Search Results - (Author, Cooperation:S. B. Felix)

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  1. 1
    Staff View
    Publication Date:
    2018-01-26
    Publisher:
    Wiley-Blackwell
    Electronic ISSN:
    1097-4652
    Topics:
    Biology
    Medicine
    Published by:
    http://www.wiley.com/wiley-blackwell

    Latest Papers from Table of Contents or Articles in Press
  2. 2
    A. E. Locke ; B. Kahali ; S. I. Berndt ; A. E. Justice ; T. H. Pers ; F. R. Day ; C. Powell ; S. Vedantam ; M. L. Buchkovich ; J. Yang ; D. C. Croteau-Chonka ; T. Esko ; T. Fall ; T. Ferreira ; S. Gustafsson ; Z. Kutalik ; J. Luan ; R. Magi ; J. C. Randall ; T. W. Winkler ; A. R. Wood ; T. Workalemahu ; J. D. Faul ; J. A. Smith ; J. Hua Zhao ; W. Zhao ; J. Chen ; R. Fehrmann ; A. K. Hedman ; J. Karjalainen ; E. M. Schmidt ; D. Absher ; N. Amin ; D. Anderson ; M. Beekman ; J. L. Bolton ; J. L. Bragg-Gresham ; S. Buyske ; A. Demirkan ; G. Deng ; G. B. Ehret ; B. Feenstra ; M. F. Feitosa ; K. Fischer ; A. Goel ; J. Gong ; A. U. Jackson ; S. Kanoni ; M. E. Kleber ; K. Kristiansson ; U. Lim ; V. Lotay ; M. Mangino ; I. Mateo Leach ; C. Medina-Gomez ; S. E. Medland ; M. A. Nalls ; C. D. Palmer ; D. Pasko ; S. Pechlivanis ; M. J. Peters ; I. Prokopenko ; D. Shungin ; A. Stancakova ; R. J. Strawbridge ; Y. Ju Sung ; T. Tanaka ; A. Teumer ; S. Trompet ; S. W. van der Laan ; J. van Setten ; J. V. Van Vliet-Ostaptchouk ; Z. Wang ; L. Yengo ; W. Zhang ; A. Isaacs ; E. Albrecht ; J. Arnlov ; G. M. Arscott ; A. P. Attwood ; S. Bandinelli ; A. Barrett ; I. N. Bas ; C. Bellis ; A. J. Bennett ; C. Berne ; R. Blagieva ; M. Bluher ; S. Bohringer ; L. L. Bonnycastle ; Y. Bottcher ; H. A. Boyd ; M. Bruinenberg ; I. H. Caspersen ; Y. D. Ida Chen ; R. Clarke ; E. W. Daw ; A. J. de Craen ; G. Delgado ; M. Dimitriou ; A. S. Doney ; N. Eklund ; K. Estrada ; E. Eury ; L. Folkersen ; R. M. Fraser ; M. E. Garcia ; F. Geller ; V. Giedraitis ; B. Gigante ; A. S. Go ; A. Golay ; A. H. Goodall ; S. D. Gordon ; M. Gorski ; H. J. Grabe ; H. Grallert ; T. B. Grammer ; J. Grassler ; H. Gronberg ; C. J. Groves ; G. Gusto ; J. Haessler ; P. Hall ; T. Haller ; G. Hallmans ; C. A. Hartman ; M. Hassinen ; C. Hayward ; N. L. Heard-Costa ; Q. Helmer ; C. Hengstenberg ; O. Holmen ; J. J. Hottenga ; A. L. James ; J. M. Jeff ; A. Johansson ; J. Jolley ; T. Juliusdottir ; L. Kinnunen ; W. Koenig ; M. Koskenvuo ; W. Kratzer ; J. Laitinen ; C. Lamina ; K. Leander ; N. R. Lee ; P. Lichtner ; L. Lind ; J. Lindstrom ; K. Sin Lo ; S. Lobbens ; R. Lorbeer ; Y. Lu ; F. Mach ; P. K. Magnusson ; A. Mahajan ; W. L. McArdle ; S. McLachlan ; C. Menni ; S. Merger ; E. Mihailov ; L. Milani ; A. Moayyeri ; K. L. Monda ; M. A. Morken ; A. Mulas ; G. Muller ; M. Muller-Nurasyid ; A. W. Musk ; R. Nagaraja ; M. M. Nothen ; I. M. Nolte ; S. Pilz ; N. W. Rayner ; F. Renstrom ; R. Rettig ; J. S. Ried ; S. Ripke ; N. R. Robertson ; L. M. Rose ; S. Sanna ; H. Scharnagl ; S. Scholtens ; F. R. Schumacher ; W. R. Scott ; T. Seufferlein ; J. Shi ; A. Vernon Smith ; J. Smolonska ; A. V. Stanton ; V. Steinthorsdottir ; K. Stirrups ; H. M. Stringham ; J. Sundstrom ; M. A. Swertz ; A. J. Swift ; A. C. Syvanen ; S. T. Tan ; B. O. Tayo ; B. Thorand ; G. Thorleifsson ; J. P. Tyrer ; H. W. Uh ; L. Vandenput ; F. C. Verhulst ; S. H. Vermeulen ; N. Verweij ; J. M. Vonk ; L. L. Waite ; H. R. Warren ; D. Waterworth ; M. N. Weedon ; L. R. Wilkens ; C. Willenborg ; T. Wilsgaard ; M. K. Wojczynski ; A. Wong ; A. F. Wright ; Q. Zhang ; E. P. Brennan ; M. Choi ; Z. Dastani ; A. W. Drong ; P. Eriksson ; A. Franco-Cereceda ; J. R. Gadin ; A. G. Gharavi ; M. E. Goddard ; R. E. Handsaker ; J. Huang ; F. Karpe ; S. Kathiresan ; S. Keildson ; K. Kiryluk ; M. Kubo ; J. Y. Lee ; L. Liang ; R. P. Lifton ; B. Ma ; S. A. McCarroll ; A. J. McKnight ; J. L. Min ; M. F. Moffatt ; G. W. Montgomery ; J. M. Murabito ; G. Nicholson ; D. R. Nyholt ; Y. Okada ; J. R. Perry ; R. Dorajoo ; E. Reinmaa ; R. M. Salem ; N. Sandholm ; R. A. Scott ; L. Stolk ; A. Takahashi ; F. M. Van't Hooft ; A. A. Vinkhuyzen ; H. J. Westra ; W. Zheng ; K. T. Zondervan ; A. C. Heath ; D. Arveiler ; S. J. Bakker ; J. Beilby ; R. N. Bergman ; J. Blangero ; P. Bovet ; H. Campbell ; M. J. Caulfield ; G. Cesana ; A. Chakravarti ; D. I. Chasman ; P. S. Chines ; F. S. Collins ; D. C. Crawford ; L. A. Cupples ; D. Cusi ; J. Danesh ; U. de Faire ; H. M. den Ruijter ; A. F. Dominiczak ; R. Erbel ; J. Erdmann ; J. G. Eriksson ; M. Farrall ; S. B. Felix ; E. Ferrannini ; J. Ferrieres ; I. Ford ; N. G. Forouhi ; T. Forrester ; O. H. Franco ; R. T. Gansevoort ; P. V. Gejman ; C. Gieger ; O. Gottesman ; V. Gudnason ; U. Gyllensten ; A. S. Hall ; T. B. Harris ; A. T. Hattersley ; A. A. Hicks ; L. A. Hindorff ; A. D. Hingorani ; A. Hofman ; G. Homuth ; G. K. Hovingh ; S. E. Humphries ; S. C. Hunt ; E. Hypponen ; T. Illig ; K. B. Jacobs ; M. R. Jarvelin ; K. H. Jockel ; B. Johansen ; P. Jousilahti ; J. W. Jukema ; A. M. Jula ; J. Kaprio ; J. J. Kastelein ; S. M. Keinanen-Kiukaanniemi ; L. A. Kiemeney ; P. Knekt ; J. S. Kooner ; C. Kooperberg ; P. Kovacs ; A. T. Kraja ; M. Kumari ; J. Kuusisto ; T. A. Lakka ; C. Langenberg ; L. Le Marchand ; T. Lehtimaki ; V. Lyssenko ; S. Mannisto ; A. Marette ; T. C. Matise ; C. A. McKenzie ; B. McKnight ; F. L. Moll ; A. D. Morris ; A. P. Morris ; J. C. Murray ; M. Nelis ; C. Ohlsson ; A. J. Oldehinkel ; K. K. Ong ; P. A. Madden ; G. Pasterkamp ; J. F. Peden ; A. Peters ; D. S. Postma ; P. P. Pramstaller ; J. F. Price ; L. Qi ; O. T. Raitakari ; T. Rankinen ; D. C. Rao ; T. K. Rice ; P. M. Ridker ; J. D. Rioux ; M. D. Ritchie ; I. Rudan ; V. Salomaa ; N. J. Samani ; J. Saramies ; M. A. Sarzynski ; H. Schunkert ; P. E. Schwarz ; P. Sever ; A. R. Shuldiner ; J. Sinisalo ; R. P. Stolk ; K. Strauch ; A. Tonjes ; D. A. Tregouet ; A. Tremblay ; E. Tremoli ; J. Virtamo ; M. C. Vohl ; U. Volker ; G. Waeber ; G. Willemsen ; J. C. Witteman ; M. C. Zillikens ; L. S. Adair ; P. Amouyel ; F. W. Asselbergs ; T. L. Assimes ; M. Bochud ; B. O. Boehm ; E. Boerwinkle ; S. R. Bornstein ; E. P. Bottinger ; C. Bouchard ; S. Cauchi ; J. C. Chambers ; S. J. Chanock ; R. S. Cooper ; P. I. de Bakker ; G. Dedoussis ; L. Ferrucci ; P. W. Franks ; P. Froguel ; L. C. Groop ; C. A. Haiman ; A. Hamsten ; J. Hui ; D. J. Hunter ; K. Hveem ; R. C. Kaplan ; M. Kivimaki ; D. Kuh ; M. Laakso ; Y. Liu ; N. G. Martin ; W. Marz ; M. Melbye ; A. Metspalu ; S. Moebus ; P. B. Munroe ; I. Njolstad ; B. A. Oostra ; C. N. Palmer ; N. L. Pedersen ; M. Perola ; L. Perusse ; U. Peters ; C. Power ; T. Quertermous ; R. Rauramaa ; F. Rivadeneira ; T. E. Saaristo ; D. Saleheen ; N. Sattar ; E. E. Schadt ; D. Schlessinger ; P. E. Slagboom ; H. Snieder ; T. D. Spector ; U. Thorsteinsdottir ; M. Stumvoll ; J. Tuomilehto ; A. G. Uitterlinden ; M. Uusitupa ; P. van der Harst ; M. Walker ; H. Wallaschofski ; N. J. Wareham ; H. Watkins ; D. R. Weir ; H. E. Wichmann ; J. F. Wilson ; P. Zanen ; I. B. Borecki ; P. Deloukas ; C. S. Fox ; I. M. Heid ; J. R. O'Connell ; D. P. Strachan ; K. Stefansson ; C. M. van Duijn ; G. R. Abecasis ; L. Franke ; T. M. Frayling ; M. I. McCarthy ; P. M. Visscher ; A. Scherag ; C. J. Willer ; M. Boehnke ; K. L. Mohlke ; C. M. Lindgren ; J. S. Beckmann ; I. Barroso ; K. E. North ; E. Ingelsson ; J. N. Hirschhorn ; R. J. Loos ; E. K. Speliotes
    Nature Publishing Group (NPG)
    Published 2015
    Staff View
    Publication Date:
    2015-02-13
    Publisher:
    Nature Publishing Group (NPG)
    Print ISSN:
    0028-0836
    Electronic ISSN:
    1476-4687
    Topics:
    Biology
    Chemistry and Pharmacology
    Medicine
    Natural Sciences in General
    Physics
    Keywords:
    Adipogenesis/genetics ; Adiposity/genetics ; Age Factors ; *Body Mass Index ; Continental Population Groups/genetics ; Energy Metabolism/genetics ; Europe/ethnology ; Female ; Genetic Predisposition to Disease/genetics ; *Genome-Wide Association Study ; Glutamic Acid/metabolism ; Humans ; Insulin/metabolism/secretion ; Male ; Obesity/*genetics/*metabolism ; Polymorphism, Single Nucleotide/genetics ; Quantitative Trait Loci/genetics ; Synapses/metabolism
    Published by:
    http://www.nature.com/

    Latest Papers from Table of Contents or Articles in Press
  3. 3
    Lin, H., van Setten, J., Smith, A. V., Bihlmeyer, N. A., Warren, H. R., Brody, J. A., Radmanesh, F., Hall, L., Grarup, N., Muller-Nurasyid, M., Boutin, T., Verweij, N., Lin, H. J., Li-Gao, R., van den Berg, M. E., Marten, J., Weiss, S., Prins, B. P., Haessler, J., Lyytikainen, L.-P., Mei, H., Harris, T. B., Launer, L. J., Li, M., Alonso, A., Soliman, E. Z., Connell, J. M., Huang, P. L., Weng, L.-C., Jameson, H. S., Hucker, W., Hanley, A., Tucker, N. R., Chen, Y.-D. I., Bis, J. C., Rice, K. M., Sitlani, C. M., Kors, J. A., Xie, Z., Wen, C., Magnani, J. W., Nelson, C. P., Kanters, J. K., Sinner, M. F., Strauch, K., Peters, A., Waldenberger, M., Meitinger, T., Bork-Jensen, J., Pedersen, O., Linneberg, A., Rudan, I., de Boer, R. A., van der Meer, P., Yao, J., Guo, X., Taylor, K. D., Sotoodehnia, N., Rotter, J. I., Mook-Kanamori, D. O., Trompet, S., Rivadeneira, F., Uitterlinden, A., Eijgelsheim, M., Padmanabhan, S., Smith, B. H., Volzke, H., Felix, S. B., Homuth, G., Volker, U., Mangino, M., Spector, T. D., Bots, M. L., Perez, M., Kahonen, M., Raitakari, O. T., Gudnason, V., Arking, D. E., Munroe, P. B., Psaty, B. M., van Duijn, C. M., Benjamin, E. J., Rosand, J., Samani, N. J., Hansen, T., Kaab, S., Polasek, O., van der Harst, P., Heckbert, S. R., Jukema, J. W., Stricker, B. H., Hayward, C., Dorr, M., Jamshidi, Y., Asselbergs, F. W., Kooperberg, C., Lehtimaki, T., Wilson, J. G., Ellinor, P. T., Lubitz, S. A., Isaacs, A.
