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Biomedical subjects

G Steurer

Publications and source records attributed to G Steurer.

32 records · Page 2Linked to original sources
PubMed1988

Recurrent paradoxical embolism complicating severe thromboembolic pulmonary hypertension.

A patient with a three-year history of recurrent pulmonary embolism is presented. Thromboembolic pulmonary hypertension was proven in the final stage of disease in the presence of repeated episodes of systemic embolic events. Paradoxical embolism was assumed to be present on the basis of blood-gas analysis and contrast echocardiography that demonstrated a right-to-left shunt at atrial level. Autopsy revealed a patent foramen ovale and provided strong evidence for the accuracy of the clinical diagnosis.

Adult↗
PubMed1988

The platelet rebound phenomenon during PGI2-infusion occurs at the receptor level.

In 6 patients treated with continuous prostaglandin I2 (PGI2)-infusion using a portable pump at a rate of 5 ng/kg/min for 7 days drug receptor interaction of [3H]Iloprost, a stable PGI2 analogue, with a particulate platelet membrane fraction was investigated. Saturation binding experiments of the high affinity platelet prostacyclin receptor performed before and at the end of PGI2 infusion revealed a significant increase of dissociation constant (Kd) and increase in maximal number of binding sites (Bmax). These findings suggest that continuous long-term PGI2 infusion results in a functional desensitization of the membrane-bound PGI2 platelet receptor with a decrease in receptor affinity and an increase in number of binding sites as suggested earlier based upon platelet sensitivity behaviour.

Aged↗
PubMed1986

Assessment of the sensitivity of leukaemic cells to cytotoxic drugs by bioluminescence measurement of ATP in cultured cells.

A short-term test in vitro is described, which can be used to detect resistance to cytostatic agents in leukaemic cells. Leukaemic cell suspensions were incubated with cytostatic agents and the resulting intracellular ATP concentrations were measured by a bioluminescence ATP assay. There was a clear dose-effect relationship in acute leukaemia and chronic lymphocytic leukaemia cells for drugs used in the treatment of leukaemias. A good correlation was found between the ATP content of leukaemic cells and cell viability as determined by the trypan blue dye exclusion test. Preliminary individual clinical correlations suggest a correlation between the chemosensitivity in vitro and the response patterns in vivo in leukaemia patients. This simple, fast and sensitive method may have application for determination of drug-induced cytotoxicity in leukaemic cells in vitro.

Acute Disease↗
PubMed1984

Interaction of the antihypertensive drug urapidil with cardiac beta-adrenoceptors in vitro.

A possible interaction of the antihypertensive drug, urapidil with beta-adrenoceptors was investigated in a guinea-pig ventricular membrane preparation. Urapidil at concentrations above 1 microM antagonized the isoproterenol-induced stimulation of adenylate cyclase activity. Urapidil 10 microM shifted the concentration-response curve for isoproterenol in a parallel manner to the right by a factor of 16. Urapidil competed with specific beta-adrenoceptor binding of [125I]iodocyanopindolol with an IC50 of 12 microM. Since the affinity of urapidil to beta-adrenoceptors appeared rather low, any beta-adrenoceptor blocking property may be of relevance in vivo at high dosages only.

Adenylyl Cyclases↗
PubMed1984

Phosphorylated adenosine derivatives as low-affinity adenosine-receptor agonists. Methodological implications for the adenylate cyclase assay.

