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Biomedical subjects

E Miyajima

Publications and source records attributed to E Miyajima.

At least 37 records · Page 2Linked to original sources

Improvement of multiple coronary risk factors in obese hypertensives by reduction of intra-abdominal visceral fat.

The association of obesity and hypertension is well documented, and the combination is important as a coronary risk factor, but its non-pharmacological management is very difficult. Japanese hypertensive obese subjects (HO, n = 95) selected from 321 non-medicated obese subjects with a body mass index > 25 kg/m2 were characterized by the clinical features of significant diaphragmatic elevation, higher heart rate (HR), fasting blood glucose (FBS), total cholesterol (Tch), uric acid and gamma GTP values and lower vital capacity (VC) compared to those of normotensive-obese subjects (NO, n = 226) (p < 0.01). During a diet therapy program (about 1,200 kcal/day) for HO (n = 55), 25 subjects were treated with a non-drug-dependent pulse-synchronized transpercutaneous electric abdominal muscle stimulator (PEM) (ca. 30,000 muscle contractions/day) for 4 weeks. These subjects showed significant improvement with reduction in body weight (9.4%, 7.4 kg), intra-abdominal visceral fat (VF) CT scan area (29%), abdominal subcutaneous area (10%) at the level of the umbilicus, blood pressure (BP), HR, FBS, gamma GTP, Tch, plasma norepinephrine, plasma renin activity and plasma insulin, an increase of VC and lowering of the diaphragm (p < 0.05). The reductions in weight, BP, FBS and Tch in the diet group (n = 30, 1,200 kcal/day for 4 weeks) were smaller than those in the PEM-diet group (p < 0.05). The Japanese hypertensive obese patients had complications of many other coronary risk factors, and the reduction in weight and VF with PEM-diet therapy seems to be effective for improving these risk factors.

Abdominal Muscles↗

Circadian variation of haemodynamics in patients with essential hypertension: comparison between early morning and evening.

OBJECTIVE: An increased incidence of cardiovascular accidents in the morning has been reported, but the reason why is not clear. We measured 24-h haemodynamics and focused on its change in the morning. DESIGN: To study the circadian variation of haemodynamics, we recorded 24-h direct blood pressure and electrocardiogram using a telemetry method, in 21 untreated inpatients with essential hypertension, and measured cardiac output using the dye-dilution method in the morning, in the evening and during sleep. We also determined the beat-to-beat cardiac output (using the pulse-contour method), the total peripheral resistance and the ratio of low- to high-frequency components (using power spectral analysis of the R-R interval during 24 h), and made comparisons between morning and evening values. RESULTS: Both systolic and diastolic blood pressure increased rapidly in the early morning. Although the comparison of blood pressure between morning and evening showed no difference, total peripheral resistance and low- to high-frequency ratio were significantly higher in the morning than in the evening, but cardiac output was lower in the morning. CONCLUSIONS: Sympathetic nervous activity and vascular resistance seem to be higher in the morning than in the evening, and these haemodynamic changes may stress the cardiovascular system.

Adult↗

Relationship between blood pressure and heart rate while awake and asleep in patients with mild essential hypertension.

Blood pressure (BP) and heart rate (HR) (BP waveforms) are affected by external stress during waking and BP is reduced to its lowest level (base BP) during sleep. This study investigated the relationship between BP waveforms while awake and base BP waveforms during sleep. The intra-arterial BPs of 64 inpatients (34 males and 30 females, age: 42 +/- 11, mean +/- SD) with mild essential hypertension were measured for 24 h by the telemetry method. The average ln (SBP/DBP) (m) while awake and the m at base BP (ln: natural logarithm, SBP: systolic BP, DBP: diastolic BP) had approximately the same values in each patient (mean difference: -0.02 +/- 0.07). The product of the RR interval (60/HR) and DBP (RR x DBP) while awake and at base BP had almost the same value (mean difference: -3.2 +/- 10 mmHg.sec). According to the Windkessel model, the RR interval during which blood-flow volume in relation to the m value is at its highest can be inferred as S (em-1)/(em-m-1) (S: systolic time). Using this formula, we developed a formula to estimate base RR from waking m, BP, and RR. Calculations with this estimate formula produced a very slight difference (0.0 +/- 0.1 sec) between estimated and actual values for base RR. For the most part, it was possible to infer the base DBP value from the estimated base RR using RR x DBP while awake (mean difference: -3.7 +/- 7.0 mmHg). These results suggest that the base BP waveform may be the most efficient pattern, and that waking BP waveforms change based on the base BP waveform during sleep.

