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Biomedical subjects

M Anlauf

Publications and source records attributed to M Anlauf.

67 records · Page 4Linked to original sources
PubMed1975

[Clinical experimental studies in patients with asympathicotonic hypotension].

Three patients with postural hypotension (two of the idiopathic type, one possibly due to familial dysautonomia) were found to have not only the pathognomonic postural hypotension, without rise in heart rate, cardiac output and peripheral vascular resistance, but also a similarly abnormal regulatory mechanism on ergometric stress when recumbent. There was a delayed-response to the bloodpressure fall on Valsalva a manoeuvre, and the blood volume was reduced. A combined effect of these factors explains that these patients have a more marked impairment of physical capcity than might be expected merely from the orthostatic hypotension. The actions of noradrenaline, adrenaline, phenylephrine, isoproterenol, angiotensin and tyramine on blood pressure and heart rate were different from normal. Plasma-renin activity was reduced in all three patients and could not be raised. Urinary excretion of adrenaline and noradrenaline was markedly diminished. Reactions to noradrenaline and tyramine, as well as the excretion pattern of the catecholamine metabolites suggest a disorder of active adrenaline liberation. Furthermore, different disorders of catecholamine metabolism underlie idiopathic orthostatic hypotension and familial autonomia. Therapeutic trials with fludrocortisone, beta-receptor blockers and levodopa brought improvement, but long-term results are not yet available.

Achievement↗
PubMedDate not supplied

Noninvasive, quantitative determination of muscle blood flow in man by a combination of venous-occlusion plethysmography and computed tomography.

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.

Adult↗
PubMedDate not supplied

From the cholinergic gene locus to the cholinergic neuron.

The cholinergic gene locus (CGL) was first identified in 1994 as the site (human chromosome 10q11.2) at which choline acetyltransferase and a functional vesicular acetylcholine transporter are co-localized. Here, we present recent neuroanatomical, developmental, and evolutionary insights into the chemical coding of cholinergic neurotransmission that have been gleaned from the study of the CGL, and its protein products VAChT and ChAT, which comprise a synthesis-sequestration pathway that functionally defines the cholinergic phenotype.

Animals↗
PubMedDate not supplied

Correlation between lymphocyte beta 2-adrenoceptor density and mean arterial blood pressure: elevated beta-adrenoceptors in essential hypertension.

In 41 normotensive volunteers (diastolic pressure, less than 90 mm Hg) the beta 2-adrenoceptor density in lymphocytes was determined by (+/-)-125 iodocyanopindolol (ICYP) binding and compared with that in nine patients with borderline hypertension (diastolic pressure, 90-95 mm Hg) and 45 patients with established essential hypertension (diastolic pressure, greater than 95 mm Hg). The mean number of beta 2-adrenoceptors for controls was 774 +/- 49 (range, 300-1,500) ICYP binding sites/cell. In borderline hypertension it was significantly higher, with 1,037 +/- 22 (range, 950-1,150) sites/cell, and increased further in patients with essential hypertension to 1,424 +/- 72 (range, 700-2,700) sites/cell. The KD values for ICYP, however, were nearly the same in all groups (approximately 50 pM). Calculation of the data of all 95 subjects resulted in a significant positive correlation between beta 2-adrenoceptor density and mean arterial blood pressure (r = 0.637; p less than 0.001). Since the properties of beta 2-adrenoceptors in human lymphocytes resemble those in other tissues, the hypothesis is presented that the increased density of beta 2-adrenoceptors may reflect sympathetic hyperactivity in essential hypertension, which might contribute (perhaps via enhanced release of endogenous noradrenaline through stimulation of presynaptic beta 2-adrenoceptors by adrenaline) to the elevation of blood pressure.

Adult↗
PubMedDate not supplied

Expression of vesicular monoamine transporters in endocrine hyperplasia and endocrine tumors of the oxyntic stomach.

BACKGROUND: Gastric enterochromaffin-like (ECL) cells selectively express the vesicular monoamine transporter (VMAT) VMAT2, and enterochromaffin (EC) cells the VMAT1 isoform. AIMS: We investigated whether VMAT isoform selection indicates the origin of endocrine hyperplasia and neoplasia from oxyntic ECL or EC cells and may be of prognostic significance in different types of gastric carcinoids. METHODS: Tissue from patients with chronic atrophic gastritis (CAG), Zollinger-Ellison-syndrome (ZES), gastric carcinoids and neuroendocrine carcinoma (NEC) was investigated by immunohistology and in situ hybridization. RESULTS: Endocrine cells forming diffuse, linear, and micronodular hyperplasia in CAG and ZES, as well as oxyntic microcarcinoids expressed both VMAT2 and chromogranin A (CgA) but neither VMAT1 nor serotonin. In five of six sporadic carcinoids VMAT2 and CgA but not VMAT1 were detected. One carcinoid was copositive for VMAT1 and serotonin but negative for VMAT2. Electron microscopy confirmed the VMAT2-positive tumors as ECLoma and the VMAT1-immunoreactive carcinoid as EComa. CONCLUSIONS: VMAT2 and VMAT1 are reliable markers for differentiation of gastric endocrine hyperplasia and neoplasia from ECL and EC cells, respectively. The significance of VMAT2 and VMAT1 as prognostic markers lies in the relatively poor prognosis for EComa compared to ECLoma, characterized by VMAT2 positivity. The absence of both VMAT2 and VMAT1 in NEC may indicate poor prognosis.

Adult↗