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Biomedical subjects

U Moser

Publications and source records attributed to U Moser.

At least 91 records · Page 5Linked to original sources
PubMed1984

Detection of organic hydroperoxides in rabbit lung lavage fluid, but not in lung tissue homogenate, using GSH peroxidase and GSH reductase.

A specific method for the detection of organic hydroperoxides in lung lavage fluid (lung surfactant system) and lung tissue homogenate is described. After the inactivation of endogenous GSH peroxidase and GSH reductase and preincubation with catalase, organic hydroperoxides are consumed by addition of GSH and GSH peroxidase. The increase of GSSG, compared to a blank without addition of GSH peroxidase, is measured in a second enzymatic step with GSH reductase. The recoveries of t-butyl hydroperoxide and of peroxidized, free fatty acids added to lavage fluid or to lung homogenate are higher than 85% in each case. The detection limits of this assay for organic hydroperoxides are 0.9 nmol/mg surfactant phospholipid (molar ratio of 0.00066) and 40 nmol/g wet lung weight. The assay detects organic hydroperoxides in the surfactant system of normal rabbit lungs, but not in lung tissue homogenate.

Animals↗
PubMed1984

The failure of ascorbic acid therapy to alter the induction or remission of murine amyloidosis.

It has been claimed that ascorbic acid enhances the in vitro degradation of AA amyloid fibrils. This raises the possibility that ascorbic acid may be of benefit in systemic AA amyloidosis, a condition with serious morbidity and mortality for which there is as yet no specific treatment. The effect was therefore tested of oral or injected supplements of ascorbic acid on the induction of AA amyloidosis in mice. Amyloid was induced either by repeated injections of casein or by injection of 'amyloid enhancing factor' and silver nitrate. Mice with established amyloidosis were also treated with additional ascorbic acid. Despite the fact that plasma ascorbic acid levels were significantly higher in orally supplemented mice than in controls there was no demonstrable effect on the induction, the extent and distribution or the progression of amyloidosis.

Amyloid↗
PubMed1984

Uptake of ascorbic acid by human granulocytes.

The uptake of ascorbic acid by isolated human granulocytes is investigated under different conditions. The rate of uptake depends on the concentration of ascorbic acid in the incubation medium as well as on temperature, with a maximum at 40 degrees C. At 0 degrees C no uptake can be observed. N-formylated peptides being known to stimulate human granulocytes, considerably increase ascorbic acid uptake, but the non-formylated methionyl-leucyl-phenylalanine is without effect. Glucose is a strong inhibitor of ascorbate uptake with a Ki of 3.7 mM and a stoichiometry of 1:1. Fructose does not inhibit at all and galactose only at elevated concentrations. Phlorizin, a known inhibitor of glucose transport, inhibits the uptake of ascorbic acid to the same extent as that of glucose. Elevated glucose levels do not induce a release of ascorbic acid out of the cells. It is concluded that ascorbic acid is actively accumulated in human granulocytes and that stimulated cells respond with a pronounced increase of ascorbate uptake. The site of ascorbic acid transport across the membrane is probably the same as of glucose.

Ascorbic Acid↗
PubMed1983

Influence of aprotinin and gabexate mesilate on arachidonic acid release by the Ca-ionophore A 23187 in the lung.

