Library

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Electronic Resource
    Electronic Resource
    The electron-deficient olefin 2,2-bis(trifluoromethyl)ethylene-1,1-dicarbonitrile: hydride abstractions from allyl and isobutenyl ethers and thioethers (1991)
    s.l. : American Chemical Society
    The @journal of organic chemistry 56 (1991), S. 1677-1679 
    Details
    ISSN: 1520-6904
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1021/jo00005a001
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    2,2-Bis(trifluoromethyl)ethylene-1,1-dicarbonitrile as a unique enophile (1991)
    s.l. : American Chemical Society
    The @journal of organic chemistry 56 (1991), S. 1679-1681 
    Details
    ISSN: 1520-6904
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1021/jo00005a002
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Cardioprotective actions of KC 12291 I. Inhibition of voltage-gated Na+ channels in ischemia delays myocardial Na+ overload (1998)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 358 (1998), S. 547-553 
    Details
    ISSN: 1432-1912
    Keywords: Abstract To characterize KC 12291 (1-(5-phenyl-1 ; 2 ; 4-thiadiazol-3-yl-oxypropyl)-3-[N-methyl-N-[2-(3 ; 4-dimethoxyphenyl) ethyl] amino] propane hydrochloride) ; a newly synthezised inhibitor of voltage-gated Na+ channels ; the effects of the agent on Na+ current and ischemia-induced Na+ overload were investigated in isolated cardiomyocytes ; atria and saline-perfused hearts. As measured by the patch clamp technique ; KC 12291 (1 µM) significantly reduced peak Na+ current after activation of voltage-gated Na+ channels in rat cardiomyocytes. Partial depolarization enhanced the inhibitory effects during steady state conditions of the channel. In isolated guinea pig atria ; 1 µM KC 12291 had no effect on contractility under basal conditions but effectively delayed the onset and reduced the extent of anoxic contracture. The concentration-response curve was clearly shifted to the left when atria were partially depolarized by increased extracellular K+. As measured by 23Na NMR spectroscopy in isolated perfused guinea pig hearts ; intracellular Na+ rose more than four-fold in a linear fashion ; during 60 min of low-flow ischemia. KC 12291 (1 µM) prevented Na+ overload within the initial 12 min of ischemia; thereafter the slope of Na+ accumulation was identical to controls. Electrical excitability of hearts ; evaluated by intracardial ECG ; completely ceased within 15 min after the onset of ischemia. KC 12291 (1 µM) accelerated this process by more than 6 min. The data provide first evidence that KC 12291 reduces Na+ influx through voltage-gated Na+ channels during ischemia and thus delays Na+ overload by enhancing the inexcitability of the heart. ; Key words Heart ; Ischemia ; Na+ overload ; Na+ channels ; Inhibition ; 23Na NMR spectroscopy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/PL00005291
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    Evidence for adenosine receptor-mediated isoprenaline-antagonistic effects of the adenosine analogs PIA and NECA on force of contraction in guinea-pig atrial and ventricular cardiac preparations (1985)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 331 (1985), S. 131-139 
    Details
    ISSN: 1432-1912
    Keywords: (−)-N6-Phenylisopropyladenosine ; 5′-N-Ethylcarboxamideadenosine ; Adenosine receptor ; Guinea-pig heart ; Adenylate cyclase ; Transmembrane action potential
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of the adenosine agonists (−)-N6-phenylisopropyladenosine (PIA) and 5′-N-ethylcarboxamideadenosine (NECA) on force of contraction, adenylate cyclase activity and normal as well as slow action potentials were studied in guinea-pig isolatedatrial (left auricles) andventricular preparations (papillary muscles). Inauricles PIA and NECA exerted concentration-dependent negative inotropic effects with similar potenticies (mean EC50:0.05 μmol l−1 for PIA and 0.03 μmol l−1 for NECA). Similar results were obtained in the presence of isoprenaline. Inpapillary muscles PIA and NECA alone had no effect on force of contraction but produced negative inotropic effects in the presence of isoprenaline (mean EC50:0.19 μmol l−1 for PIA and 0.10 μmol l−1 for NECA). In both preparations, the negative inotropic effects of PIA and NECA in the presence of isoprenaline were antagonized by the adenosine receptor antagonist 8-phenyltheophylline. In both preparations, PIA and NECA did not affect adenylate cyclase activity, both in the absence and presence of isoprenaline. Inauricles the negative inotropic effects of both nucleosides were accompanied by shortening of the action potential. This effect was also observed in the presence of isoprenaline. Inpapillary muscles the adenosine