    American Heart Association (AHA)
    Published 2018
    Staff View
    Publication Date:
    2018-05-11
    Publisher:
    American Heart Association (AHA)
    Print ISSN:
    1942-325X
    Electronic ISSN:
    1942-3268
    Topics:
    Medicine
    Keywords:
    Electrophysiology, Epidemiology, Genetic, Association Studies
    Published by:
    http://www.americanheart.org/

    Latest Papers from Table of Contents or Articles in Press
  4. 4
    Bihlmeyer, N. A., Brody, J. A., Smith, A. V., Warren, H. R., Lin, H., Isaacs, A., Liu, C.-T., Marten, J., Radmanesh, F., Hall, L. M., Grarup, N., Mei, H., Muller-Nurasyid, M., Huffman, J. E., Verweij, N., Guo, X., Yao, J., Li-Gao, R., van den Berg, M., Weiss, S., Prins, B. P., van Setten, J., Haessler, J., Lyytikainen, L.-P., Li, M., Alonso, A., Soliman, E. Z., Bis, J. C., Austin, T., Chen, Y.-D. I., Psaty, B. M., Harrris, T. B., Launer, L. J., Padmanabhan, S., Dominiczak, A., Huang, P. L., Xie, Z., Ellinor, P. T., Kors, J. A., Campbell, A., Murray, A. D., Nelson, C. P., Tobin, M. D., Bork-Jensen, J., Hansen, T., Pedersen, O., Linneberg, A., Sinner, M. F., Peters, A., Waldenberger, M., Meitinger, T., Perz, S., Kolcic, I., Rudan, I., de Boer, R. A., van der Meer, P., Lin, H. J., Taylor, K. D., de Mutsert, R., Trompet, S., Jukema, J. W., Maan, A. C., Stricker, B. H. C., Rivadeneira, F., Uitterlinden, A., Volker, U., Homuth, G., Volzke, H., Felix, S. B., Mangino, M., Spector, T. D., Bots, M. L., Perez, M., Raitakari, O. T., Kahonen, M., Mononen, N., Gudnason, V., Munroe, P. B., Lubitz, S. A., van Duijn, C. M., Newton-Cheh, C. H., Hayward, C., Rosand, J., Samani, N. J., Kanters, J. K., Wilson, J. G., Kaab, S., Polasek, O., van der Harst, P., Heckbert, S. R., Rotter, J. I., Mook-Kanamori, D. O., Eijgelsheim, M., Dorr, M., Jamshidi, Y., Asselbergs, F. W., Kooperberg, C., Lehtimaki, T., Arking, D. E., Sotoodehnia, N.
    American Heart Association (AHA)
    Published 2018
    Staff View
    Publication Date:
    2018-01-12
    Publisher:
    American Heart Association (AHA)
    Print ISSN:
    1942-325X
    Electronic ISSN:
    1942-3268
    Topics:
    Medicine
    Keywords:
    Electrophysiology, Genetic, Association Studies
    Published by:
    http://www.americanheart.org/

    Latest Papers from Table of Contents or Articles in Press
  5. 5
    Staff View
    ISSN:
    1432-1440
    Keywords:
    Key words Coronary heart disease ; Genotype ; angiotensinogen ; Angiotensin-converting enzyme ; E-selectin
    Source:
    Springer Online Journal Archives 1860-2000
    Topics:
    Medicine
    Notes:
    Abstract  Previous association studies between angiotensin-converting enzyme (ACE) and angiotensinogen (AGT) polymorphisms and several cardiovascular diseases have reported variable results. Therefore we examined the association of the DNA variants of ACE and AGT with early, severe coronary heart disease (CHD). In addition, we compared the genotypes of both polymorphisms and the recently discovered polymorphism in the E-selectin gene in both patients and an unselected population. This study included 113 patients with severe CHD (50 years old or less) and up to 197 control subjects. The frequencies of the ACE I/D variants were 48% I and 52% D in the controls and 46% I and 54% D in the patients. The frequencies of the AGT-M235T polymorphism were 60.8% M and 39.2% T in controls and 49.1% M and 50.9% T in the patients. The frequencies of the S128R polymorphism of the E-selectin were 91.3% S and 8.7% R in controls and 84.5% S and 15.5% R in the patients. In our studies the DD genotype of ACE was not associated with early severe CHD. We found a correlation between the M235T molecular variant of AGT and the S128R variant of E-selectin to early severe CHD.
