with ileus, polyuria and hypercalcemia: a case of recurrence 17 years after the initial operation.

A case of malignant pheochromocytoma, with a recurrence 17 years after the initial diagnosis of benign pheochromocytoma, was presented. The autopsy revealed multiple metastases of pheochromocytoma to the bone marrow of the thoracic and lumbar vertebrae. Of particular note is the fact that the patient was associated with paralytic ileus, polyuria and hypercalcemia and that he died of hypercalcemia crisis. Cases like this appear to be very rare.

Adrenal Gland Neoplasms↗

Prevalence of hypertension in diabetes mellitus--its relation to diabetic nephropathy.

The prevalence of hypertension was studied in 374 patients with non-insulin dependent diabetes mellitus (NIDDM) and in 1197 non-diabetic controls. The diagnosis of hypertension was made when the mean systolic pressure of three measurements on different occasions was 151 mmHg or greater, or the mean diastolic pressure was 91 mmHg or greater. The prevalence was 42.8% in the diabetics and 17.8% in the controls. It showed a significant difference over age 31 (p less than 0.05). Proteinuria (p less than 0.001), abnormal ECG (p less than 0.01), hyperlipidemia (p less than 0.05) and hypertensive or sclerotic changes of the retina (p less than 0.001) were more frequently observed in the diabetics than in the controls. Hypertension was found in 71% of those with proteinuria, 48% with diabetic retinopathy, 61% with abnormal ECG and 54% with hyperlipidemia in the diabetics. The incidence of proteinuria was 22.8% in the diabetic hypertensives and was 8.3% in the non-diabetic hypertensives (p less than 0.001). 24 subjects out of 119 diabetics, who were normotensive at their initial visits, became hypertensive within 10 years (N-H), and 95 remained normotensive (N-N). 38% of N-H showed proteinuria already on their initial examinations and 3% of N-N did. 73% of those who showed proteinuria on their initial examination became hypertensive and 13% of those who were free from proteinuria did (p less than 0.001). The results suggest that diabetic nephropathy plays an important role in developing hypertension in diabetics.

Adult↗

[A case of adrenocortical carcinoma with Cushing's syndrome presenting unusual urinary 17-ketosteroid fractionation].

A patient with adrenocortical carcinoma with Cushing's syndrome is presented. This case seems to be most characterized by its very unusual urinary 17-ketosteroid (KS) fractionation, since markedly increased etiocholanolone was not accompanied by increments of either DHEA or androsterone. Determination of the plasma adrenocorticosteroids of the patient revealed normal DHEA and DHEA-S levels, moderately increased 17-OH-pregnenolone, and markedly increased 11-deoxycortisol. Therefore, it seems plausible that the unique 17-KS fractionation of this patient would have ensued as a result of remarkably decreased C17-20 lyase activity sufficient to nullify the increased 17-OH-pregnenolone and that markedly increased etiocholanolone might have been converted from 11-deoxycortisol.

17-Hydroxycorticosteroids↗