M Anlauf

University of Duisburg-Essen, Essen, North Rhine-Westphalia, Germany

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Publications (34)76.83 Total impact

  • K D Bock, M Anlauf
    Versicherungsmedizin / herausgegeben von Verband der Lebensversicherungs-Unternehmen e.V. und Verband der Privaten Krankenversicherung e.V 04/2009; 61(1):1-3.
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    ABSTRACT: 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.
    Medizinische Klinik 10/1990; 85(9):517-22. · 0.34 Impact Factor
  • F Weber, M Anlauf
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    ABSTRACT: 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.
    Journal of hypertension. Supplement: official journal of the International Society of Hypertension 01/1990; 7(6):S286-7.
  • F Weber, M Anlauf, R D Müller
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    ABSTRACT: 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.
    European Journal of Clinical Pharmacology 02/1989; 37(5):517-20. · 2.74 Impact Factor
  • F Weber, M Anlauf, M Serdarevic
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    ABSTRACT: Because of the lack of non-invasive methods for measuring muscle blood flow, quantitative investigations of blood flow in the skeletal muscle of hypertensive subjects are rare. We therefore developed a new method for the determination of muscle blood flow noninvasively and quantitatively by a combination of computed tomography and venous occlusion plethysmography (strain-gauge method). At two sites on one forearm (p = site of the largest diameter, d = 1 cm proximal to the epicondyle lat.) the volumes of tissues [Vt = total volume, VM = muscle volume, VSk = bone volume, VR = residual volume = Vt - (VM + VSk)] were determined by computed tomograms and total forearm blood flow (Fp and Fd, respectively in ml/100 ml tissue x min) measured by strain-gauge plethysmography. After correcting for the bone volume at the different sites, Fp and Fd were transformed into the absolute influx rates of blood volume (Qp and Qd). From Qp and Qd and the different tissue volumes, the muscle blood flow (FM in ml/100 ml muscle x min) could be calculated: (formula; see text) Results thus derived were compared with data from the literature Cooper et al. (17). At rest there was neither a significant difference in Fp (own results: 3.62 +/- 1.67, Cooper: 3.25 +/- 1.42 ml/100 ml tissue x min, means +/- S.D.) nor in FM (4.08 +/- 2.07 and 3.66 +/- 1.57 ml/100 ml muscle x min, respectively), however, Fp and FM were significantly different (p less than 0.05). In the mean, FM was 13% greater than Fp, range: -40 to +38% (Cooper 15%, range: -17 to +43%). The individual difference could not be predicted by any of the parameters. Testing the procedure by means of a pharmacological agent (clonidine) with known effects on muscle blood flow (no change) and skin blood flow (decrease) revealed the correct reproduction of this hemodynamic pattern with our method. The usual identification of total with muscle blood flow would have led to false conclusions.
    Archiv für Kreislaufforschung 01/1988; 83(3):327-41. · 5.90 Impact Factor
  • K D Bock, M Anlauf, F Weber
    Lebensversicherungs Medizin 10/1987; 39(5):151-4.
  • Medizinische Klinik 04/1986; 81(6):202-7. · 0.34 Impact Factor
  • F Weber, M Anlauf
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    ABSTRACT: 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.
    European Journal of Clinical Pharmacology 02/1985; 28(2):139-42. · 2.74 Impact Factor
  • M Anlauf, O-E Brodde
    Journal of Hypertension - J HYPERTENSION. 01/1985; 3(4).
  • Journal of Cardiovascular Pharmacology - J CARDIOVASC PHARMACOL. 01/1984; 6(4):678-682.
  • New England Journal of Medicine 05/1983; 308(17):1033-4. · 51.66 Impact Factor
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    ABSTRACT: 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.
    Clinical and experimental hypertension. Part A, Theory and practice 02/1983; 5(2):225-38.
  • Die Medizinische Welt 12/1982; 33(47):1723-5.
