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Biomedical subjects

M Anlauf

Publications and source records attributed to M Anlauf.

At least 19 recordsLinked to original sources
PubMed1995

[Amlodipine in long-term treatment of mild and moderate hypertension. A multicenter study].

METHOD: An open, multicenter study was conducted to investigate the antihypertensive efficacy and safety of amlodipine in the long-term treatment of patients with mild to moderate essential hypertension of a period of 178 weeks (3.4 years). RESULTS: 92 of the 110 patients participating in the study received amlodipine treatment throughout the total study period, with 77 patients on amlodipine monotherapy (mean daily dose 6.3 mg), and 15 patients on combination antihypertensive therapy including amlodipine (mean daily dose 7.1 mg). After 8 weeks of treatment the diastolic target blood pressure of < or = 90 mmHg was achieved in 86 out of 92 patients (93.5%). The mean diastolic blood pressure reduction was retained throughout the treatment, both in patients receiving monotherapy and those on combination therapy. The incidence of adverse events was highest during the first 12 weeks of treatment (30.0%); after another 54 weeks it dropped to 18.1%, and to 7.3% during the last 112 weeks. The side effects reported most frequently were headaches and edema. CONCLUSION: These results indicate that amlodipine effects sustained reduction in diastolic blood pressure over a period of more than 3 years in patients with mild to moderate hypertension.

Adult↗
PubMed1993

[Circadian antihypertensive effect of sustained-release isradipine in patients with essential hypertension in comparison to placebo].

In this multicenter, placebo-controlled study, 16 patients with mild to moderate essential hypertension were treated with 10 mg/day isradipine retard (PN 200-110, Lomir SRO, CAS 75695-93-1) for 3 weeks. The study started with a 2 week placebo wash out phase. 13 patients were randomised to an exclusive placebo therapy. After the placebo wash out phase, following the 1st medication in active therapy and after the end of therapy, 24-h blood pressure profiles were recorded. The profile under placebo on the 1st medication was separated by a one-week intervening placebo therapy for all patients. On active therapy, the systolic as well as the diastolic blood pressure (day time, night time and 24-h mean values) were significantly reduced. The antihypertensive effect of the active therapy became already manifest after the 1st medication and was augmented after 3 weeks of therapy. In the placebo group no parameter of the 24-h profiles changed significantly. The tolerability of treatment was excellent in 14 (87.5%) of the isradipine patients and in 10 (76.9%) of the placebo group. In one of 16 patients in the active group, adverse events (flush and ankle oedema) were observed. However, therapy could be continued. In one patient of the placebo group, oedema of the fingers was noticed, in another headache was documented. In the placebo group two patients discontinued the study due to inefficacy, in the isradipine group one patient for the same reason; a second patient was excluded from this group due to a concomitant disease unrelated to the study drug.

Adult↗
PubMed1992

[Self measurement of blood pressure: automation and management problems].

In the Federal Republic of Germany, the introduction of clinical testing of devices designed for the self-measurement of blood pressure resulted in an improvement of quality of these devices during the last ten years. Further progress seems to be possible by more restrictive administrative prescriptions. Now, electronic devices have the same accuracy as stethoscope devices. They facilitate self-measurement especially in handicapped persons. Devices working by the oscillometric method do not measure blood pressure more accurately than Korotkow devices, but they are a bit less sensitive for wrong placing of the bladder. In most devices automation of the prescribed deflation rate (2 to 3 mmHg/s) was successful.

Blood Pressure Determination↗
PubMed1990

[Prevalence, causes and effects of increased iron storage in patients with kidney transplantation].

Patients on chronic hemodialysis often need blood transfusions due to erythropoietin deficiency. Even after successful kidney transplantation iron overload may persist. Former histological studies have revealed siderosis of the liver in 69% of all patients whose serum ferritin was above 1100 ng/ml. The aim of the present study was to evaluate the influence of iron overload on liver function. In 146 symptom free patients with renal allografts serum ferritin was determined to detect possible iron overload. Serum ferritin between 4 and 5480 ng/ml were found (women: 358.7 +/- 105.3; men 282.4 +/- 63.3 ng/ml; x +/- SEM). Twelve patients (8.1%) had ferritin levels higher than 1100 ng/ml. These twelve patients as well as another group of eight patients with renal allografts whose serum ferritin was known to be higher than 1100 ng/ml were included for further evaluation. Their data were matched and compared with those of a control group also patients with renal allograft (same age and sex) whose serum ferritin was lower than 1100 ng/ml. Transaminases (SGPT 22.6 +/- 3.6 vs. 15.4 +/- 6.0 U/l; SGOT 14.7 +/- 2.0 vs. 13.0 +/- 4.8 U/l) and plasma glucose (90.5 +/- 7.1 vs. 76.8 +/- 3.7 mg/dl) were found to be significantly higher (p less than 0.05) in patients with serum ferritin levels above 1100 ng/ml. Elevated transaminases were significantly more frequent in patients with high serum ferritin (9 vs. 2; p less than 0.02) as compared with the control. Ferritin levels significantly correlated with the number of preceding blood transfusions (p less than 0.002). Hbs-persistence was detected in six out of 20 patients with high ferritin levels but only in one out of 20 in the control group (p less than 0.05) whereas anti-Hbs prevalence was not different in the two groups. These data indicate that chronic iron overload should be considered as a possible cause of chronic liver disease in patients with renal allografts.