Adult↗

Blood pressure during sleep: antihypertensive medication.

To investigate whether excessive reduction of blood pressure (BP) by antihypertensive medications correlates with myocardial infarction, especially during sleep in elderly patients, we used telemetry and cuvette dye-dilution methods to assess the direct BP and the hemodynamics of 68 inpatients with essential hypertension during wakefulness and sleep. There were 25 patients greater than or equal to 60 years old (OH-group) and 43 were less than or equal to 59 years old (YH-group). Of the OH-group, 36% showed high BP during the day, with marked decreases (minimum BP less than 110/70 mm Hg) during sleep. Average cardiac index (CI) of the OH-group was low during wakefulness and extremely low during slow-wave sleep. Changes of mean BP in the OH-group correlated with changes in total peripheral vascular resistance index (TPRI) during sleep, but this correlation was not observed in the YH-group. The antihypertensive effects on nocturnal BP of the various medications was: central adrenergic inhibitors less than or equal to beta blockers with intrinsic sympathomimetic activity less than or equal to alpha (alpha beta) blockers less than or equal to angiotensin-converting enzyme inhibitors less than or equal to calcium antagonists. Because BP and CI were found to be very low and TPRI seems to play an important role in BP regulation in sleeping elderly patients, excessive antihypertensive medication may be harmful to this subgroup. However, because the effects on nocturnal BP differ among various antihypertensive treatments, further research is required on the relation between antihypertensive medication and the hemodynamics of sleeping elderly hypertensive patients.

Adult↗

Neurilemoma of the retroperitoneum.

A case is presented in which suprarenal neurilemoma was associated with paroxysmal attacks of hypertension, headache and sweating with elevated plasma and urinary catecholamines. Pheochromocytoma was excluded using an overnight clonidine suppression test. Ultrasonography, computed tomography and magnetic resonance imaging, which showed cystic mass with a pedicle continuing to the widened intervertebral foramen, were helpful for the preoperative diagnosis of retroperitoneal neurilemoma. The excised tumor was revealed to be benign neurilemoma and contain detectable levels of adrenaline, noradrenaline and dopamine. The relationships between tumor catecholamines and clinical manifestations will be discussed.

Aged↗

Augmented sympathetic nerve activity in response to stressors in young borderline hypertensive men.

To determine whether there may be an abnormality in sympathetic nerve activity in response to physical and psychological stressors, we microneurologically recorded muscle sympathetic nerve activity in 11 normotensive and 9 borderline hypertensive, age-matched men. Supine blood pressure, plasma levels of epinephrine and norepinephrine and muscle sympathetic nerve activity were measured before and during a cold pressor test or a mental arithmetic test. The resting basal values of muscle sympathetic nerve activity, blood pressure and plasma epinephrine were significantly higher in the borderline hypertensives than in the normotensives (P less than 0.05). Plasma norepinephrine levels tended to be higher in the borderline hypertensives than in the normotensives but not to a significant extent (P less than 0.10). The cold test produced significantly exaggerated pressor and muscle sympathetic nerve responses (P less than 0.05) with a trend towards an increase in plasma norepinephrine (P less than 0.10) in the borderline hypertensives as compared with normotensives. The mental arithmetic test produced significantly enhanced pressor and plasma epinephrine responses in the borderline hypertensives as compared with the normotensives (P less than 0.05). During the mental arithmetic test the muscle sympathetic nerve activity decreased significantly in the normotensives (P less than 0.05) but not in the borderline hypertensives. These findings indicate that in people with borderline hypertension an abnormality exists in sympathetic nerve activity at rest and in response to stressors.

Adult↗

Muscle sympathetic nerve activity in renovascular hypertension and primary aldosteronism.

