Biomedical subjects
Publications and source records attributed to M Nihei.
A case of apocrine carcinoma of the breast is reported herein. Apocrine carcinoma is a rare tumor characteristically composed of large cells with eosinophilic cytoplasm. This case involves a 34-year old woman who underwent a modified radical mastectomy and is now doing well with no evidence of recurrence, 10 months after her surgery.
The circadian blood pressure rhythm was compared in patients with Cushing's syndrome, essential hypertension, and primary aldosteronism. In patients with essential hypertension or primary aldosteronism, a clear nocturnal fall in systolic and diastolic blood pressure and heart rate was observed. This fall was seen in untreated subjects as well as in patients receiving combined treatment with a calcium antagonist, diuretic, converting enzyme inhibitor, alpha-blocker and beta-blocker, or sympatholytic drug. In these groups, there was a positive correlation between heart rate and systolic or diastolic blood pressure. On the other hand, in patients with Cushing's syndrome, there was no nocturnal fall in blood pressure but in some patients a rise was observed. In all patients there was a nocturnal fall in heart rate. Thus, there was no significant correlation between heart rate and blood pressure in these patients. Exogenous glucocorticoid eliminated the normal nocturnal fall of blood pressure in patients with chronic glomerulonephritis or systemic lupus erythematosus. These results suggest that the changed circadian blood pressure pattern in patients with Cushing's syndrome is not due to antihypertensive treatment or to the mineralocorticoid excess accompanying this disease, but it is attributable to excess glucocorticoid or the associated disturbance in the adrenocorticotropic hormone-glucocorticoid system (or both). This conclusion also implies that the normal circadian rhythm of blood pressure may be regulated at least in part by the adrenocorticotropic hormone-glucocorticoid system.
The hypotensive mechanism of percutaneous transluminal dilatation (PTD) in renovascular hypertension due to bilateral renal artery was investigated in two patients. Blood pressure was monitored continuously before, during and after PTD by use of a new automated blood pressure monitoring device based on finger volume-oscillometry. Plasma renin activity was measured repeatedly before, during and after PTD. A hypotensive effect appeared immediately after PTD and blood pressure remained low in the following observation period without any hypotensive medication. In these cases, the hypotension was accompanied by a transient decrease in heart rate immediately after PTD. The hypotensive response to PTD was not parallel to the basal plasma renin activity, suggesting that the renin-angiotensin system is not necessarily involved in the maintenance of the hypertension before PTD. The autonomic nervous system seemed to play a certain role. Since the hypotension was accompanied by a transient decrease in heart rate immediately after PTD, the hypotension may be induced either by a decrease in sympathetic tone or by an increase in vagal tone at least just after PTD. It is hypothesized that these changes in autonomic nervous activity are mediated centrally through the renal afferent mechanism in response to rapid changes in renal hemodynamics induced by PTD.
A new portable device for the indirect measurement of arterial blood pressure was successfully applied to detect paroxysmal hypertension and circadian fluctuation of blood pressure in patients with phaeochromocytoma. The device utilizes the volume-oscillometric technique, it is equipped with a microprocessor and allows long-term automatic monitoring of indirect blood pressure in the human finger. Compared with conventional fully automated portable devices of the arm-cuff type, our current equipment is lighter, less noisy, and causes less discomfort. With this device repeated measurements can be made without causing stress or discomfort, and without disturbing sleep. The arterial pressure measurement obtained using this device was reliable and reproducible. In some patients certain symptoms, possibly due to phaeochromocytoma, had been observed for several years before the study, although hypertension had not been identified. While these patients had consistently high circulating catecholamine levels, nocturnal falls in blood pressure were clearly documented. This suggests that plasma catecholamines released from the phaeochromocytoma, though excessive, may be of less physiological importance than other regulatory mechanisms concerned with circadian fluctuation of blood pressure, e.g. the sympathetic nervous system and/or hypothalamo-pituitary-adrenal system. This new device has proved to be a reliable means of monitoring long-term blood pressure and is useful in the diagnosis of paroxysmal hypertension in patients with phaeochromocytoma.
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Hereditary deficiencies in early and late complement components are well known to predispose to SLE-like syndromes or recurrent infection. Hitherto reported C9 deficient cases have usually been healthy subjects, however, and it is not considered that C9 deficiency is associated with any specific disease. We describe a completely C9 deficient patient with possible Sjögren's syndrome and discuss the relationship.
The circadian rhythm of blood pressure (BP) was compared between patients with Cushing's syndrome and those with essential hypertension. In patients with essential hypertension, clear nocturnal falls in systolic and diastolic BP and heart rate (HR) were observed, and there was a positive correlation between HR and systolic or diastolic BP. On the other hand, in patients with Cushing's syndrome, there was no nocturnal fall in BP and instead a rise in some cases. In all cases with Cushing's syndrome there was a nocturnal fall in HR, and consequently no significant correlation between HR and BP in these patients. The present results imply that the normal circadian rhythm of blood pressure may be regulated at least in part by the hypothalamo-pituitary-adrenal system.