Adolescent↗
PubMed1989

Changes in muscle blood flow after smoking a cigarette determined by a new noninvasive method.

In 9 healthy subjects the effect of smoking one cigarette (nicotine content 0.9 mg) on blood pressure, heart rate and total and muscle blood flow in the forearm was measured. Blood flow was measured by a new noninvasive plethysmographic method that simultaneously gives quantitative data about total and muscle blood flow. Smoking the cigarette did not significantly affect blood pressure or heart rate. Total blood flow in the forearm did not change but the flow to the muscle was increased and resistance in this vascular bed was decreased. The pattern of haemodynamic changes in the forearm indicates that epinephrine may be the mediator of the circulatory effects of nicotine.

Adult↗
PubMed1989

Vasodilation in the vascular bed of skeletal muscle after intravenous nifedipine in normotensives and hypertensives.

The aim of the study was to investigate the effect of nifedipine on blood flow and resistance in the forearm vascular bed of skeletal muscle in 10 male patients with primary hypertension and 10 age-matched male normotensives. We measured the effects of increasing doses of intravenous nifedipine on blood pressure, heart rate, total forearm blood flow and muscle blood flow. Muscle blood flow was determined by a combination of computed tomography and strain-gauge plethysmography. The nifedipine-induced increases in total forearm blood flow were the same in both groups. However, both the increase in muscle blood flow and the decrease in the resistance of the muscle vasculature were more pronounced in the hypertensives than in the normotensives (P less than 0.05). The data provide an explanation for the blood pressure reduction induced by nifedipine in hypertensives and support the hypothesis that elevated vascular resistance is an important functional component in primary hypertension.

Adult↗
PubMed1985

Beta-adrenoceptor subtype of the venous capacity system: characterization by venous occlusion plethysmography.

In order to characterize the beta-adrenoceptor subtype of the venous vessel wall, venous occlusion plethysmograph studies were carried out in 7 healthy volunteers. Venous distensibility (VD) was considered to be a measure of venous tone. Infusion of the beta 1- and beta 2-adrenoceptor agonist isoproterenol (I), of the predominantly beta 2-adrenoceptor agonist fenoterol (F) and of the predominantly beta 1-adrenoceptor agonist dobutamine (D) in increasing doses led to a significant increase in VD by I and F but not by D. Administration of the beta 1-adrenoceptor antagonists betaxolol (B) and metoprolol (M) did not significantly change VD. Neither beta-adrenoceptor antagonist prevented the increase in VD provoked by subsequent administration of I or F. It is concluded that beta-adrenoceptors in the venous vessel wall belong to the beta 2-adrenoceptor subtype.

Adrenergic beta-Agonists↗
PubMed1985

[Comparison of the measurement accuracy of electronic blood pressure self measurement devices 1980-1983].

The accuracy of 21 new electronic devices designed for self-measurement of blood pressure has been tested on an average of 22-24 subjects each by simultaneous measurements on the same arm. Compared with electronic devices made in 1980 the accuracy has improved, especially with regard to the estimation of diastolic blood pressure. Nevertheless, most devices still give too low a value for diastolic blood pressure. In agreement with former results the systolic differences are greater in women and in normotensive subjects, whereas the diastolic differences are more pronounced in younger subjects, in males and in hypertensive patients. Despite the differences due to different sites of auscultation, the results of the best devices tested show that electronic devices may estimate the same blood pressure values over the brachial artery as measured by auscultation in the antecubital fossa. We therefore suggest stronger regulations for the licensing of new electronic devices.

Blood Pressure↗
PubMed1983

Subclassification of human beta-adrenergic receptors mediating renin release.

To determine the beta-adrenoceptor subtype controlling renin release from the kidneys, several beta-adrenoceptor subtype selective agonists and antagonists were administered to 15 healthy volunteers. While isoprenaline infusion (1, 2 and 4 micrograms/min for 5 min each) markedly increased plasma renin activity (PRA), the beta 2-selective agonist fenoterol failed to change PRA. The isoprenaline induced rise in PRA could be completely prevented by the beta 1-selective antagonists metoprolol (10 mg i.v. 45 min prior to isoprenaline infusion) and betaxolol (5 mg i.v. 45 min prior to infusion) indicating that renin release is mediated by beta 1-adrenoceptors. Binding studies with the highly specific beta-adrenoceptor radioligand (+/-)-125iodocyanopindolol demonstrated that membranes from human kidney cortical slices contain predominantly, if not exclusively, beta 1-adrenoceptors. These in vivo and in vitro results support the view that the beta-adrenoceptor mediating renin release from the human kidney is of the beta 1-subtype.

Adrenergic beta-Agonists↗
PubMed1982

Age-dependent decrease of alpha 2-adrenergic receptor number in human platelets.

In 36 healthy subjects of various ages (14-76 years) the number of alpha 2-adrenergic receptors in platelets - as determined by [3H]yohimbine binding - and plasma catecholamine levels were measured. A highly significant negative correlation (r = -0.666, P less than 0.001) between the number of alpha 2-adrenergic receptors and age was found; on the contrary, plasma catecholamine concentrations increased with increasing age. Thus, reduced responses in the elderly to adrenergic stimuli may be due to reduced number of adrenergic receptors.

Adolescent↗