Previous studies, including our own, have demonstrated that muscle sympathetic nerve activity (MSNA) is increased in patients with essential hypertension compared with normotensive subjects. However, the features of sympathetic nerve activity are still unknown in secondary hypertension. We examined MSNA in eight patients with renovascular hypertension and in 11 patients with primary aldosteronism. Twenty patients with essential hypertension and 20 normotensive subjects who were age-matched to the patients with renovascular hypertension and those with primary aldosteronism were also studied. The MSNA of a bundle of the tibial nerve was recorded by microneurography in supine subjects and expressed as both burst rate (bursts/min) and burst incidence (bursts/100 heart beats). Plasma renin activity and the plasma concentration of angiotensin II and aldosterone were also measured. MSNA was increased in the patients with renovascular hypertension compared with the patients with primary aldosteronism and those with essential hypertension and the normotensive subjects (p less than 0.01 for each). MSNA was decreased in the patients with primary aldosteronism compared with those with essential hypertension (p less than 0.01), and it was smaller than in the normotensive subjects (p less than 0.1). Furthermore, MSNA, plasma renin activity, and the plasma concentration of angiotensin II decreased significantly in five patients with renovascular hypertension 4-10 days after successful percutaneous renal angioplasty. Thus, the changes in MSNA seem to characterize the pathophysiology of renovascular hypertension and primary aldosteronism. Activation of the renin-angiotensin system may be involved in the increase in the central outflow of sympathetic nerve activity, thus exacerbating hypertension in patients with renovascular hypertension.

Adolescent↗

Enhanced sympathetic pressor responses to intracerebrovascularly infused saline in awake salt-loaded rats.

Osmotic minipumps were used to infuse hypertonic saline intracerebroventricularly into conscious rats fed high-salt diets to determine if combining high-salt intake with ICV saline infusion would elevate blood pressure more than either procedure alone. Mean aortic pressures became progressively elevated in all rats infused with saline and the magnitude of the elevation was significantly larger in those fed high-salt diets instead of the regular chow. Added pressor effects of high-salt feeding were unaffected by pharmacologic vasopressin or angiotensin blockade thereby indicating that humoral mediation by either peptide was not involved. A general increase in cardiovascular reactivity also seemed unlikely since pressor responsiveness to injected norepinephrine did not differ between rat groups. Sympathetic hyperactivity was considered to be a logical explanation because enhancement by high-salt feeding was abolished following either ganglion blockade with pentolinium or chemical sympathectomy with 6-hydroxydopamine. These findings are compatible with the interpretation that high-salt feeding enhanced pressor responses to centrally-infused saline by increasing sympathetic vasomotor tone.

Angiotensin II↗

Fully automatic, noninvasive measurement of cardiac output by means of the CO2 rebreathing method and its clinical application to hypertensive patients.

A new device (called a hemodynamometer) employing the principle of the CO2 rebreathing method has been developed for the noninvasive automatic measurement of pulmonary blood flow (cardiac output = CO). The device can also measure oxygen consumption (VO2) and indirect blood pressure and record electrocardiographs (heart rate) at the same time and can automatically calculate total peripheral vascular resistance (TPR) by means of a computer. In this study, the hemodynamometer was used in 28 normotensive subjects and 42 patients with essential hypertension (27 with WHO stage I and 15 with WHO stage II) to evaluate hemodynamics during rest or ergometer exercise. To evaluate accuracy, the dye-dilution (cuvette) method was simultaneously employed in some subjects. The correlation coefficient (r) between CO measured by means of the hemodynamometer and CO measured by the cuvette method was 0.96 (n = 39) with a differential of 0.08 +/- 0.53 l/min and reproducibility was good (r = 0.88, n = 70). The average CO index for normotensive subjects at rest was 3.22 +/- 0.37 l/min/m2 (VO2 = 210 +/- 30 ml/min/m2) and agreed with previously reported values. A significant difference was observed between the hemodynamics (CO and TPR indices) of the WHO-I group and those of the WHO-II group during rest or mild exercise (25-watt load). Because it can measure CO and TPR easily and noninvasively, the hemodynamometer is considered useful for evaluating hemodynamic changes in hypertensive patients.

Adult↗

Inhibition of cytokine-induced MHC class II but not class I molecule expression on mouse islet cells by niacinamide and 3-aminobenzamide.