analogs did not detectably alter the shape of the normal action potential. Ca2+-dependent slow action potentials elicited in potassium-depolarized preparations also remained unaltered in the presence of PIA or NECA alone. However, the isoprenaline-induced enhancement of the maximal rate of depolarization of slow action potentials was attenuated by PIA or NECA. It is concluded that in guinea-pig atrial and ventricular cardiac preparations the adenosine analogs PIA and NECA exert isoprenaline-antagonistic effects on force of contraction via adenosine receptors the existence of which can thus be shown in a functional way. These receptors are not detectably coupled to the adenylate cyclase. The negative inotropic effect in theauricle is most likely due to a shortening of the action potential resulting from an activation of potassium channels, which in turn indirectly reduces the Ca2+ influx during the action potential. In theventricle the adenosine receptor is either not linked to these potassium channels or adenosine-sensitive potassium channels do not exist in the ventricle. Instead the activation of the receptor causes a decrease of the slow Ca2+ inward current but this effect is observed only when the slow Ca2+ inward current had previously been enhanced by a cyclic AMP-dependent mechanism.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00634229
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 5
    Electronic Resource
    Electronic Resource
    Effects on transmembrane action potential, slow inward current and force of contraction in ventricular cardiac muscle of BRL 31660, a new antiarrhythmic drug with class I and class IV activity (1985)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 329 (1985), S. 86-93 
    Details
    ISSN: 1432-1912
    Keywords: BRL 31660 ; Lidocaine ; Antiarrhythmic drug ; Action potential ; Slow inward current
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of 1–30 μmol l−1 BRL 31660 on transmembrane action potential and force of contraction were investigated in guinea-pig electrically driven papillary muscles. Lidocaine was studied for comparison. BRL 31660 depressedV max of the action potential without changing the resting potential, decreased the force of contraction and decreased the action potential duration. Similar effects were obtained with lidocaine. BRL 31660 inhibited the recovery ofV max from inactivation, the time constant of which was estimated to be about 1,100 ms in the presence of 10 μmol l−1 BRL 31660. The depressive effect onV max was particularly pronounced at low (less negative) membrane potentials. BRL 31660 can thus be classified as a class I antiarrhythmic agent of the lidocaine type. Additional voltage-clamp experiments in cow ventricular trabeculae provided evidence that BRL 31660 also depressed the slow inward current at concentrations similar to those producing the effects on the transmembrane action potential. BRL 31660 thus exerted an additional class IV action. This effect was not shared by lidocaine. It is concluded that BRL 31660 is a new antiarrhythmic agent which depresses both the fast and slow inward current at similar concentrations. The dual effects of BRL 31660 conceivably contribute to its antiarrhythmic activity, but the clinical relevance of these results remains to be elucidated.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00695197
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 6
    Electronic Resource
    Electronic Resource
    The positive inotropic effect of phenylephrine in the presence of propranolol. Increase in time to peak force and in relaxation time without increase in c-AMP (1978)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 303 (1978), S. 205-211 
    Details
    ISSN: 1432-1912
    Keywords: Phenylephrine in the presence of propranolol ; Positive inotropic effect ; c-AMP ; Time to peak force ; Relaxation time
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of phenylephrine on the shape of the contraction curve and on the cyclic adenosine 3′,5′-monophosphate (c-AMP) content were studied in electrically driven (frequency 0.2 Hz) cat papillary muscles. All experiments were done in the presence of 1 μM propranolol in order to minimize interference from β-adrenoceptors. 1. Phenylephrine increased the force of contraction in a concentration-dependent manner. Maximal effects (about 200% of control) occurred at 30 μM phenylephrine. 2. The positive inotropic effect (PIE) of phenylephrine was antagonized by phentolamine. Phentolamine, 5μM, produced a parallel shift of the concentration-response curve for the PIE of phenylephrine by about two log units to the right. 3. The PIE of 30 μM phenylephrine occurred without any detectable increase in the c-AMP levels of the preparations. 