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Biomedical subjects

E Miyajima

Publications and source records attributed to E Miyajima.

At least 55 records · Page 3Linked to original sources
PubMed1988

A new compact 24-hour indirect blood-pressure recorder and its clinical application.

A new portable noninvasive recorder (4 X 6.5 X 14 cm in size, 390 g in weight) was developed for monitoring 24-hour blood pressure and its clinical applicability was investigated. Employing an ordinary-size cuff, this is the lightest and the most compact apparatus of its kind ever developed. It is powered by a rechargeable battery. The cuff is pressurized by a miniature, low-noise, rotary micropump. To eliminate noises resulting from body motion, two microphones are used to distinguish Korotkoff sounds. Systolic blood pressure (SBP), diastolic blood pressure (DBP), and heart rate (HR) are measured automatically at intervals of 1 to 60 min throughout 24 hours. These data can be stored as many as 600 times in the recorder's semiconductor memory. After measurement, mean values; standard deviations (SD); and trendograms of SBP, DBP, and HR are printed out by means of an appurtenant, miniature analyzer measuring 5 X 7.5 X 15 cm. A comparison of values obtained with this new instrument and the values obtained with a conventional auscultatory method showed average errors of -1.2 +/- 4.7 (SD)mmHg for SBP and -2.7 +/- 5.0 mmHg for DBP. The correlation coefficient (r) of values obtained by two methods was r = 0.99 for SBP and r = 0.96 for DBP (n = 185). In 38 male and 31 female normotensive subjects (average casual BP: male 126 +/- 11/76 +/- 7 mmHg; female 116 +/- 13/69 +/- 10 mmHg), average 24-hour BP values recorded by the new recorder were 115 +/- 7.5 (SBP)/70 +/- 6 (DBP)mmHg for the males and 106 +/- 6/63 +/- 5 mmHg for the females. The new recorder seems to be convenient, easy to operate, and clinically useful in ambulatory monitoring.

Adult↗
PubMed1988

Neurogenic abnormalities in young borderline hypertensives.

Although neurogenic abnormalities have been postulated to be involved in the pathogenesis of borderline hypertension, no direct evidence has been documented. We continuously recorded muscle sympathetic nerve activity (MSNA) using a microelectrode in the tibial nerve, along with arterial pressure (AP) and heart rate (HR) during the cold pressor or isometric handgrip test in 16 male adolescents with borderline hypertension (BHT) and 10 normotensive adolescents (NT). Baroreflex changes in MSNA were also assessed during the pressor responses to intravenous phenylephrine. During the cold pressor test, both MSNA and AP gradually increased, but the HR responses were inconsistent. The resulting changes in MSNA, AP and HR were all augmented in BHT compared with NT. By contrast during the isometric handgrip test, MSNA, AP, and HR increased in both groups, but none of the differences between the groups was significant. Furthermore, baroreflex inhibition of MSNA were significantly reduced in BHT. Thus, some neurogenic abnormalities exist in BHT, which can be easily detected by recording MSNA.

Adolescent↗
PubMed1987

Presence of functional receptors for atrial natriuretic peptide in human pheochromocytoma.

Pheochromocytoma, a catecholamine-secreting adrenomedullary tumor, has been shown to contain the functional receptor for human atrial natriuretic peptide(h-ANP). Release of catecholamines from tissue slices of pheochromocytoma was inhibited by h-ANP in a dose-dependent manner. Binding assays using 125I-ANP revealed a single class of high affinity binding sites for ANP. When covalently tagged with 125I-ANP and electrophoresed under non-reducing and reducing conditions, the receptor migrated as a 140-kDa band and a 70-kDa band, respectively, reflecting its disulfide-linked subunit structure. The presence of ANP receptor in pheochromocytoma was further demonstrated by immunohistochemistry; the tumor was positively stained with an antireceptor antiserum. The antiserum was also useful to establish the zona glomerulosa localization of ANP receptor in the normal human adrenal gland.