In a model of isolated, ventilated rabbit lungs, perfused with Krebs-Henseleit albumin buffer in a recirculating system, increased availability of free AA (arachidonic acid) results in an increase in pulmonary vascular resistance and permeability. The former can be ascribed to cyclooxygenase products of AA, among which thromboxane A2 is mainly responsible. The increase of vascular permeability is, at least partly, due to lipoxygenase products of AA. Availability of free AA for the different oxygenation pathways can be achieved either by direct application of free AA to the perfusion fluid or by stimulation of AA release from the membrane phospholipid pool by the Ca-ionophore A 23187. The serine proteinase inhibitor gebaxate mesilate in a concentration range between 1 microM and 10 microM and aprotinin in a concentration range between 8 and 200 KIE/ml dose-dependently reduce the increase in vascular resistance after stimulation with A 23187. Correspondingly the increase in vascular permeability due to A 23187 is significantly reduced by gabexate mesilate (5 microM) to 52% and by aprotinin (200 KIE/ml) to 73%. On the contrary the increase in pulmonary vascular resistance and permeability after direct application of free AA to the perfusion fluid is not affected by gabexate mesilate and aprotinin. AA metabolism by cyclooxygenase from ram vesicular gland microsomes is inhibited in vitro by gabexate mesilate and by aprotinin only in very high concentrations (greater than 1mM respectively greater than 2130 KIE/ml). Measurements with porcine pancreas and bee venom phospholipase A2 reveal no influence of aprotinin on these enzymes. Gabexate mesilate inhibits pancreas phospholipase A2 in concentrations more than 10-fold higher than those necessary in the isolated lungs (IC50 = 430 microM), bee venom phospholipase A2 not being affected at all. It is thus apparent that the release of AA from the membrane phospholipid pool rather than any particular step in its oxygenation metabolism is the site of action of these proteinase inhibitors in the pulmonary vascular bed. The possible involvement of an intracellular proteinase is discussed.

Animals↗
PubMed1983

[Structure- and conformation-activity relationships of heterocyclic acetylcholine analogues. 16. Conformational behaviour and cholinergic properties of isoarecaidine and sulfoisoarecaidine esters].

In the course of investigations of structure- and conformation-activity relationships of heterocyclic acetylcholine analogues, both the methyl esters of the tertiary and quaternary isoarecaidine and the sulfoisoarecoline were tested for their cholinergic properties. The electronic structures and the conformational behaviour of these cholinergics were investigated by quantum chemical calculations using Extended Hückel Theory (EHT) and Complete Neglect of Differential Overlap (CNDO/2)MO methods. The results show that the muscarinic potency of the heterocyclic compounds is dependent on structure and conformational behaviour of the onium center. The divergent charge distribution around the cationic heads of the ammonium and sulfonium derivatives, respectively, as well as differences in the dimensions of the two heterocyclic systems, can not be utilized to explain the differences in muscarinic potency of the isoarecaidine and sulfoisoarecaidine methyl esters.

Acetylcholine↗
PubMed1983

[Structure- and conformation-activity relationships of heterocyclic acetylcholine analogs. 17. Conformational behavior and cholinergic properties of arecaidine and sulfoarecaidine esters].

In the course of investigations of structure and conformation-activity relationships of heterocyclic acetylcholine analogues, the tertiary and quaternary methyl esters of arecaidine and the methyl ester of sulfoarecaidine were tested for their cholinergic activities. The conformational behaviour and the electronic structures of these cholinergics were investigated by quantum chemical calculations using Extended Hückel Theory (EHT) and Complete Neglect of Differential Overlap (CNDO/2)methods. The results show that the muscarinic potency of the heterocyclic analogues is dependent on structure and conformational behaviour of the onium center. The divergent charge distribution around the cationic heads of the ammonium and sulfonium derivatives, respectively, as well as differences in the dimensions of the two heterocyclic systems, can not be utilized to explain the differences in muscarinic potency of the arecaidine and sulfoarecaidine methyl esters.

Acetylcholinesterase↗
PubMed1982

Depressor effects of isoguvacine propyl ester and isoarecaidine propyl ester due to stimulation of central GABA receptors in the cat.

Upon their simultaneous administration into the left and right vertebral artery of the cat, 2 x 30 micrograms isoarecaidine propyl ester (IAPE) and 2 x 30 micrograms isoguvacine propyl ester (IGPE) induce hypotension and bradycardia. These effects were antagonized by (+)-bicuculline or picrotoxin. IAPE is rapidly hydrolyzed by cat brain tissue in vivo. It is suggested that both IAPE and IGPE are prodrugs and that the corresponding carboxylic acids are GABA agonists and responsible for the cardiovascular effects evoked.