4. The PIE of 30μM phenylephrine developed about three times more slowly than the PIE of an equieffective concentration of isoprenaline. 5. The PIE of phenylephrine was accompanied by significant, concentration-dependent increases in both time to peak force and relaxation time. 6. It is concluded that the PIE of phenylephrine in the presence of propranolol is mediated mainly by a stimulation of α-adrenoceptors. It is unlikely to be related to an increase in c-AMP. With respect to time course and influence on the shape of the contraction curve it is qualitatively different from the effects of β-adrenoceptor stimulation. These data are taken to support the hypothesis that the mechanical effects of α-and β-adrenoceptor stimulating agents on the heart are produced by different mechanisms.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00498045
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 7
    Electronic Resource
    Electronic Resource
    Negative inotropic effect of vanadate in ventricular myocardium in the presence of 3-isobutyl-1-methylxanthine or isoprenaline (1980)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 315 (1980), S. 147-153 
    Details
    ISSN: 1432-1912
    Keywords: Vanadate ; Isobutylmethylxanthine ; Isoprenaline ; Negative inotropic effect ; Ventricular myocardium
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The influence of a low concentration of 3-isobutyl-1-methylxanthine (IBMX; 5μmol l−1) on the positive inotropic effect of vanadate (NH4VO3; 10–1,000 μmol l−1) and isoprenaline (ISO; 0.1–300 nmol l−1) was studied in electrically driven (frequency 1 Hz) papillary muscles isolated from guinea pigs. Furthermore the influence of maximally effective concentrations of IBMX (100μmol l−1), ISO (100nmol l−1) and dihydro-ouabain (DHO; 70μmol l−1) on the inotropic effect of NH4VO3 was investigated. 1. IBMX (5μmol l−1) shifted the concentrationresponse curve for ISO to the left (EC50-ratio 2.4). In contrast, the positive inotropic effect of NH4VO3 (mean EC50 81.7μmol l−1) was not influenced by IBMX at this concentration. 2. In the presence of high concentrations of IBMX or ISO, NH4VO3 exerted a concentration-dependent (10–1,000μmol l−1) atropine-insensitive negative inotropic effect with mean EC50 values of 40.1 μmol l−1 and 73.0μmol l−1, respectively. 3. In the presence of the maximally effective concentration of DHO, NH4VO3 had no effect on force of contraction, i.e. it neither further increased nor reduced the DHO-induced positive inotropic effect. 4. The negative inotropic effect of NH4VO3 in the presence of IBMX or ISO in guinea-pig papillary muscles was not accompanied by a shortening of the action potential. 5. From the failure of IBMX (5μmol l−1) to enhance the positive inotropic effect of NH4VO3 it is concluded that the recently described small increase in c-AMP, which accompanies the NH4VO3-produced increase in force of contraction in intact papillary muscles, is not of major importance in mediating the agent's positive inotropic effect. 6. The mechanism of the negative inotropic effect of NH4VO3 in the presence of high concentrations of IBMX or ISO remains obscure. Apparently, it is not due to a shortening of the action potential. A stimulation of muscarinic cholinergic receptors is also unlikely although there are obvious similarities between the negative inotropic effect of NH4VO3 and that of acetylcholine described under similar conditions in ventricular heart muscle preparations. Interestingly, all drugs hitherto found capable of evoking a negative inotropic effect of vanadate in ventricular tissue are well known to increase myocardial c-AMP levels.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00499257
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 8
    Electronic Resource
    Electronic Resource
    Role of guanine nucleotide-binding protein in the regulation by adenosine of cardiac potassium conductance and force of contraction. Evaluation with pertussis toxin (1986)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 332 (1986), S. 403-405 
    Details
    ISSN: 1432-1912
    Keywords: Pertussis toxin ; Adenosine ; Negative inotropic effect ; Potassium conductance ; Guinea-pig heart
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In atrial cardiac preparations adenosine exerts a receptor-mediated negative inotropic effect due to an increased potassium conductance. Pretreatment of guinea pigs with pertussis toxin abolished the negative inotropic and action potential shortening effect of adenosine and the adenosine analogue (−)-N6-phenylisopropyladenosine (PIA). As pertussis toxin specifically inactivates guanine nucleotide-binding proteins involved in the signal transfer from receptor binding to specific cell functions, it is concluded that a guanine nucleotide-binding protein is involved in the regulation of the receptor-mediated change in potassium conductance and force of contraction.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00500095
