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  • 1
    Electronic Resource
    Electronic Resource
    Are Electrophysiological Studies Needed Prior to Defibrillator Implantation? (2003)
    350 Main Street , Malden , MA 02148-5018 , USA , and 9600 Garsington Road , Oxford OX4 2DQ , UK . : Blackwell Futura Publishing, Inc.
    Pacing and clinical electrophysiology 26 (2003), S. 0 
    Details
    ISSN: 1540-8159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: At present, patients with documented sustained VT or resuscitated cardiac arrest (CA) are treated with ICDs. The aim of this study was to retrospectively evaluate if a routine electrophysiological study should be recommended prior to ICD implantation. In 462 patients referred for ICD implantation because of supposedly documented VT (n = 223) or CA (n = 239) , electrophysiological study was routinely performed. In 48% of the patients with CA, sustained VT or VF was inducible. Electrophysiological study suggested conduction abnormalities (n = 11) or supraventricular tachyarrhythmias (n = 3) in conjunction with severely impaired left ventricular function to have been the most likely cause of CA in 14 (5.9%) of 239 patients. Likewise, sustained VT was only inducible in 48% of patients with supposedly documented VT. Of these inducible VTs, nine were diagnosed as right ventricular outflow tract tachycardia or as bundle branch reentry tachycardia. Supraventricular tachyarrhythmias judged to represent the clinical event were the only inducible arrhythmia in 35 (16%) patients (AV nodal reentrant tachycardia [n = 7] , AV reentry tachycardia [n = 4] , atrial flutter [n = 19] , and atrial tachycardia [n = 5] ). Based on findings from the electrophysiological study, ICD implantation was withheld in 14 (5.9%) of 239 patients with CA and in 44 (19.7%) of 223 patients with supposedly documented VT. During electrophysiological study, VT or VF was only reproducible in about 50% of patients with supposedly documented VT or CA. Electrophysiological study revealed other, potentially curable causes for CA or supposedly documented VT in 12.6% (58/462) of all patients, indicating that ICD implantation can potentially be avoided or at least postponed in some of these patients. Based on these retrospective data, routine electrophysiological study prior to ICD implantation seems to be advisable. (PACE 2003; 26:1715–1721)
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1460-9592.2003.t01-1-00257.x
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  • 2
    Electronic Resource
    Electronic Resource
    Opioid receptor agonists activate pertussis toxin-sensitive G proteins and inhibit adenylyl cyclase in canine cardiac sarcolemma (1996)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 354 (1996), S. 643-649 
    Details
    ISSN: 1432-1912
    Keywords: Cardiac sarcolemma ; Opioid receptors ; Adenylyl cyclase ; Low Km ; GTPase ; G proteins
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Although both opioid receptors and endogenous opioids are abundant in cardiac tissues, the signal transduction pathways of opioids in cardiac sarcolemmal membranes have yet to be identified. In highly purified canine cardiac sarcolemmal membranes, binding of the opioid receptor antagonist [3H]diprenorphine and effects of μ, δ and κ agonists on low Km GTPase and adenylyl cyclase were measured. Equilibrium binding of [3H]diprenorphine revealed a maximal binding capacity of 7.2 pmol/mg protein and a Kd of 1.3 nmol/1. In the presence of GTP, (D-Pen2,5, p-Cl-Phe4)enkephalin and (D-Arg6)dynorphin A 1-13 fragment both inhibited adenylyl cyclase by 20–25% (from 206 ± 30to164 ± 28 pmol·min− 1·mgprotein−1, EC506 μmol/Landfrom254 ± 109to204 ± 90 pmol·min− 1·mg protein−, EC50 8 pmol/L, respectively; P〈0.001). Both substances stimulated low Km GTPase by 20%and13%,respectively(from12.7 ± 3.0 to 15.2 ± 3.7 pmol·min−1.mgprotein−1,EC50 12 μmol/L, P〈0.01, and from 9.1 ± 2.8 to 10.4 ± 3.2 pmol-min− 1·mg protein−1, EC50 6 μmol/L, P〈0.05, respectively). These effects were blocked by the opioid receptor antagonist naltrexone and by pretreatment of sarcolemmal membranes with pertussis toxin. The μ opioid receptor agonists (D-AIa2, Me Phe4, Gly-[ol]5)enkephalin and morphiceptin had no effect on either cardiac adenylyl cyclase or low Km GTPase activities. These data suggest that in cardiac sarcolemma, opioid receptors are coupled to pertussis toxin sensitive G proteins and mediate inhibition of adenylyl cyclase activity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00170840
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  • 3
    Electronic Resource
    Electronic Resource
    Inhibition of elastase improves myocardial function after repetitive ischaemia and myocardial infarction in the rat heart (1997)
    Springer
    Pflügers Archiv 433 (1997), S. 563-570 
    Details
    ISSN: 1432-2013
    Keywords: Key words Myocardial stunning ; Myocardial infarction ; Myocardial blood flow ; Regional myocardial function ; Myeloperoxidase ; Elastase ; Neutrophils