    Type of Medium:
    Electronic Resource
    URL:
    http://dx.doi.org/10.1007/s001090050087

    Articles: DFG German National Licenses
  6. 6
    Staff View
    ISSN:
    1433-8580
    Keywords:
    Isolated perfused heart ; Coronary H1- and H2-receptors ; Histamine ; Cimetidine ; Anaphylaxis
    Source:
    Springer Online Journal Archives 1860-2000
    Topics:
    Medicine
    Notes:
    Summary The present study characterizes effects of histamine in the presence of the H2-antagonist cimetidine on the coronary circulation of the isolated perfused spontaneously beating guinea pig heart. Infusion of histamine (2 ⋅ 10−8 mol/1–5 ⋅ 10−6 mol/l) induced a dose-dependent coronary dilation, comparable to the effect of isoproterenol and two highly selective H2-agonistic compounds, impromidine and dimaprit. In the presence of cimetidine (5 ⋅ 10−6 mol/l), however, coronary response to histamine was reversed in a manner that a dose-dependent coronary constriction occurred with coronary spasm and a flow rate approaching zero at histamine concentrations above 8 ⋅ 10−7 mol/l, whereas the dilatory effect of impromidine and dimaprit was completely antagonized. In contrast, the histamine-induced constriction in the presence of cimetidine could be nearly abolished by additional infusion of the H1-antagonistic compound mepyramine (5 ⋅ 10−5 mol/l). Is is concluded that H1- and H2-receptors are present in the coronary smooth muscle, H1-receptors mediating constriction and H2-receptors mediating coronary dilation. Speculation is provided that histamine may have hazardous effects in anaphylactic states if cimetidine is administered simultaneously, e.g., to prevent or cure peptic ulcer. Other possible clinical implications will be discussed.
    Type of Medium:
    Electronic Resource
    URL:
    http://dx.doi.org/10.1007/BF01852292

    Articles: DFG German National Licenses
  7. 7
    Staff View
    ISSN:
    1420-908X
    Source:
    Springer Online Journal Archives 1860-2000
    Topics:
    Medicine
    Notes:
    Abstract The heart is a target organ of anaphylaxis. In isolated perfused hearts, an anaphylactic reaction is characterized by arrhythmias, coronary constriction, and severe impairment of ventricular contractile force. Various mediators such as PAF, thromboxane A2 and leukotrienes, are responsible for anaphylactic coronary constriction and negative inotropic effects. The cardiac effects of anaphylactic histamine release are related to the stimulation of two antagonistic receptor types. Histamine induces atrioventricular conduction delay and constriction of the epicardial coronary vessels via H1-receptor stimulation. H2-receptors, however, mediatecoronary vasodilation and an increase in heart rate and myocardial contractility. It may therefore be concluded that administration of histamine H2-receptor antagonists is disadvantageous. During anaphylactic states, the cardiodepressive effects of the other mediators of anaphylaxis are unmasked, resulting in a sustained coronary constriction and impairment of myocardial contractility. To verify this speculation, we investigated the effects of H1- and H2-receptor antagonists on cardiovascular function of guinea pigs during systemic anaphylaxis. In guinea pigs, sensitization was produced by subcutaneous application of ovalbumin. Fourteen days after sensitization, the effects of an intravenous infusion of ovalbumin were tested in the anesthetized artificially ventilated guinea pigs. The renewed administration of the antigen induced severe cardiac dysfunction. Within a few minutes, cardiac output markedly decreased and left ventricular end-diastolic pressure increased significantly, indicating left ventricular pump failure. In the same time range, ECG recordings uniformly showed signs of acute myocardial ischemia. In addition, arrhythmias occurred in terms of an atrioventricular block. After 4 min, blood pressure rapidly declined. All animals died within 12 min. Pretreatment with the selective H1-receptor antagonist astemizol (5 mg/kg i.v.) delayed the onset of myocardial ischemia, arrhythmias and cardiac pump failure. After 10 min, however, left ventricular contractility and blood pressure steadily declined, leading to severe hypotension within 30 min. In the case of a pretreatment with astemizol (5 mg/kg i.v.) and the H2-receptor antagonist famotidine (10 mg/kg i.v.), no relevant changes of cardiovascular function were seen compared to pretreatment with astemizol alone. It is therefore concluded that endogenous histamine, via H1-receptor stimulation plays an important part during the early phase of systemic anaphylaxis, whereas mediators other than histamine are involved at a later stage of the process. Furthermore, H2-receptor-mediated effects are of minor importance in cardiovascular manifestation of anaphylaxis. Pretreatment with H2-receptor antagonists has no detrimental effects on cardiovascular function during anaphylactic reactions in guinea pigs underin vivo conditions.