Adrenal Gland Neoplasms↗
PubMed1987

Pharmacokinetics and depressor effect of delapril in patients with essential hypertension.

The pharmacokinetics and depressor effect of a nonsulfhydryl angiotensin-converting enzyme inhibitor, delapril, was assessed by administering a single dose of 30 mg to nine patients with mild to moderate essential hypertension. Orally administered delapril is a prodrug and must be deesterified to its active metabolites, delapril diacid and 5-hydroxy delapril diacid. The pharmacokinetic parameters for delapril, delapril diacid, and 5-hydroxy delapril diacid were, respectively: t 1/2 0.30, 1.21, and 1.40 hours; Cmax 489, 635, and 229 ng/ml; AUC 572, 1859, and 948 ng X hr/ml. Delapril produced significant decreases in systolic blood pressure and angiotensin-converting enzyme activity 24 hours after dosing. There were no significant changes in the endogeneous creatinine clearance after the drug. Thus delapril may represent a useful antihypertensive agent for control of blood pressure in patients with essential hypertension.

Adult↗
PubMed1987

Pharmacokinetics of a single dose of ramipril in patients with renal dysfunction: comparison with essential hypertension.

The acute effects and pharmacokinetic properties of an angiotensin converting enzyme (ACE) inhibitor, ramipril, and its potent active diacid metabolite, ramiprilate, were investigated. Hypertensive patients with impaired renal function (IRF; n = 6) and with normal renal function (NRF; n = 5) were studied. The terminal half-life of ramiprilate in IRF was longer than that in NRF. The peak plasma concentrations of ramipril and ramiprilate in IRF were higher than those in NRF. The area under the plasma level-time curves of ramipril and ramiprilate in IRF were greater than those in NRF. A significant inverse correlation was found between creatinine clearance and area under the plasma level-time curve.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1987

Antihypertensive effects and pharmacokinetics of single and consecutive administration of doxazosin in patients with mild to moderate essential hypertension.

A single dose of doxazosin, a long-acting postsynaptic alpha 1-adrenoceptor antagonist, was administered to seven patients with essential hypertension. Following administration of a single dose, all the patients except one who was forced to be discharged from the hospital for work, continuously received doxazosin once daily (o.d.) for evaluation of its consecutive dosing effect. The antihypertensive effect, pharmacokinetics, and effects on the plasma renin activity (PRA) of doxazosin were investigated. Following a 2-mg single dose of doxazosin, the systolic blood pressure (SBP) decreased significantly up to 12 h, whereas consecutive dosing produced a significant decrease in the SBP up to 24 h and a significant decrease in the mean blood pressure up to 24 h as compared with placebo. The pharmacokinetic parameters of doxazosin in both single- and consecutive-dose study were 18.9 and 25.8 ng/ml in Cmax, 11.1 and 12.9 h in half life (t1/2), and 182.0 and 273.0 ng h/ml in area under the curve (AUC)24(0), respectively. No significant changes were observed in PRA and plasma concentration of catecholamines. Neither were there any observable changes in endogenous creatinine clearance and in the urinary excretion rates of Na, K, and Cl. Doxazosin was well tolerated by all patients, and no untoward effects were observed. Doxazosin effectively reduces blood pressure and, because of its long t1/2 and minimal effects on PRA catecholamines, and electrolytes, seems to be a useful antihypertensive agent in patients with essential hypertension.

Adult↗
PubMed1987

Exacerbation of central baroreflex impairment in Dahl rats by high-salt diets.

To determine whether baroreflex impairment progresses in hypertensive Dahl rats, we recorded reflex responses to drug-induced changes in blood pressure in hypertension-sensitive (DS) and hypertension-resistant (DR) rats maintained on low- or high-salt diets for 7 wk. Chronotropic responses, manifested as either bradycardia for phenylephrine or tachycardia for sodium nitroprusside, were always smaller in awake DS rats on high-salt diet than in any others. When the same rats were later anesthetized, related changes in afferent aortic and efferent splanchnic nerve activity were similarly reduced. Regardless of dietary salt intake, reflex bradycardia elicited by electrical stimulation of aortic nerve afferents was also weaker in DS than in DR rats, but attendant decreases in mean aortic pressure and splanchnic nerve activity did not differ significantly. These results are compatible with an impairment of afferent and central components of the reflex arc. Even though exact sites of dysfunction were not identified, our findings suggest that in hypertensive DS rats high-salt diets may aggravate baroreflex impairment, at least in part, by acting centrally.