Normal mouse islet cells express low levels of MHC class I molecules and undetectable or extremely low levels of MHC class II molecules. Class I expression was dose-dependently augmented by incubation with interferon-gamma (IFN-gamma) or tumor necrosis factor (TNF). Although neither IFN-gamma nor TNF alone induce class II molecules on islet cells, synergistic interaction of IFN-gamma (200 U/ml) and TNF (200 U/ml) may induce class II expression on approximately 50% of islet cells. Niacinamide and 3-aminobenzamide, both inhibitors of ADP ribosylation and scavengers of free radicals, attenuated the class II expression induced by IFN-gamma and TNF. Twenty millimolar niacinamide and 10 mM 3-aminobenzamide reduced the rates of class II antigen-positive cells to mean +/- SD 3.6 +/- 0.3 and 6.1 +/- 1.9%, respectively. The agents did not affect the cytokine-induced augmentation of class I antigens. The inhibition of class II molecule expression may at least partly account for the preventive effect of niacinamide on autoimmune-associated beta-cell damage in NOD mice.

Animals↗

[Adrenal tumors associated with renal cell carcinoma].

We experienced two cases with renal cell carcinoma who showed enlargement of the contralateral adrenal gland. In case 1, the enlarged adrenal gland was a non-functioning adrenal adenoma, and in case 2, it was a metastatic adrenal tumor. Non-functioning adrenal adenomas are benign tumors of the adrenal cortex often found incidentally at autopsy or on computed tomography (CT) studies of the upper abdomen. Adrenal adenomas have been reported to occur in 9.5-14% of patients with renal cell carcinoma, while the incidence being 1.5-8.7% in the general population. Since metastases of renal cell carcinoma to the adrenal glands are not uncommon, it is important to distinguish between non-functioning adrenal adenomas and metastatic tumors. Therefore, we studied the incidence of adrenal tumors (including metastatic tumors and benign tumors) in patients with renal cell carcinoma who underwent the abdominal CT study in our hospital. From 1982 to 1989, CT had been performed in 67 patients with renal cell carcinoma. Six adrenal masses were identified with CT in these patients. Three out of the 6 patients probably had metastatic tumors and one of the 3 adrenal masses was pathologically diagnosed as metastatic tumor. The other three masses were benign on pathology and only one of them was pathologically diagnosed as non-functioning adrenal adenoma. The incidence of adrenal adenomas on the CT study was lower than that of previous studies based on autopsy. The reasons of this difference in results between their studies and ours are not clear.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenoma↗

Age-related changes in muscle sympathetic nerve activity in essential hypertension.

To investigate the pathophysiological role of the sympathetic nervous system in essential hypertension, this study recorded the muscle sympathetic nerve activity (MSNA) of the tibial nerve and examined the age-related changes in patients with essential hypertension and in normotensive persons. There were 43 normotensive subjects (16-69 years old) and 63 patients with essential hypertension (18-67 years old) in the study. The MSNA at rest, recorded by microneurography, was evaluated by burst rate (bursts/min), burst incidence (bursts/100 heart beats), and spike frequency (spikes/min). The MSNA recording showed a high reproducibility with a correlation coefficient of 0.86 (p less than 0.01) in repeated studies. The MSNA was significantly greater in the hypertensive patients than in the normotensive subjects, irrespective of activity units (p less than 0.01), and this finding was consistent in the young (30 years old or less), middle-aged (31-50 years old), and old groups (51 years old or more). Furthermore, MSNA showed a significant positive correlation with age both in the normotensive subjects (r = 0.43, p less than 0.01 for burst rate; r = 0.49, p less than 0.01 for burst incidence; and r = 0.50, p less than 0.01 for spike frequency) and in the hypertensive patients (r = 0.40, p less than 0.01 for burst rate; r = 0.44, p less than 0.01 for burst incidence; and r = 0.40, p less than 0.01 for spike frequency).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

Functional atrial natriuretic peptide receptor in human adrenal tumor.

