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At least 1,495 records · Page 83Linked to original sources
PubMed1977

Morphometric changes in rabbit ventricular myocardium produced by long-term beta-adrenoceptor blockade.

In rabbits long-term beta-adrenoceptor blockade did not cause any change in the morphology of individual organelles in the ventricular myocardium. There were, however, striking and significant changes in their relative distribution: (1) the relative volume of the mitochondria was reduced and was replaced by an equivalent relative increase in sarcoplasm; and (2) the relative volume of vascular elements was increased and the interfibrillar volume was decreased, so that the path from capillary to cell wall was reduced. The relative volumes of myofibrils and nuclei were unchanged. The doses used were well within the range used clinically, so that the results could be relevant to the efficacy of beta-blockers in angina pectoris, because the relative increase in capillaries and shorter diffusion pathway for oxygen could raise oxygen availability. The reduced rate of growth of the heart in young rabbits during beta-blockade may also be relevant to the treatment of infants with hypertrophic obstructive cardiomyopathy by beta-blockers.

Animals↗
PubMed1986

Drugs in exacerbation of psoriasis.

Drugs that have been associated with the precipitation or exacerbation of psoriasis include lithium, beta adrenergic receptor blocking agents, and antimalarials. The withdrawal of corticosteroids has been reported to activate pustular psoriasis. Nonsteroidal anti-inflammatory drugs, such as indomethacin, have recently been reported to exacerbate psoriasis, although additional well-controlled studies are still needed. Drugs used for treatment of psoriasis will sometimes cause a flare because of irritation, phototoxicity, or hypersensitivity reaction resulting in a Koebner phenomenon. Because psoriasis is a very complex disease and its activity is often unpredictable, clinical studies on adverse drug effects on psoriasis have been difficult to conduct. This review evaluates clinical, histologic, and biochemical evidence in the literature for drug-associated onset or exacerbation of psoriasis.

Adrenal Cortex Hormones↗
PubMed1985

Stimulation of cyclic adenosine 3',5'-monophosphate formation in rabbit choroid plexus by beta-receptor agonists and vasoactive intestinal polypeptide.

The formation of cyclic adenosine 3',5'-monophosphate (cAMP) was determined in blood-free choroid plexus homogenates from all ventricles of rabbit using a competitive protein binding technique. Previous stimulation of the intact plexus tissue in vitro with sympathomimetic drugs or vasoactive intestinal polypeptide (VIP) leads to increased local synthesis of cAMP. Tests with selective beta-receptor agonists and antagonists suggested that beta 1-receptors predominate, which is consistent with studies of sympathomimetic effects on cerebrospinal fluid production in vivo.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1981

Determination of prenalterol in plasma and in urine by gas-liquid chromatography.

A description is given of a gas-liquid chromatographic method for the quantitative determination of unchanged prenalterol in plasma and for the total (free and conjugated) prenalterol in urine. After addition of an adequate internal standard, prenalterol together with the internal standard, is extracted with diethyl ether and derivatized with heptafluorobutyric anhydride-pyridine to form a tri-heptafluorobutyric derivative. This derivative has favourable properties for its estimation by gas-liquid chromatography using electron-capture detection. A large percentage of prenalterol is excreted as sulfate conjugate in man. Thus a hydrolysis step is added to the urine assay. The sensitivity of the method is about 2ng/ml.

Chromatography, Gas↗
PubMed1982

Assay of prenalterol in plasma and urine by gas chromatography-mass spectrometry.

A sensitive and selective method for the quantitative analysis of prenalterol in plasma and urine is described. Prenalterol and the internal standard, deuterated prenalterol, are extracted with diethyl ether at pH 9.9 under salting-out conditions. Derivatization is performed by means of pentafluoropropionic anhydride in toluene before separation in the gas chromatograph. Detection and quantification of the triacyl derivatives are done by mass spectrometry in the selected ion monitoring mode. The method allows determination of concentrations down to 5 nmol/l (1 ng/ml) in 1 ml of sample, with a relative standard deviation below 10%.

Gas Chromatography-Mass Spectrometry↗