Animals↗
PubMed1982

Centrally induced cardiovascular effects and kinetic behaviour of isoarecaidine propyl ester in the cat.

The present investigation deals with effects of isoarecaidine propyl ester (IAPE) on blood pressure and heart rate of the anaesthetized cat. The kinetic behaviour of the drug in plasma and various brain tissues was also studied. The results indicate that the ester (4 mg.kg-1) induces a depressor effect and bradycardia after i.v. administration. Injection of IAPE (up to 60 micrograms.kg-1) into the left vertebral artery lowers blood pressure in a dose-dependent manner. When administered simultaneously into the left and right vertebral artery, low doses (6 micrograms. kg-1) produce a substantial fall in blood pressure. Although the fall in blood pressure after i.v. injection lasts for more than 60 min, plasma half life is extremely short (t1/2 = 6.3 sec). The possible metabolism of the ester was studied in the pons, medulla oblongata and cerebellum. Thirty min after the injection into the left vertebral artery, IAPE is almost entirely hydrolyzed in the pontomedullary region. This degradation is prevented by pretreatment with paraoxon, that abolishes the depressor action of IAPE. It is suggested that accumulated isoarecaidine in the pontomedullary region is responsible for the depressor response to IAPE. Since IAPE does not seem to influence blood pressure and heart rate via a peripheral mechanism and lowers blood pressure and cardiac frequency by a central action, this drug is considered to be of pharmacological interest. The mechanism of action is discussed.

Animals↗
PubMed1981

Muscarinic effects of various isoarecaidine esters in sympathetic ganglia.

1 The pressor effects of various tertiary and quaternary isoarecaidine esters in both pithed and anaesthetized rats are reported. In order to elucidate the mechanism of action, various experiments were carried out with the quaternary isoarecaidine methyl ester (Q-4-Me). 2 Treatment with mecamylamine, dexetimide, reserpine and phentolamine abolished or reduced the pressor response to Q-4-Me, whereas pretreatment with cocaine gave rise to a prolonged pressor effect. Plasma noradrenaline levels were significantly increased after the infusion of Q-4-Me. 3 From the results it can be concluded that the pressor effects brought about by the quaternary compounds can be attributed to stimulation of nicotinic and muscarinic receptors in sympathetic ganglia. The consequences of interaction with muscarinic receptors predominate over the effects due to minimal interference with nicotinic receptors by the drug.

Anesthesia↗
PubMed1980

[Increasing suicides of psychiatric inpatients: reality or artefact? (author's transl)].

In several countries the suicide rate for psychiatric inpatients has increased more than that for admissions and suicides in the general population. This was also the case in our clinic. This hypothesis was tested: today, because of more liberal management, suicides are committed during hospitalization that in an earlier and more restrictive age would have taken place after discharge. All suicides taking place 1960-1979 in the clinic's main catchment area were examined for previous hospitalization. The hypothesis was not supported. Over twenty years neither the suicide cases nor all discharged patients changed significantly in distribution of age, sex, number of previous admissions, duration of hospitalization, or diagnosis. Therefore, none of these variables explain the increase. In both decades, on the other hand, patients that committed suicide during their stay at the clinic had been hospitalized longer; those that committed suicide within three months after discharge had been hospitalized for a shorter time than the sum of discharged patients. Among the suicides that occurred after discharge, the percentage of depressives and addicts was higher and the percentage of schizophrenic patients was smaller than among all discharged patients. A change in patient management (more time off, more working outside, more open wards) has preceded the increase in suicides; medical staff, however, has doubled over the decades considered here. Rising pressure for resocialization to avoid hospitalism may heighten suicidal behavior. Preventive measures are discussed.

Adult↗