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    ABSTRACT: The effect of clonidine on the number of 2-adrenoceptors in human platelet membranes, determined by3H-yohimbine binding, was investigatedin vitro andin vivo. Incubation of platelet membranes with clonidine (1–100 M) for 16 h at 25 C led to a concentration-dependent decrease in the number of3H-yohimbine binding sites of 10–25%; the affinity of3H-yohimbine to the sites was not changed (KD approximately 3–4 nM). In such desensitized membranes, inhibition of3H-yohimbine binding by clonidine resulted in steep, monophasic displacement curves, which in comparison to the curves from control membranes (IC50 for clonidine 90 nM), were shifted to the right (IC50: 321 nM) and were not affected by 10–4M guanosine-5-triphosphate (GTP).Treatment of 3 hypertensive patients with clonidine (3150 g/d for 7 days) reduced blood pressure and heart rate. Simultaneously, both3H-yohimbine binding sites on platelet membranes and plasma catecholamine levels decreased within three days and remained at a reduced level during treatment. After abrupt cessation of clonidine treatment, blood pressure, heart rate and plasma catecholamines rapidly increased, reaching values after two days similar to or higher than those before treatment.3H-yohimbine binding sites, however, initially decreased further before returning to control values. In platelet membranes derived from hypertensive patients treated with clonidine for at least three weeks, GTP (10–4M) had no influence on inhibition of3H-yohimbine binding by (—)-adrenaline and clonidine. It is concluded that clonidine desensitizes 2-adrenoceptors in human platelet membranesin vitro andin vivo. An important step in the desensitization process is the uncoupling of receptor occupancy by agonists and adenylate cyclase activity, as indicated by loss of the regulatory activity of GTP on desensitized membranes. The clonidine withdrawal syndrome may be caused by enhanced release of endogenous catecholamines not adequately regulated by presynaptic 2-adrenoceptors, which have become subsensitive after chronic clonidine treatment.
    European Journal of Clinical Pharmacology 08/1982; 23(5):403-409. · 2.74 Impact Factor
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    ABSTRACT: 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.
    European Journal of Pharmacology 08/1982; 81(2):345-7. · 2.59 Impact Factor
  • European Journal of Clinical Pharmacology 02/1982; 23(5):403-9. · 2.74 Impact Factor
  • M Anlauf, K D Bock
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    ABSTRACT: A diagnostic examination may be called rational if it leads to a short, less costly and especially more certain diagnosis for the patient. Among other things, sensitivity and specificity, i.e. the proportion of correct positive to correct negative results of the separates steps of the examination determine the reliability of the answers to diagnostic questions. In most hypertensive patients the diagnosis can be completed in medical general practise. First results in West Germany show that only about 5 to 10% of patients require further investigations in special practices, general hospitals or special departments.
    MMW, Münchener medizinische Wochenschrift 12/1981; 123(47):1785-90.
  • K D Bock, M Anlauf
    MMW, Münchener medizinische Wochenschrift 07/1978; 120(23):787-8.
  • N Graben, W Cremer, M Anlauf, K D Bock
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    ABSTRACT: Between 1972 and 1976 15 patients with chronic renal failure of different aetiology and varying severity were observed who developed 23 hypercalcaemic phases during treatment with calcium-containing drugs. 12 instances of hypercalcaemia occurred during conservative treated during conservative treatment (serum creatinine 177-1061 mumol/l, equivalent to 20-120 mg/l) and 11 during chronic haemodialysis (serum creatinine 707-1061 mumol/l, equivalent to 80-120 mg/l). In 15 cases hypercalcaemia was caused by a hexacalciumhexasodium-heptacitratehydrate complex (Acetolyt), in 6 cases by the combined use of this drug with calcium ion-exchange resins on a calciumpolystyrolsulfonate base, and in two cases by the use of calcium tablets and calciumpolystyrolsulfonate, respectively. The daily doses of these drugs were in the usual therapeutic range in most cases. Deterioration of renal function was observed in two cases and coma in a further two cases. In 5 cases gastric ulcers were demonstrated. Three patients died. In no patient was there evidence of florid hyperparathyroidism. Treatment with calcium-containing drugs in patients with renal failure should only be carried out under regular control of calcium concentrations.
    DMW - Deutsche Medizinische Wochenschrift 01/1978; 102(52):1903-7. · 0.65 Impact Factor
  • Verhandlungen der Deutschen Gesellschaft für Kreislaufforschung 02/1977; 43:229-30.