Biomedical subjects

H Pelzer

Publications and source records attributed to H Pelzer.

At least 55 records · Page 3Linked to original sources

PubMed1986

New approaches for the detection of early activation products in thrombotic states.

The occurrence of a consumption coagulopathy as well as prethrombotic and thrombotic states are connected with the formation of thrombin. The proteinase acts upon physiological substrates leading to activation products, e.g. fibrinopeptides, platelet factors or thrombin-antithrombin III-complex. For the determination of such products we have developed immunochemical assays, which detect parameters of a direct or indirect action of thrombin in a specific and sensitive manner: 1. ELISA for determination of platelet factor 4; 2. Latex-test for determination of D-Dimer; 3. ELISA for determination of thrombin-antithrombin III complex. Preliminary results from clinical investigations indicate that the determination of these parameters can be valuable for the diagnosis of activation processes of the clotting system.

Blood Coagulation Disorders↗

PubMed1986

Biochemical pharmacology of pirenzepine. Similarities with tricyclic antidepressants in antimuscarinic effects only.

5,11-Dihydro-11-[(4-methyl-1-piperazinyl) acetyl]-6H-pyrido[2,3-b][-1,4]-benzodiazepin-6-one dihydrochloride (pirenzepine, Gastrozepin) and some tricyclic antidepressant drugs which show a very close relationship concerning the chemical structure were investigated in numerous binding, uptake and enzymatic studies in vitro. With pirenzepine a high affinity binding could be demonstrated only to muscarinic receptors (Ki = 58 nmol/l). In all other studies pirenzepine had a very weak or no effect at all. In contrast, tricyclic antidepressants bound with high but different affinities to various receptors as known from numerous publications. The highest affinities were found with imipramine at the specific imipramine binding sites (Ki = 9.8 nmol/l) and at the alpha 1-receptor (Ki = 39 nmol/l), with desipramine at the muscarinic receptors (Ki = 88 nmol/l), with mianserin at the H1-(Ki = 3.4 nmol/l) and 5HT2-receptors (Ki = 7.3 nmol/l). Moreover, imipramine and desipramine showed their known substantial inhibition of noradrenaline and/or 5-hydroxytryptamine uptake. Thus, a homogeneous affinity or activity profile of the antidepressants studied does not exist. The only common property of pirenzepine and the tricyclic antidepressants was found to be the high affinity binding to the muscarinic receptors which might explain the common antisecretory action of these agents. Because of the unique specificity of pirenzepine lacking all other effects of the tricyclic antidepressants as demonstrated in this study, it is very unlikely that this drug exerts any antidepressant-like central action.

Animals↗

PubMed1985

Pharmacological properties of an extremely selective beta 1-adrenoceptor antagonist, 2-[4-[3-(tert-Butylamino)-2-hydroxypropoxy] phenyl]-3-methyl-6-methoxy-4(3H)-quinazolinone [+/-)HX-CH 44 BS).

2-[4-[3-(tert-Butylamino)-2-hydroxypropoxy] phenyl]-3-methyl-6-methoxy-4(3H)-quinazolinone (+/-)HX-CH 44 BS) is a new beta 1-selective adrenoceptor antagonist. Affinity for beta 1-adrenoceptors was determined in isolated guinea-pig papillary muscle (pA2 = 7.4), in isoprenaline-stimulated guinea-pig cardiac adenylate cyclase (pA2 = 7.3) and in receptor binding experiments with rat heart membranes (pKi = 8.0). Due to a direct relaxing action of (+/-)HX-CH 44 in smooth muscles its beta 2-affinity could only be estimated from receptor binding experiments (pKi = 5.0). (+/-)HX-CH 44 BS shows an extremely high beta 1/beta 2-affinity ratio of about 800 and therefore appears to be much more selective than atenolol or metoprolol (beta 1/beta 2 = 10-50). In contrast to propranolol or atenolol, (+/-)HX-CH 44 hardly antagonized bronchodilation induced by i.v. isoproterenol in anaesthetized guinea-pigs in vivo. Furthermore, cardiac actions of the beta 1-selective agonist norepinephrine in cats in vivo were competitively antagonized by (+/-)HX-CH 44 whereas inotropic and chronotropic effects of the non-selective beta-agonist epinephrine were not. This phenomenon may be explained by the mixed population of beta 1-and beta 2-adrenoceptors in cat heart and by the high beta 1-selectivity of (+/-)HX-CH 44.

Acetylcholine↗

PubMed1981

Murein biosynthesis in ether permeabilized Escherichia coli starting from early peptidoglycan precursors.

ETB, ether treated bacteria, from E. coli and other Gram-negative strains, contain in a cell-free system all enzymes necessary for murein biosynthesis. Starting with a variety of combinations of peptidoglycan precursors, high yields of sodium dodecylsulfate (SDS, 4%) insoluble murein or murein like material were synthesized. The amount of newly synthesized SDS insoluble material (NSM) was dependent upon the growing phase at which cells had been harvested for preparation of ETB. This data may provide some insight into the regulation of peptidoglycan biosynthesis. Starting from early peptidoglycan precursors, the cell-free synthesis of NSM was inhibited by specific inhibitors of murein synthesis, such as D-cycloserine, D-fluoroalanine, 2-amino-ethylphosphonate, analogues of D-alanyl-D-alanine and beta-lactam antibiotics at appropriate concentrations. Some D-alanyl-D-alanine analogues and 4-chlorodiaminopimelic acid were incorporated into NSM in place of their corresponding natural substrates.

Cell Membrane Permeability↗

PubMed1980

Inhibition of peptidoglycan synthesis in ether-permeabilized Escherichia coli cells by structural analogs of D-alanyl-D-alanine.

Several analogs of D-alanyl-D-alanine have been proved to be competitive inhibitors of murein (cross-linked peptidoglycan) synthesis in either-permeabilized cells of Escherichia coli. Some analogs, distinguished from D-alanyl-D-alanine only by minor structural deviations, were incorporated into a murein-like sodium dodecyl sulfate-insoluble material in place of the natural substrate. These analogs therefore could be designated as competitive substrates of the cross-linked end product of murein synthesis. In contrast, others, even those containing bulky residues at the methyl group of the amino-terminal D-alanine, exhibited inhibition of murein synthesis. The last-mentioned group of analogs also inhibited a blank value which seems to be a characteristic feature of this system without added D-alanyl-D-alanine. From this data, a steady-state concentration of D-alanyl-D-alanine or D-alanine or both in growing cells of E. coli could be calculated as approximately 0.4 x 10(-3) M.

Anti-Bacterial Agents↗

PubMed1975

Bis-(p-hydroxyphenyl)-pyridyl-2-methane: The common laxative principle of Bisacodyl and sodium picosulfate.

After both oral and rectal administration in humans (4,4'-diacetoxy-diphenyl)-(pyridyl-2)-methane (bisacodyl, Dulcolax) and 4,4'-(2-pyridyl-methylene)-diphenol-disulfuric acid semiester disodium (sodium picosulfate, Laxoberal) are hydrolyzed to bis-(p-hydroxyphenyl)-pyridyl-2-methane (BHPM). In both cases BHPM is responsible for the laxative action. Experiments in rats and guinea pigs have shown that the hydrolysis of picosulfate, in contrast to that of bisacodyl, is attributable to the microorganisms of the intestinal flora.

Administration, Oral↗

PubMed1974