Afferent Pathways↗
PubMed1987

Measurements of base blood pressure during sleep and its clinical significance in hypertensive patients.

The intra-arterial blood pressure (BP) was measured during 24 hours on 52 patients with essential hypertension using a portable device. The minimum BP inherent to each subject (base BP) was determined from the systolic and diastolic BP histograms during sleep. In this study the systolic and diastolic BPs were presented as a mean BP (BP) and a base BP, and the average of BPs during waking hours was considered as the sum of the base BP and the additional BP increment. The clinical significance of the base BP and BP increment was examined by comparing them with the results of clinical examinations. The comparison showed that the base BP was closely related with the left ventricular hypertrophy and severity of hypertension, while the BP increment correlated with the baroreflex sensitivity and plasma norepinephrine concentration. In this paper, a new tonometry was developed to indirectly record the BP of the superficial temporal artery. The tonometry correlated well with the intra-arterial BP measurement, and was available for the indirect base BP evaluation at an outpatient-clinic.

Adult↗
PubMed1987

Renal haemodynamics and comparative effects of captopril in patients with benign- or malignant-essential hypertension, or with chronic renal failure.

Effects of captopril on arterial pressure (AP) and renal function were investigated in patients with non-malignant "benign" or malignant phase essential hypertension (EH group), or with chronic renal failure (CRF group). After captopril administration, AP and renal vascular resistance (RVR) decreased significantly, and renal blood flow (RBF) and plasma renin activity (PRA) increased in both groups. Glomerular filtration rate (GFR) increased in the EH group, but was unchanged in CRF. Filtration fraction decreased in the malignant hypertension and CRF groups. Significant correlations were found between baseline PRA and baseline RVR, and the captopril-induced decrease in mean AP, decrease in RVR, increase in RBF, and increase in GFR in the EH group, while these associations were not observed in CRF. These results indicate that the high AP, RVR, suppressed RBF and GFR in the EH group were closely related to activity of the renin-angiotensin system, but not so the low RBF and GFR in CRF. Small doses of captopril may improve impaired renal function in EH, and may not cause deterioration in the CRF group.

Captopril↗
PubMed1987

Preoperative lateralisation of aldosteronomas by aldosterone/cortisol ratios in adrenal venous plasma.

Data from adrenal scintigraphy with 6 beta-[131I]-iodomethyl-19-norcholesterol (AS), computed tomography (CT), adrenal venography and adrenal venous sampling were compared for their accuracy in locating small aldosteronomas in 17 patients. Final confirmation of location was by surgery. Seventeen out of 18 adrenals whose aldosterone/cortisol (A/C) ratio was 5.0 x 10(-3) or higher were found to have aldosteronomas (94.4%). All 14 adrenals whose A/C ratios were less than 5.0 x 10(-3) contained no aldosteronomas (100%). AS successfully lateralised nine out of 17 aldosteronomas (52.9%), CT 3 out of 5 (60.0%), adrenal venography 12 out of 17 (70.6%), adrenal venous aldosterone concentration 12 out of 15 (80.0%). The most frequent problem with adrenal venous sampling was the varying degrees of mixture with non-adrenal venous blood, mainly from renal vein and inferior vena cava blood. The A/C ratio of adrenal venous plasma proved to be the most useful diagnostic tool, using cortisol concentration as an indicator of any non-adrenal venous mixture.

Adenoma↗
PubMed1986

Impaired sympathetic baroreflexes in prehypertensive Dahl hypertension-sensitive rats.