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 9
    Electronic Resource
    Electronic Resource
    Preparation of α-chiral crotylsilanes by retro-[1,4]-brook rearrangements. A stereochemical study (1995)
    Weinheim : Wiley-Blackwell
    Liebigs Annalen 1995 (1995), S. 385-400 
    Details
    ISSN: 0947-3440
    Keywords: Asymmetric induction ; Diastereoselectivity ; 1,3-Diol ; Lithiation, reductive ; Rearrangement, retro-Brook ; Silane, α-chiral ; Silane, crotyl- ; Silane, γ-hydroxy- ; Chemistry ; Organic Chemistry
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Chemistry and Pharmacology
    Notes: Treatment of alcohols cis-22, cis-23, and trans-23 with PPh3/ Ph2S2 provided three mixtures of isomers of α, γ-disubstituted allyl phenyl sulfides. They consisted of diastereomers and -except starting from trans-23-of regioisomers. Each mixture was lithiated reductively by lithium naphthalenide at -78°C in THF. α, γ-Disubstituted allyllithium compounds resulted which underwent retro-[1,4]-Brook rearrangements within 30-90 min. A high degree of stereocontrol by 1,3-asymmetric induction was observed in the rearrangement starting from a 5:1 mixture of the tBuPh2Si-containing sulfide regioisomers cis-25 and iso-25 (each regioisomer consisting of more than one diastereomer): The α-chiral crotylsilane anti, trans-26 was formed as a racemic mixture with ds = 93:7:0:0 in preference to isomer syn,trans-26 which possesses the opposite configuration at the silicon-bearing stereocenter and in preference to the corresponding cis isomers (Scheme 5). The rearrangements of the two other sulfide mixtures were much less stereoselective and exhibited ds = 49:44:4:3 starting from the two tBuPh2Si-containing diastereomers of the isomeric sulfide trans-25 (Scheme 5) and ds = 59:41 starting from the 3.5:1 mixture of the MePh2Si-containing sulfide regioisomers cis-24 and iso-24 (each regioisomer consisting of more than one diastereomer; Scheme 9). The stereostructures of the rearrangement products were determined by chemical correlations, NMR analogies, and a crystal structure analysis of 27. It was proven that the stereochemical outcome of the retro-[1,4]-Brook rearrangements of the MePh2Si-containing 3.5:1 mixture of sulfides cis-24/iso-24 is kinetically rather than thermodynamically controlled (Scheme 10). Mechanistic aspects are discussed in Schemes 11-13.
    Additional Material: 1 Tab.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jlac.199519950247
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 10
    Electronic Resource
    Electronic Resource
    Strategy for the Synthesis of Epoxide- and Carbonate-Containing Dienediyne Models of the Neocarzinostatin Chromophore - Application to the 6-Ring/11-Ring Case[1] (1997)
    Weinheim : Wiley-Blackwell
    Liebigs Annalen 1997 (1997), S. 947-959 
    Details
    ISSN: 0947-3440
    Keywords: C-C coupling ; Dienediynes ; Enol triflates ; McMurry reaction ; Neocarzinostatin ; Synthetic methods ; Chemistry ; Organic Chemistry
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Chemistry and Pharmacology
    Notes: A novel synthetic strategy leading to bicyclic dienediyne models of the chromophore 1 of the anti-tumor antibiotic neocarzinostatin is described. Its key step is a ring-closing McMurry reaction of the dienediyne keto aldehydes 17 or 23. It leads to dienediynediols (compounds 19 and 24, respectively) or to trienediynes (compounds 18 and 25, respectively). Low temperatures favor the formation of dienediynediols while high temperatures favor the formation of trienediynes, so that the McMurry reactions of keto aldehyde 23 show an almost perfect temperature-dependent chemoselectivity (Scheme 6). The trienediyne 25 contains a ketal group which was removed by acid-catalyzed methanolysis (Scheme 8). The resulting diol 31 was mono-tert-butylsilylated to provide the allyl alcohol 36 (Scheme 10). It was epoxidized regio- and stereoselectively with Sharpless' asymmetric epoxidation reagent. The resulting epoxide 37 was converted into the dienediyne epoxycarbonate syn-33 in the final step of a sequence totaling seven steps and 5% yield starting from the bistriflate 3b; 3b itself is accessible from 2-formylcyclohexa none in two steps and 47% overall yield. The dienediyne epoxycarbonate syn-33 is the first synthetic congener of the neocarzinostatin chromophore furnished both with the - correctly configured - epoxide and carbonate rings.
    Additional Material: 1 Tab.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jlac.199719970526
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...