The effects of synthetic human atrial natriuretic peptide (ANP) on the release of catecholamines, aldosterone, or cortisol were observed in human adrenal tumors obtained surgically from patients with pheochromocytoma, primary aldosteronism, or Cushing's syndrome, respectively. Each tumor tissue or adjacent normal cortical tissue was sectioned into slices, which were incubated in medium-199 in the presence or absence of adrenocorticotrophin (ACTH) and ANP. The amounts of epinephrine, norepinephrine, aldosterone, or cortisol released into the medium were measured. Existence of ANP receptors on the adrenal tissues was examined by binding assays, affinity labeling, and immunohistochemistry. Release of catecholamines from pheochromocytoma tissues was inhibited by ANP, and the presence of the ANP receptor on pheochromocytoma was further demonstrated by both binding assays and affinity labeling; Scatchard analysis revealed a single class of binding sites for ANP with a Kd of 1.0 nM and a Bmax of 0.4 pmol/mg of protein and the molecular size was estimated as 140 and a 70 kDa under nonreducing and reducing conditions, respectively. The presence of ANP receptors in pheochromocytoma was demonstrated by immunohistochemistry. ANP inhibited both basal and ACTH-stimulated aldosterone secretion in the slices of normal cortex, and localization of ANP receptors in zona glomerulosa cells was also demonstrated. However, ANP did not inhibit basal and ACTH-stimulated aldosterone and cortisol secretion in both tissue slices from aldosteronoma and Cushing's adenoma. Consistent with these observations, the absence of ANP receptors in adenoma tissues was determined by binding assays, affinity labeling, and immunohistochemistry.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Cortex↗

Angiotensin II inhibits baroreflex control of muscle sympathetic nerve activity and the heart rate in patients with essential hypertension.

This study examined the effects of angiotensin II (Ang II) on blood pressure, heart rate and muscle sympathetic nerve activity in patients with essential hypertension and normotensive subjects. Muscle sympathetic nerve activity was measured by a microneurographic method. Graded doses of phenylephrine (0.5 and 1.0 g/kg per min) or Ang II (5, 10 and 20 ng/kg per min) were intravenously infused into supine subjects for 10 min at 30-min intervals. Although the pressor responses to Ang II and phenylephrine were enhanced in the hypertensives compared with the normotensives (both P less than 0.05), the reduction in muscle sympathetic nerve activity during infusion of phenylephrine and Ang II and the reduction in the heart rate during infusion of phenylephrine were significantly smaller in the hypertensives than in the normotensives. The decrease in the heart rate in response to Ang II was not significant in either group. Furthermore, in the two groups, the decreases in muscle sympathetic nerve activity and the heart rate were significantly smaller during infusion of Ang II than during infusion of phenylephrine. These results suggest that angiotensin II impairs the baroreflex function in patients with essential hypertension and in normotensive subjects, and that the blunted response of sympathetic nerve activity and the heart rate observed in the hypertensives may underlie the maintenance of high blood pressure.

Angiotensin II↗

Impaired baroreflex changes in muscle sympathetic nerve activity in adolescents who have a family history of essential hypertension.

To evaluate the baroreflex changes and basal sympathetic vasomotor tone among three groups of adolescent normotensives or borderline hypertensives with and normotensives without a family history of hypertension, we continuously recorded muscle sympathetic nerve activity, arterial pressure and heart interval. Baroreflex slopes were calculated either by plotting the heart interval against the preceding peak systolic arterial pressure, or by relating the percentage changes in muscle sympathetic nerve activity to the mean changes in systolic arterial pressure produced by intravenous phenylephrine. The baroreflex slopes for the heart interval were significantly smaller in borderline hypertensive offspring (14 +/- 2 ms/mmHg) than in control normotensives (23 +/- 2 ms/mmHg) or normotensive offspring (19 +/- 3 ms/mmHg), whereas those for muscle sympathetic nerve activity were significantly smaller both in normotensive offspring (-8.3 +/- 1.0%/mmHg) and borderline hypertensive offspring (-7.9 +/- 0.5%/mmHg) than in control normotensives (-16.3 +/- 1.4%/mmHg). Baseline muscle sympathetic nerve activity was higher in borderline hypertensive offspring (20.1 +/- 3.0 bursts/min) than in control normotensives (10.1 +/- 1.2 bursts/min) or normotensive offspring (12.8 +/- 1.4 bursts/min), and also the depressor responses to trimethaphan were significantly enhanced in borderline hypertensive offspring [-19.2 +/- 2 versus 14 +/- 1 (normotensive offspring) or 12 +/- 2 (control normotensives)]. These results indicate that baroreflex inhibition of muscle sympathetic nerve activity was reduced in adolescents with a family history of hypertension even when they were normotensive. This reduced reflex sympatho-inhibition could lead to the development of hypertension by increasing sympathetic vasomotor tone.

Adult↗