    Type of Medium:
    Electronic Resource
    URL:
    http://dx.doi.org/10.1007/BF01980881

    Articles: DFG German National Licenses
  8. 8
    Staff View
    ISSN:
    1420-908X
    Source:
    Springer Online Journal Archives 1860-2000
    Topics:
    Medicine
    Notes:
    Summary In vivo anaphylaxis is associated with respiratory distress and cardiovascular failure. The present investigation was designed to further characterize respiratory and cardiac anaphylactic events. In guinea pigs, sensitization was produced by subcutaneous application of ovalbumin together with Freund's adjuvant. Fourteen days after sensitization, the effects of an intravenous infusion of ovalbumin were tested in the anesthetized artificially ventilated guinea pigs. The renewed application of the antigen induced an initial increase of left ventricular pressure which was followed by a rapid decrease 5 min after antigenic challenge. Enddiastolic left ventricular pressure increased within 3 min, thus indicating left ventricular pump failure. In the same time range, ECG recordings uniformly showed signs of acute myocardial ischemia. In addition, heart rate steadily decreased. All animals died within 15 min. Simultaneously with cardiac anaphylactic malfunction, severe arterial hypoxia and carbon dioxide retention occurred, revealing respiratory distress. Histamine is known as a potent bronchoconstrictor via histamine H1-receptor stimulation. Administration of H1-recpetor antagonists to improve respiration may therefore provide further information on the contribution of pulmonary malfunction to anaphylactic cardiovascular shock. Therefore, additional experiments were performed with sensitized guinea pigs pretreated with the histamine H1-receptor blocker mepyramine. In these experiments the antigenic challenge induced a dissociation of cardiac and respiratory manifestation of anphylaxis. Despite inhibition of hypoxia and carbon dioxide retention, left ventricular pump failure and occurrence of myocardial ischemia were delayed but not suppressed. It is concluded that histamine is an important mediator of anaphylactic respiratory distress. However, vasoactive anaphylactic mediators other than histamine are primarily involved in anaphylactic cardiac malfunction occurring during the later phase of systemic anaphylaxis.
    Type of Medium:
    Electronic Resource
    URL:
    http://dx.doi.org/10.1007/BF01986585

    Articles: DFG German National Licenses
  9. 9
    Kieback, A. G. ; Grohmann, A. ; Kalb, G. ; Baumann, G. ; Felix, S. B.
    Springer
    Published 2000
    Staff View
    ISSN:
    1435-1420
    Keywords:
    Key words Cardiac output – continuous measurement – thermodilution – heart failure – Swan-Ganz catheter – sodium nitroprusside ; Schlüsselwörter Herzzeitvolumen – kontinuierliche Messung – Thermodilution – Herzinsuffizienz – Swan-Ganz-Katheter – Nitroprussid-Natrium
    Source:
    Springer Online Journal Archives 1860-2000
    Topics:
    Medicine
    Description / Table of Contents:
    Zusammenfassung Wir untersuchten die Korrelation zweier unterschiedlicher Messverfahren zur Bestimmung des Herzzeitvolumens (HZV) bei 12 herzinsuffizienten Patienten (NYHA III–IV) während der Applikation von Nitroprussid-Natrium (NPN). Dabei sollte geprüft werden, ob beide Messverfahren vergleichbar eine Änderung des Herzzeitvolumens erfassen. Mittels eines Swan-Ganz-Katheters (Baxter 746H-8F) wurde das HZV durch die Thermodilution entsprechend dem Bolusverfahren (TDB) sowie kontinuierlich nach der „continuous cardiac output” (CCO)-Methode über ein in den Katheter integriertes thermisches Filament bestimmt. Nitroprussid-Natrium wurde in 4 steigenden Dosierungen intravenös verabreicht. Die Dosissteigerungen erfolgten nach jeweils 60 Minuten. Messungen wurden zu 11 Zeitpunkten durchgeführt (3 unter Basalbedingungen sowie jeweils 2 in 30-minütigen Abständen während jeder NPN-Dosisstufe). Die Korrelationen zu den einzelnen Messzeitpunkten wurden nach dem Spearman-Verfahren berechnet.¶   Ergebnisse: Im Vergleich des HZV (TDB) und HZV (CCO) errechneten sich zu 8 von 11 Messzeitpunkten signifikante Korrelationen (p〈0,05).¶   Schlussfolgerung: Das CCO-Verfahren ermöglicht die schnelle und zuverlässige Bestimmung des HZV auch bei einer medikamentös verursachten schnellen Veränderung der Hämodynamik.
    Notes:
    Summary We examined the correlation between two different methods to measure cardiac output in 12 patients with chronic heart failure (NYHA III–IV).¶   Using a Swan-Ganz catheter (Baxter 746H-8F) we measured cardiac output according to the thermodilution bolus method and to the continuous thermodilution method, which works automatically by delivering pulses of energy from a thermal filament on the catheter. Sodium nitroprusside was infused in four increasing doses. Every 60 minutes, the dose was increased. We performed measurements at 11 time points (3 at baseline and 8 every 30 minutes during application of sodium nitroprusside). Statistical analysis was calculated according to the Spearman formula.¶   Results: The values for cardiac output by the thermodilution bolus method and the continuous method showed significant correlation at 8 of 11 time points.¶   Conclusion: The continuous method allows fast and reliable measurement of cardiac output while pharmacologically changing hemodynamics.
