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Biomedical subjects

E Lindner

Publications and source records attributed to E Lindner.

At least 55 records · Page 3Linked to original sources
PubMed1980

Exercise induced changes of catecholamines and potassium in plasma of dogs after treatment with propranolol.

Previous studies in man have shown that during beta-adrenoceptor blockade physical exercise caused a significantly greater elevation of plasma catecholamines than without blockade. After blockade of beta-adrenoceptors, increased levels of circulating catecholamines should have an unopposed effect on adrenergic alpha-receptors. In order to elucidate such an effect, experiments were performed with 7 trained dogs before and after acute beta-adrenoceptor blockade (0.1 mg/kg (-)-propranolol i. v.). Exercise was performed on a conveyor (10 min, 10 km/h, slope 10%). Besides catecholamine concentrations in plasma, as an index of alpha-receptor-stimulation potassium concentrations in plasma were determined. Immediately after exercise, plasma noradrenaline was increased from 310 to 579 pg/ml, plasma adrenaline from 136 to 222 pg/ml and plasma potassium from 4.23 to 4.6 mmol/l. After beta-adrenoceptor blockade exercise caused a significantly higher increase in plasma noradrenaline from 352 to 755 pg/ml and plasma adrenaline from 172 to 260 pg/ml. Also plasma potassium concentrations were significantly elevated from 4.03 to 5.05 mmol/l. The results indicate an enhanced reflex activation of sympatho-neuronal and sympatho-adrenal mechanisms during exercise after beta-adrenoceptor blockade; the increased concentrations of noradrenaline at the adrenoceptors might reduce the efficiency of beta-blockade. Concomitantly, increased stimulation of alpha-adrenoceptors is elicited, which becomes obvious by an increase of potassium concentration in plasma.

Animals↗
PubMed1979

Methods of heavy metal electron microscopic histochemistry applied to frog lung surfactant.

Four heavy metal staining methods have been applied to frog lung surfactant. Among them, the iodoplatinate method is the only one that almost exclusively visualizes the phospholipid moiety being produced in the lamellated bodies of the pulmonary epithelial cells and forming the backbone of organized structures within the extracellular lining layer. The other three techniques-ruthenium red-osmium tetroxide, osmium tetroxide-ferrocyanide, acidic phosphotungstic acid in chromatic (Rambourg technique)--more or less give electron contrast to glycoproteins and to a lesser extent to the hydrophilic parts of phospholipids. They all show the extracellular lining layer to be a two component system: the content of the lamellar bodies form--when released--membranous configurations, similar to those observed in mammalian lungs; they unfold in an amorphous hypophase, which is apparently secreted by goblet cells of the pulmonary epithelium.

Animals↗
PubMed1979

Ultrahistochemical investigations of dog lung surfactant with ruthenium red and iodoplatinate reactions.

Dog lungs have been fixed by immersion and submitted to two histochemical procedures. An iodoplatinate reaction technique to demontrate choline phospholipids stains cell membranes, inclusion bodies of type II alveolar epithelial cells and tubular myelin figures of pulmonary surfactant, the latter as electron-dense lines measuring 5 nm. The ruthenium red procedure gives rise to an intense contrast of the free surface of alveolar epithelium. The 5 nm-lines of the pulmonary surfactant are seen as electron-lucent lines, but bordered by electron-dense rims. Though both techniques have limitations in their interpretation, which are discussed in this paper, they demonstrate the tubular myelin figures to be a highly organized mixture of phospholipids and glycoproteins.

Animals↗
PubMed1979

[14,15-beta-oxido analog of proscillaridin (HOE 040). A new cardiac glycoside with low arrhythmic activity and greater absorption ratio].

The 14,15-beta-oxido analogue of proscillaridin A (HOE 040), in a dose 4 times higher showed equally positive-inotropic effect on the isolated guinea pig heart as did proscillaridin A. In the dog in vivo HOE 040 was equally positive-inotropic, as measured by the increase of dp/dt of the left ventricle of the heart, as proscillaridin A. In combination with aconitine, HOE 040 also in 4fold higher dose caused less cardiac fibrillation on the isolated guinea pig heart than did proscillaridin A. The dose of HOE 040 which by infusion in the guinea pig in vivo precipitates cardiac arrhythmias was 4 times higher than that of proscillaridin A, the lethal dose was 5 times higher. In dogs in vivo the dose of HOE 040 by infusion causing prolongation of PQ or cardiac arrhythmias, resp., was twice the dose necessary of proscillaridin A, the lethal dose was nearly 5 times higher. The decrease of cardiac activity in Rhesus monkeys amounted to 69% in 24 h, whereas proscillaridin A decreased cardiac activity only by 41% in 24 h. The absorption of HOE 040 from the duodenum of dogs anesthetized with pentobarbital amounted to 72%, whereas proscillaridin A is observed by only between 14 and 25%. The concentration of the drug HOE 040 in hearts of rats was twice, in the hearts of dogs 3 fold that of proscillaridin A. The concentrations of both drugs in the brain of rats and dogs were not different. In the biochemical test system in vitro the blocking effect of both drugs on the Na+K+-ATPase of ox brain was not different.