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A new portable device for the indirect measurement of ambulatory blood pressure in the finger was successfully applied to normotensive and hypertensive subjects in and outside a ward setting. The device uses the volume-oscillometric technique and, equipped with a microprocessor, permits long-term ambulatory monitoring of indirect systolic and mean blood pressure at desired intervals (once every 1-10 min). Systolic and mean blood pressures obtained by this method were well correlated with those measured by the direct (Oxford) and arm-cuff methods. Systolic and diastolic blood pressure obtained by the volume-oscillometric device were almost identical with those recorded by an arm-cuff. Systolic blood pressure obtained by the volume oscillometric method was, however, significantly lower than that measured by the direct method. The new device has also been used to measure blood pressure during treadmill exercise and ice-water immersion. Mean values of blood pressure and the SD of these averaged for 24 hours, or for every hour, were reproducible when the measurements were repeated under the same condition. The present device is portable, causes minimal noise, can detect rapid change in blood pressure and causes less discomfort when compared to the conventional arm-cuff method. Regular measurements can be made with minimal sleep disturbance. This fully automatic volume-oscillometric device allows reliable 24-hour monitoring of ambulatory blood pressure not only in but also outside a ward setting, and as such is useful for studies of hypertension.
The effect of weight loss on blood pressure and on antihypertensive drug consumption was examined in 81 nonobese subjects with essential hypertension who had been chronically treated with antihypertensive drugs. A hypocaloric diet was prescribed for 5 months. A weight loss greater than 2 kg in 5 months was considered significant. Quality and quantity of antihypertensive medications were scored according to a formula. In the subjects whose medication and weight did not change, mean arterial pressure remained unchanged, whereas it decreased significantly (-7.1 +/- 1.9 mm Hg) in those who showed significant weight loss (-3.28 +/- 0.34 kg) with no change in medication. Among the subjects whose antihypertensive medication remained constant during the diet program there was a significant correlation between the change in weight and mean arterial pressure (r = 0.45, p less than 0.01). Mean arterial pressure increased significantly (+5.1 +/- 1.7 mm Hg) in subjects whose weight remained unchanged with a decrease in medication, whereas it remained significantly lower than the control (by -3.1 +/- 2.0 mm Hg) in those whose weight decreased significantly (-4.57 +/- 0.69 kg) with the decrease in medication. The weight loss-induced decrease in blood pressure occurred independently of the initial degree of obesity and the initial level of mean arterial pressure. Urinary sodium excretion in the control period and at the end of the diet program did not differ significantly between subgroups. These results indicate that, even in subjects of normal weight with essential hypertension, weight loss can induce a fall in blood pressure that leads to a reduction of antihypertensive medication.(ABSTRACT TRUNCATED AT 250 WORDS)
A new device which measures ambulatory blood pressure was used to detect paroxysmal hypertension in patients with pheochromocytoma. The device uses a finger volume-oscillometric technique for the long-term measurement of indirect arterial pressure at desired intervals. The device clearly detected crises of hypertension of short duration. This device is invaluable for the detection of paroxysmal hypertension in patients with pheochromocytoma.
In patients with essential hypertension, the pharmacokinetics of nifedipine in 2 forms (capsule, 10 mg nifedipine dissolved in an organic solvent; slow release tablet, 20 mg nifedipine) and their pharmacodynamic effectiveness on arterial pressure were studied. The maximum plasma concentration was higher and achieved more rapidly after application of the capsule than after the retard tablet (p less than 0.01). The plasma half-time of nifedipine in the capsule was shorter than that in the retard tablet (p less than 0.05). The absorption rate of nifedipine from the capsule tended to be larger than that from the retard tablet. Plasma concentrations of nifedipine, measured 12 hr after the dosing of the retard tablet during chronic treatment, were not different from those after the acute administration of the retard tablet, suggesting that no accumulation of nifedipine occurs. The capsule of nifedipine elicited prompt and profound hypotension with short duration, while the retard tablet produced a hypotensive effect with relatively slow onset and long duration. Arterial pressure reduction was maintained throughout the day using 12 hourly dose of the retard tablet. During the chronic treatment the maximum hypotensive effect was observed 4 weeks after the start of treatment. Twelve hourly administration of the retard tablet is a convenient regimen for the long-term control of mild to severe essential hypertension.
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Short-term treatment with 1-(p-carbamoyl-methylphenoxy)-3-isopropylamino)-2-propanol (atenolol, Tenormin) (100 mg/d for 5 days) was conducted in 12 patients with labile essential hypertension. Before and at the end of the treatment, cardiohemodynamics, renal hemodynamic and excretory function, and renal pressor (renin-angiotensin-aldosterone) and depressor (renal kallikrein-kinin and prostaglandin) systems were examined. Atenolol decreased cardiac output (CO) without affecting total peripheral resistance. Atenolol also decreased plasma renin activity, plasma aldosterone concentration, urinary excretion of kallikrein-kinin, and urinary excretion of potassium whereas it increased plasma potassium concentration. Urinary excretion of prostaglandin E and sodium was not affected by atenolol. Glomerular filtration rate decreased, but renal plasma flow remained unchanged during the treatment by atenolol. A significant positive correlation was found between the changes in CO and in systolic blood pressure (SBP) while negative correlation was observed between the changes in total peripheral resistance and in SBP. A significant positive correlation was also noted between urinary kallikrein excretion and renal plasma flow. The change in urinary kinin excretion was conversely correlated to that in SBP. This study demonstrates that the hypotensive mechanism of atenolol is very complex. Decrease in CO and inhibition of renin-angiotensin-aldosterone system may mainly be responsible for hypotension. It is likely that potassium retaining action of atenolol partly contributes to its hypotensive action. It is also hypothetized that renal kallikrein-kinin system may play a role in modulating the hypotensive action of atenolol.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.