    Type of Medium:
    Electronic Resource
    URL:
    http://dx.doi.org/10.1007/s003900070049

    Articles: DFG German National Licenses
  10. 10
    Kleber, F. X. ; Wensel, R. ; Felix, S. B. ; Reindl, I. ; Baumann, G.
    Springer
    Published 1996
    Staff View
    ISSN:
    1435-1803
    Keywords:
    Heart failure ; pulmonary circulation ; endothelial function ; acetylcholine ; vasodilation
    Source:
    Springer Online Journal Archives 1860-2000
    Topics:
    Medicine
    Notes:
    Abstract Elevated pulmonary vascular resistances occur to a variable degree in patients with chronic congestive heart failure (CHF). These might be caused by increased levels of endogenous vasoconstrictors, defective endothelial vasodilatory mechanisms or structural vascular abnormalities. To determine the contribution of defective endothelial mediated vasodilation, we tested 10 patients with CHF due to coronary artery disease (n=4) or dilated cardiomyopathy (n=5), and congenital corrected transposition of the great arteries (n=1) (median pulmonary artery pressure 36 mmHg, range of pulmonary vascular resistance 0.94–10.7 WE). Patients were in median functional class NYHA III, median left ventricular ejection fraction was 21%, median oxygen uptake at the anaerobic threshhold was 8.25 ml/kg/min. Flow was measured by a flow wire (0.018 inch) positioned in a pulmonary artery branch with a diameter of 3–8 mm determined by intravascular ultrasound before. Acetylcholine infusion was adjusted to 10−6, 10−5 and 10−4 molar concentrations in the pulmonary artery branch. A dose dependent increase in flow between 64 to 140% was seen in 8 out of 10 patients. We conclude: Acetylcholine mediated vasodilation is found in patients with CHF and elevated pulmonary vascular resistances.
    Type of Medium:
    Electronic Resource
    URL:
    http://dx.doi.org/10.1007/BF00788720

    Articles: DFG German National Licenses
  11. 11
    Felix, S. B. ; Baumann, G. ; Helmus, S. ; Sattelberger, U.
    Springer
    Published 1988
    Staff View
    ISSN:
    1435-1803
    Keywords:
    cardiac anaphylaxis ; anaphylactic mediators ; cardiac histaminergic H1-and H2-receptors ; coronary spasm
    Source:
    Springer Online Journal Archives 1860-2000
    Topics:
    Medicine
    Notes:
    Summary Histamine is known to act as a direct stimulator. In the heart, two types of histamine receptors are present: H1- and H2-receptors. H2-receptors cause an increase in heart rate and contractility as well as coronary vasodilatation, whereas H1-receptors mediate chronotropic effects and coronary vasoconstriction. During anaphylactic states, histamine is released from cardiac tissue where it is stored in large amounts. The present study was designed to ascertain the role of cardiac histamine release during cardiac anaphylaxis. In guinea pigs, sensitization was produced by intraperitoneal administration of ovalbumin (O). 14 days after sensitization, the effects of an intracoronary infusion of O (1.1×10−8 moles/min) were tested in the isolated perfused heart preparation. The response of the sensitized hearts to O was characterized by a rapid increase in contractile force (dp/dtmax 120% above baseline after 30 s), followed by a decrease reaching a minimum of 30% below bascline after 10 min. Over the same time range, the heart rate first increased (+24%), then decreased, concurrent with the appearance of arrhythmias, before reaching baseline level. Coronary flow decreased (−40% after 1 min) and finally stabilized at a new steady state (−20% below baseline). It is concluded that histamine might be an important mediator of these effects, since in the presence of H2-receptor blockade with cimetidine 96.2×10−7 moles/min), the positive inotropic and chronotropic effects were completely antagonized. Furthermore, a decrease in heart rate and contractility occurred (−25% and −50% after 2 min, respectively). Finally, coronary constriction was intensified and resulted in coronary spasm with flow rates approaching zero after 1 min. On the other hand, additional H1-receptor blockade with dimetinden (2.5×10−9 moles/min) did not antagonize the development of coronary spasm significantly and did not influence the decrease in contractility and the occurrence of bradycardia. The results obtained therefore suggest that besides histamine, other mediators are involved in the development of cardiac anaphylaxis. The cardiodepressant actions of these anaphylactic mediators were revealed by the H2-receptor blockade.
    Type of Medium:
    Electronic Resource
    URL:
    http://dx.doi.org/10.1007/BF01906682

    Articles: DFG German National Licenses
  12. 12
    Felix, S. B. ; Baumann, G. ; Raschke, P. ; Maus, C. ; Berdel, W. E.