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  We investigated the potential of inhibition of elastase, a granulocyte-derived proteolytic enzyme, in ameliorating the effects of myocardial stunning caused by repetitive ischaemia (RI) and myocardial infarction (MI) for the first time in an in situ, perfused, rat heart model. The effects of the elastase-inhibitors Elafin (EL, 10 mg/kg/h) and ICI 200,880 (ICI,5 mg/kg/h) on myocardial blood flow (MBF, H2 clearance), regional myocardial function (FT, pulsed doppler) and neutrophil extravasation (myocardial myeloperoxidase activity, MPO) were investigated in RI (5×10 min ligature of the anterior descending ramus (LAD), 5×20 min reperfusion) and MI (50 min LAD ligature, 60 min reperfusion). Under control conditions, MBF and FT were significantly reduced and MPO was significantly increased after RI (n=8) and MI (n=8) in the ischaemic area compared with baseline. Pretreatment with EL (n=7) or ICI (n=7) did not improve MBF significantly and did not influence the successive attenuation of peak values of reactive hyperaemia. However, both EL and ICI significantly improved FT and significantly reduced MPO after RI and MI compared with control conditions. Additionally, both the area at risk and MI size were reduced significantly by both inhibitors. These results demonstrate that elastase inhibitors significantly improve the reduction of FT both in myocardial stunning and in myocardial infarction in the rat without significant improvement of MBF. It is concluded that elastase inhibitors exert a cardioprotective effect against reperfusion injury, probably by inhibition of leukocyte extravasation as indicated by the decrease in MPO activity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004240050315
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  • 4
    Electronic Resource
    Electronic Resource
    Phosphotransfer reactions as a means of G protein activation (1996)
    Springer
    Molecular and cellular biochemistry 157 (1996), S. 59-63 
    Details
    ISSN: 1573-4919
    Keywords: nucleoside diphosphate kinase ; G proteins ; phosphate transfer reactions
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Heterotrimeric guanine nucleotide-binding regulatory proteins (G proteins) serve to transduce information from agonist-bound receptors to effector enzymes or ion channels. Current models of G protein activation-deactivation indicate that the oligomeric GDP-bound form must undergo release of GDP, bind GTP and undergo subunit dissociation, in order to be in active form (GTP bound α subunits and free βγ dimers) and to regulate effectors. The effect of receptor occupation by an agonist is generally accepted to be promotion of guanine nucleotide exchange thus allowing activation of the G protein. Recent studies indicate that transphosphorylation leading to the formation of GTP from GDP and ATP in the close vicinity, or even at the G protein, catalysed by membrane-associated nucleoside diphosphate kinase, may further activate G proteins. This activation is demonstrated by a decreased affinity of G protein-coupled receptors for agonists and an increased response of G protein coupled effectors. In addition, a phosphorylation of G protein β subunits and consequent phosphate transfer reaction resulting in G protein activation has also been demonstrated. Finally, endogenously formed GTP was preferentially effective in activating some G proteins compared to exogenous GTR The aim of this report is to present an overview of the evidence to date for a transphosphorylation as a means of G protein activation (see also refs [1 and 2] for reviews). (Mol Cell Biochem 157: 593, 1996)
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00227881
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  • 5
    Electronic Resource
    Electronic Resource
    Evidence against a regulation of Na+/K+-ATPase by Gi proteins. Failure to detect an influence of G proteins on Na+/Ca2+-exchange in cardiac sarcolemmal membranes (1996)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 353 (1996), S. 505-512 
    Details
    ISSN: 1432-1912
    Keywords: Sarcolemmal membranes ; Gi proteins ; Adenosine A1 receptor ; Muscarinic ; M2 receptor ; Na+/Ca2+ exchange ; Na+/K+-ATPase ; K+O2NPhPase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In the myocardium the inhibitory guanine nucleotide-binding regulatory proteins (Gi proteins) mediate negative chronotropic and negative inotropic effects by activation of K+ channels and inhibition of adenylyl cyclase. The concept of a uniform inhibitory action of Gi proteins on myocardial cellular activity has been questioned by the recent observations of adenosine-induced activation of the Na+/Ca2+ exchange and a carbachol-induced inhibition of the Na+/K+-ATPase activity in cardiac sarcolemmal membranes. The aim of the present study, therefore, was to reinvestigate the putative regulation of Na+/Ca2+ exchange and Na+/K+-ATPase activity in purified canine sarcolemmal membranes. These membranes were enriched in adenosine A1 (Maximum number of receptors, B max 0.033 pmol/mg) and muscarinic M2 (B max 2.9 pmol/mg) receptors and contained Gi2 and Gi3, two Gi protein isoforms, and Go, another pertussis toxin-sensitive G protein, as detected with specific antibodies. The adenosine A1-selective agonist, (−)-N 6-(2-phenylisopropyl)-adenosine, and the muscarinic agonist, carbachol, both inhibited isoprenaline-stimulated adenylyl cyclase activity by 25% and 35% respectively, and the stable GTP analogue 5′-guanylylimidodiphosphate inhibited forskolin-stimulated adenylyl cyclase activity by 35% in these membranes. The characteristics of Na+/Ca2+ exchange and Na+/K+-ATPase activity as well as those of the ouabain-sensitive, K+-activated 4-nitrophenylphosphatase, an ATP-independent, partial reaction of the Na+/K+-ATPase, were in agreement with published data with regard to specific activity, time course of activity and substrate dependency. However, none of these activities were influenced by adenosine, (−)-N 6-(2-phenylisopropyl)-adenosine, carbachol, or stable GTP analogs, suggesting that Na+/Ca2+ exchange and Na+/K+-ATPase are not regulated by Gi proteins in canine cardiac sarcolemmal membranes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00169169
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