Animals↗
PubMed1978

Induction of microsomal drug-metabolizing enzymes caused by hexobarbital.

Hexobarbital was given to anaesthetized mice for a period of 7 h by repeated i. p. injection, first of 100 mg/kg,then several times of 50 mg/kg. A high level of hexobarbital was maintained in the liver. The activity of microsomal drug-metabolizing enzymes was induced by this treatment with hexobarbital. 30 min after a single i. p. injection of 100 mg/kg of hexobarbital, there was a significant inhibition of aminopyrine N-demethylase but none of cytochrome c and neotetrazolium reductases. Hexobarbital in vitro inhibits aminopyrine N-demethylase but not cytochrome c reductase.

Aminopyrine N-Demethylase↗
PubMed1978

Positive inotropic and blood pressure lowering activity of a diterpene derivative isolated from Coleus forskohli: Forskolin.

Forskolin is a diterpene derivative isolated from the Indian plant Coleus forskohli. Forskolin has positive inotropic action on the isolated guinea pig heart, on the isolated left atrium of the guinea pig heart and on the dog and cat heart in situ. It increases the heart rate. The positive inotropic effect on the increase of heart rate are not blocked by beta-blockers. On reserpinized dogs the actions on the heart could also be seen. With high doses the action potential of the guinea pig papillary muscle is shortened. The positive inotropic effect could be differentiated from the effects of theophylline, cardiac glycosides and veratrine. Forskolin lowers the blood pressure in dogs and cats and also in spontaneously hypertensive and renal hypertensive rats.

Action Potentials↗
PubMed1976

Hypotensive and antiarrhythmic effects of a new alkaloid, the 13-hydroxylupanine-2-pyrrolcarbonic acid ester, from the Madagascan plant Cadia ellisiana.

The alkaloid 13-hydroxylupanine-2-pyrrolcarbonic acid ester (Hoe 933) from the Madagascan plant Cadia ellisiana has an hypotensive and antiarrhythmic effect. The hypotensive effect in dogs, monkeys, and rats anaesthetized with barbiturates reaches its maximum with 0.2 mg/kg i.v. However, the hypotensive effect is much weaker in conscious animals. The enteral absorption in the dog is good; an intraduodenal dose of only 0.5 mg/kg lowered the blood pressure. In the isolated rabbit heart whose accelerator nerves were intact, the perfusion with concentrations of 0.6 mug/min Hoe 933 (total dose 6 mug) decreased the release of norepinephrine from the nerve endings, reduced the positive inotropic effect, and diminished the increase in heart rate produced by electrical stimulation of the accelerator nerve. The effect of the stimulation of the accelerator nerve on dp/dt in dogs in situ was considerably diminished by such low doses as 10 and 25 mug/kg i.v. Consequently, the alkaloid inhibits sympathetic impulse transmission. Sympathetic circulatory reflexes are weakened by the compound. The alkaloid has also a ganglionic blocking effect, which is demonstrated on the upper cervical ganglion of the cat. The effect of preganglionic stimulation of the nictitating membrane was reduced with 200 mug Hoe 933/kg i.v. In the isolated guinea pig heart the effect of nicotine on heart rate and contraction was diminished. In this respect the ganglion blocker pentolinium is 8 times more active. The antifibrillatory effect of Hoe 933 was demonstrated with 0.3 mg/kg i.v. in supercooled cats, the antiarrhythmic activity was evident with 0.5 mg/kg i.v. in dogs intoxicated with K-strophanthin. In isolated hearts of guinea pigs, a dose of only 6 mug/heart inhibited ventricular fibrillation induced by aconitine and digitoxin. Even the toxicity of digoxin was diminished by previous administration of 300 mug/kg i.v. The relative refractory period and the duration of the action potential were prolonged in the isolated papillary muscle of the guinea pig heart.

Alkaloids↗