In cellular systems provided with activatory (Ra-site) receptors for adenosine, such as rat cerebral microvessels and rat liver plasma membranes, the adenosine-receptor antagonist 8-phenyltheophylline (10 microM) significantly decreased adenylate cyclase activity if ATP was the substrate and only if GTP was present. With dATP as substrate, adenylate cyclase activities in both preparations remained unaffected by 8-phenyltheophylline. In rat cerebral-cortical membranes, with inhibitory (Ri-site) receptors for adenosine, 8-phenyltheophylline significantly enhanced adenylate cyclase activity only in the presence of GTP and if ATP was the substrate. In rat cardiac ventricular membranes, which are devoid of any adenylate cyclase-coupled adenosine receptor, the methylxanthine had no GTP-dependent effect, irrespective of the substrate used. All assay systems contained sufficiently high amounts of adenosine deaminase (2.5 units/ml), since no endogenous adenosine, formed from ATP, was found chromatographically. In order to demonstrate a direct influence of phosphorylated adenosine derivatives on adenylate cyclase activity, we investigated AMP in a dATP assay system. AMP was verified chromatographically to remain reasonably stable under the adenylate cyclase assay conditions. In the microvessels, AMP increased enzyme activity in the range 0.03-1.0 mM, an effect competitively antagonized by 8-phenyltheophylline. In the cortical membranes, 0.1 mM-AMP inhibited adenylate cyclase, which was partially reversed by the methylxanthine. The presence of GTP was again necessary for all observations. In the ventricular membranes, AMP had no effect. Since the efficacy of adenosine-receptor agonists and, probably, that of other hormones on adenylate cyclase activity can be more efficiently measured with dATP as the enzyme substrate, this nucleotide seems preferable for adenylate cyclase measurements in systems susceptible to modulation by adenosine.

Adenine Nucleotides↗
PubMed1982

Functional identification of adenylate cyclase-coupled adenosine receptors in rat brain microvessels.

It was investigated whether adenosine affects the adenylate cyclase system of microvessels, isolated from the rat cerebral cortex, via an external receptor recently classified as R-site receptor. Several adenosine analogs caused GTP-dependent stimulation of adenylate cyclase. The rank order of potency: NECA (5'-(N-ethylcarboxamido)-adenosine, EC50 0.2 microM) greater than adenosine (0.71 microM) = 2-chloroadenosine (0.72 microM) greater than L-PIA (N6-(L-phenylisopropyl)-adenosine, 1.03 microM) greater than D-PIA (N6-(D-phenylisopropyl)-adenosine, 5.27 microM) is consistent with that for agonism at activatory (Ra-site) adenosine receptors in other tissues. Adenylate cyclase stimulation by PIA displayed stereoselectivity. The action of NECA was competitively antagonized by 8-phenyltheophylline. These findings provide functional evidence for Ra-site adenosine receptors in rat brain microvessels. However, direct identification of these receptors by binding studies was not possible. Binding of [3H]NECA to rat brain microvessels displayed rapid on-off kinetics and saturability, but equivocal specificity.

Adenosine↗
PubMedDate not supplied

The cardiac and brain microvessel adenylate cyclase system in deoxycorticosterone acetate-hypertensive rats.

A decrease in isoproterenol-stimulated adenylate cyclase activity has been shown in various tissues of hypertensive rats, a finding often associated with decreased beta-adrenoceptor number. The present study was undertaken to investigate whether adenylate cyclase stimulation by other hormones is similarly affected. Adenylate cyclase activity in cerebral microvessels under control conditions and following stimulation by isoproterenol, prostaglandin E1, and the adenosine analog 5'-(N-ethylcarboxamide)-adenosine (NECA) was significantly diminished in deoxycorticosterone acetate (DOCA)-hypertensive rats as compared with control rats, as was adenylate cyclase stimulation by GTP, fluoride, and forskolin. Similar results were obtained in cardiac ventricular membranes, apart from the fact that NECA did not influence adenylate cyclase activity in the heart, either in normotensive or in hypertensive rats. In both the heart preparation and the microvessel preparation, beta-adrenoceptor numbers were reduced in DOCA-hypertensive rats. Because the adenylate cyclase data also pointed to functional alteration at the guanine nucleotide regulatory site of the adenylate cyclase complex, the influence of DOCA hypertension on receptor-adenylate cyclase coupling was investigated by competition studies for beta-adrenoceptor binding. In ventricular membranes prepared from DOCA-hypertensive rats, the isoproterenol competition curve for [125I]iodocyanopindolol binding was only slightly altered in the presence of guanylyl imidodiphosphate (50 microM), in contrast to normotensive control rats, in which it was shifted to the right and became significantly steeper. These results are suggestive of decreased guanine nucleotide sensitivity of adenylate cyclase-coupled receptors in DOCA hypertension.

Adenylyl Cyclases↗