Baroreflex responsiveness was assessed in Dahl rats that had been fed a low-salt diet to retard subsequent development of hypertension. After five weeks there were no differences in baseline pressures, but all responses elicited reflexly by elevating blood pressure with phenylephrine were less pronounced in hypertension-sensitive (DS) than in hypertension-resistant (DR) rats. Diminished responses included the following: acceleration in afferent aortic nerve activity, bradycardia, and inhibition of splanchnic and renal sympathetic nerve activity. By contrast, opposite responses elicited by lowering blood pressure with sodium nitroprusside did not differ significantly. Selective baroreflex attenuation (i.e. which was demonstrable only when blood pressure was elevated but not when it was lowered) in DS rats may have been due to differences either in pharmacology of the two drugs, or in sinoaortic vessel wall geometry. The baroreflex impairment shown here could represent a genetic predisposition that eventually elevates blood pressure in DS rats by increasing sympathetic vasomotor tone in the renal and splanchnic vascular beds.

Animals↗
PubMed1985

Anterior hypothalamic lesions impair reflex bradycardia selectively in rats.

To determine whether removal of the anterior hypothalamus would alter baroreflex activity, reflex inhibition of heart rate and renal nerve activity during pressor responses to intravenous phenylephrine was examined in rats with bilateral anterior hypothalamic lesions. Although there were no differences in basal blood pressure and heart rate 10 days after surgery, reflex bradycardia was significantly reduced in awake lesioned rats compared with sham-operated controls. The differences in reflex bradycardia were abolished by cholinergic blockade with atropine but unaltered by beta-adrenergic blockade with propranolol. Because attenuation of chronotropic reflexes by anterior hypothalamic lesions resembled that produced by cholinergic blockade, vagal inhibition must be at least partly responsible. Reflex bradycardia was still attenuated even in lesioned rats anesthetized with alpha-chloralose, but renal nerve activity was as inhibited as in sham-operated rats. These results suggest that the anterior hypothalamus participates in baroreflex regulation of heart rate by altering parasympathetic tone but without affecting cardiac or renal sympathetic nerve activity.

Animals↗
PubMed1985

Dietary salt loading produces baroreflex impairment and mild hypertension in rats.

Mild hypertension with reduced chronotropic baroreflex sensitivity to phenylephrine occurred in Sprague-Dawley rats fed a high-salt diet for 5 wk. Progressive elevation of systolic and mean pressures, detected initially by indirect tail-cuff measurement, was later verified by direct recording of phasic pressures from indwelling aortic catheters in the same rats. Reflex bradycardia during pressor responses to phenylephrine was consistently less pronounced in salt-loaded than in control rats, whether tested while rats were awake or anesthetized. However, attendant decreases in renal nerve activity were not appreciably altered. Neither central nor carotid baroreceptor mechanisms were considered likely but aortic baroreceptors must have somehow been depressed because increases in afferent aortic nerve activity elicited during intravenous infusion of phenylephrine were invariably smaller in salt-loaded than in control rats. Whatever the underlying mechanisms may be, our results show that when hypertension develops during dietary salt loading, baroreflex chronotropic responses are selectively inhibited while attendant decreases in renal nerve activity are preserved.

Action Potentials↗
PubMed1984

Chronic cerebroventricular infusion of hypertonic sodium chloride in rats reduces hypothalamic sympatho-inhibition and elevates blood pressure.

