Biomedical subjects

D Martens

Publications and source records attributed to D Martens.

8 recordsLinked to original sources

PubMed1990

[Alcohol withdrawal syndrome in the postoperative phase--therapy or prevention?].

In a prospective study 50 patients who reported regular ethanol consumption and who underwent neck dissection were evaluated by clinical examination and the Munich alcohol test (MALT). 31 patients were not classified as alcohol abusers and none of them developed withdrawal symptoms (WS) postoperatively. 19 patients were diagnosed as alcohol abusers; 9 of them (group 1) received symptomatic therapy with clomethiazol and haloperidol, 10 patients (group 2) received continuous ethanol infusions (2-4 g/h) postoperatively as prophylaxis for WS. 6 patients in group 1 developed WS; none of group 2 developed WS. Thus the period of intensive care therapy of group 2 was significantly shorter (3.0 versus 11.5 days). It was concluded that postoperative continuous ethanol infusions prevent the occurrence of WS and should be administered to severely alcoholic patients.

Alcohol Withdrawal Delirium↗

PubMed1988

[3H]-8-cyclopentyl-1,3-dipropylxanthine binding to A1 adenosine receptors of intact rat ventricular myocytes.

The purpose of the present study was the identification of A1 adenosine receptors in intact rat ventricular myocytes, which are thought to mediate the negative inotropic effects of adenosine. The adenosine receptor antagonist [3H]-8-cyclopentyl-1,3-dipropylxanthine was used as radioligand. Binding of the radioligand to intact myocytes was rapid, reversible, and saturable with a binding capacity of 40,000 binding sites per cell. The dissociation constant of the radioligand was 0.48 nM. The adenosine receptor antagonists 8-cyclopentyl-1,3-dipropylxanthine, "xanthine amine congener," and theophylline were competitive inhibitors with affinities in agreement with results obtained for A1 receptors in other tissues. Competition experiments using the adenosine receptor agonists R-N(6)-phenylisopropyladenosine, 5'-N-ethylcarboxamidoadenosine, and S-N(6)-phenylisopropyladenosine gave monophasic displacement curves with Ki values of 50 nM, 440 nM, and 4,300 nM, which agreed well with the GTP-inducible low affinity state in cardiac membranes. The low affinity for agonists was not due to agonist-induced desensitization, and correlated well with the corresponding IC50 values for the inhibition of cyclic AMP accumulation by isoprenaline. It is suggested that only a low affinity state of A1 receptors can be detected in intact rat myocytes due to the presence of high concentrations of guanine nucleotides in intact cells.

Animals↗

PubMed1987

Pharmacological characterization of A1 adenosine receptors in isolated rat ventricular myocytes.

The aim of the present study was the characterization of adenosine receptors in isolated rat ventricular myocytes. The cAMP-levels of rat ventricular myocytes in the presence of 1 mumol/l isoprenaline were reduced by up to 48% by adenosine analogues; the rank order of potency was: R-N6-phenylisopropyladenosine (IC50 60 nmol/l), 5'-N-ethylcarboxamidoadenosine (IC50 360 nmol/l) and S-N6-phenylisopropyladenosine (IC50 16 mumol/l). The adenosine receptor antagonist XAC ("xanthine amine congener") antagonized the effect of R-N6-phenylisopropyladenosine in a concentration-dependent manner with a Ki-value of 20 nmol/l. The A1 receptor-selective radioligand R-N6-125I-p-hydroxyphenylisopropyladenosine bound to membranes prepared from rat ventricular myocytes in a saturable manner with a Bmax of 17.7 fmol/mg protein and a KD-value of 1.1 nmol/l. Adenosine analogues competed for the binding with the same rank order of potency as for the inhibition of the isoprenaline-induced cAMP-increase. GTP inhibited radioligand binding with an IC50-value of 73 mumol/l. These results suggest the presence of A1 adenosine receptors on rat ventricular myocytes, which mediate an inhibition of adenylate cyclase. The receptors may be responsible for the effects of adenosine and its analogues on the heart.

Adenosine↗

PubMed1979