To determine whether or not salt loading restricted to the brain would elevate blood pressure, chronically implanted osmotic minipumps were used to infuse hypertonic sodium chloride solutions made in artificial cerebrospinal fluid into a jugular vein intravenously or the third cerebral ventricle, intracerebroventricularly, for 11 days in awake rats. During intracerebroventricular infusion of hypertonic sodium chloride, tail-cuff systolic pressures began to rise on day 4 and were significantly elevated by day 9. In contrast, infusions of either artificial cerebrospinal fluid alone, intracerebroventricularly, or hypertonic sodium chloride, intravenously, were ineffective. Confirming the blood pressure elevation thereby detected, systolic and mean pressures recorded directly from indwelling aortic catheters after the same rats had been anesthetized with urethane on day 11, were also significantly higher following intracerebroventricular infusion of hypertonic sodium chloride than after infusion of artificial cerebrospinal fluid alone. Magnitude of depressor and sympatho-inhibitory responses elicited by graded electrical stimulation of the anterior hypothalamus invariably increased with the current strength used for stimulation. At all current strengths used for hypothalamic stimulation, depressor responses as well as attendant decreases in sympathetic neural firing, were smaller in rats that had been infused intracerebroventricularly with hypertonic sodium chloride than in any of the controls. Inhibition seemed specific for the anterior hypothalamus because pressor responses to stimulation of the ventromedial hypothalamus were the same whether or not the intracerebroventricular infusion contained hypertonic sodium chloride. An explanation based on diminished cardiovascular sensitivity also appeared unlikely, since depressor responses to intravenously injected histamine were almost equal in both groups. Our results are compatible with the interpretation that hypertonic sodium chloride infused chronically into the 3rd ventricle acts by reducing anterior hypothalamic inhibition of sympathetic vasomotor tone, and that this, in turn, then elevates blood pressure.

Animals↗
PubMed1984

Baroreflex impairment precedes hypertension during chronic cerebroventricular infusion of hypertonic sodium chloride in rats.

Osmotic minipumps were implanted chronically for continuous 11-d infusion of hypertonic sodium chloride (NaCl) into the third cerebral ventricle (ICV) of awake rats to determine whether baroreflex sensitivity would be altered. Systolic and mean pressures, recorded from aortic catheters on day 11 while the rats were anesthetized with alpha-chloralose, were significantly higher in rats infused with artificial cerebrospinal fluid (CSF) containing hypertonic NaCl than in controls similarly infused with artificial CSF alone. Reflex changes in heart rate produced by subsequent intravenous infusions of either phenylephrine or sodium nitroprusside were inhibited, but reflex changes in renal nerve activity were unaltered. Magnitude of reflex bradycardia during pressor responses to phenylephrine, as well as of reflex tachycardia during depressor responses to sodium nitroprusside, was consistently smaller in NaCl-infused than in control rats. By contrast, group differences in attendant renal nerve firing were not significant. After sinoaortic denervation, drug-induced blood pressure effects persisted, but reflex responses in heart rate and renal nerve firing were abolished or markedly diminished. Peripheral effects produced by hypertonic NaCl leakage from the infusion site were considered unlikely because after 11 d of ICV infusion, sodium concentration, though appreciably elevated in CSF samples collected from the cisterna magna, was unaffected in corresponding serum samples. When cardiovascular responses to phenylephrine were recorded while chronic ICV infusions were in progress, awake rats receiving hypertonic NaCl were still normotensive on day 2 yet reflex bradycardia was already attenuated. In showing that baroreflex impairment preceded the development of hypertension, our results suggest that by depressing the anterior hypothalamus, chronic ICV infusion of hypertonic NaCl reduces sympatho-inhibition, and the ensuing baroreflex impairment then elevates blood pressure. However, other mechanisms could also be involved.

Animals↗
PubMed1978

Interference of an anesthetic preparation with plasma triglyceride determinations.

A marked elevation in plasma triglycerides is observed when experimental animals are anesthetized with a pentobarbital sodium injection (Nembutal), a most widely used anesthetic in animal experiments. This is proven, however, to be a false rise due to the interference of propylene glycol present in the solvent of the injection with the plasma triglyceride determinations. One mole of propylene glycol produces one mole of formaldehyde by oxidation. The formaldehyde thus generated from propylene glycol mixes with those from glycerol moiety of plasma triglycerides, and gives an enhanced color reaction to all chromogenic reactions with formaldehyde. Since most of the chemical methods for plasma triglyceride determination is based on either one of these color reactions, we have to pay attention to a hypertriglyceridemia due to such influence as exerted by a solvent additive of propylene glycol upon the triglyceride measurements.

Animals↗