    Springer
    Published 1990
    Staff View
    ISSN:
    1435-1803
    Keywords:
    platelet activating factor ; cardiovascularshock ; ventricular contractilefailure ; coronaryvasospasm ; respiratorydistress
    Source:
    Springer Online Journal Archives 1860-2000
    Topics:
    Medicine
    Notes:
    Summary The platelet activating factor (PAF), a low molecular phospholipid, plays an important role in inflammation, anaphylaxis, and shock state development. In the isolated perfused guinea pig heart, PAF induces a decrease in coronary flow and cardiac contractility and atrioventricular conduction disturbances. Furthermore, PAF mediates a powerful bronchoconstrictory action causing a severe impairment in respiratory function. In the present study an attempt was made to separate cardiac from respiratory events during PAF-induced shock in vivo. PAF was injected intravenously (0.1–10 μg/kg) into anesthetized guinea pigs ventilated with room air or 100% oxygen. Administration of 10 μg/kg PAF was uniformly lethal: already within 2 min, cardiac output decreased by 60% and end-diastolic left ventricular pressure increased markedly indicating cardiac failure. ECG recordings showed signs of acute myocardial ischemia. Arrhythmias occurred in terms of atrioventricular conduction delay. Blood pressure initially increased, then declined continuously to below baseline within 10 min. All animals died within 25 min. Ventilation with room air was paralleled by development of severe hypoxia. However, under ventilation with 100% oxygen a dissociation between PAF-mediated cardiac and respiratory effects occurred. It is concluded that the PAF-induced shock is primarily based on direct cardiac damage. Furthermore, the ECG signs of ischemia are most likely due to coronary spasms.
    Type of Medium:
    Electronic Resource
    URL:
    http://dx.doi.org/10.1007/BF01907110

    Articles: DFG German National Licenses
  13. 13
    Staff View
    ISSN:
    1435-1420
    Keywords:
    Key words Dilative cardiopulmonary – autoantibodies – immunadsorption ; Schlüsselwörter Dilatative Kardiomyopathie – Autoantikörper – Immunadsorption
    Source:
    Springer Online Journal Archives 1860-2000
    Topics:
    Medicine
    Description / Table of Contents:
    Zusammenfassung Die Prognose von Patienten mit dilatativer Kardiomyopathie (DCM) ist selbst unter optimaler medikamentöser Therapie immer noch ernst, eine kausale Therapieoption besteht derzeit nicht. Bei Hinweisen auf Störungen des Immunsystems mit Bildung von Autoantikörpern, z. B. gegen β 1-adrenerge oder muskarinerge Rezeptoren in der Pathogenese der DCM stößt die Aufklärung einer möglichen funktionellen Bedeutung dieser Autoantikörper auf verstärktes Interesse. Neben der Rolle von Autoantikörpern als Marker eines Autoimmungeschehens werden als pathogenetische Mechanismen eine direkte Toxizität sowie eine negative Beeinflussung der Myokardkontraktilität und des Energiestoffwechsels diskutiert. Die Entfernung von Autoantikörpern mittels Immunadsorptionstherapie bei DCM gibt Hinweise auf deren funktionelle Bedeutung bei diesem Krankheitsbild. Das Prinzip dieser Therapieform beruht auf der Bindung zirkulierender Antikörper an Sepharosesäulen, an die polyklonale Antikörper gegen humanes Immunglobulin gebunden sind. In einer Pilotstudie konnte bei DCM Patienten gezeigt werden, daß es unter Immunadsorption parallel zur Abnahme der Immunglobulinspiegel und zu einer signifikanten hämodynamischen und klinischen Verbesserung kommt. Diese Ergebnisse sind als Hinweise zu werten, daß Autoantikörper eine aktive Rolle bei DCM spielen und mit ihrer Entfernung durch Immunadsorption künftig möglicherweise ein vielversprechendes Therapiekonzept zur Verfügung steht.
    Notes:
    Summary For patients with dilative cardiomyopathy (DCM), the prognosis is highly unfavorable, even under conditions of optimal medication. At present, there is no option for causal therapy. Since there is increasing evidence that modifications of the immune system accompanied by the production of autoantibodies, e.g., against β 1 ad-renergic or muscarinergic receptors, are involved in the pathogenesis of DCM, the elucidation of the possible functional significance of these autoantibodies has attracted increasing interest. In addition to the role of autoantibodies as markers for an autoimmune process, discussion of the possible pathogenetic mechanisms has centered on direct toxicity as well as on negative influencing of myocardial contractility and energy metabolism. The effects gained through removal of autoantibodies by immunoadsorption therapy for DCM patients sheds light on the functional importance of autoantibodies in this syndrome. The principle of this form of therapy is based on the binding of circulating antibodies to sepharose columns, to which polyclonal antibodies against human immunoglobulin are linked. A pilot study conducted among DCM patients disclosed that immunadsorption took place in simultaneous conjunction with a reduction in the immunoglobulin level and with significant hemodynamic and clinical improvement. These results may be interpreted as indicating that autoantibodies play an active role in DCM and that their removal by immunadsorption possibly represents a highly promising future therapeutic concept.
    Type of Medium:
    Electronic Resource
    URL:
    http://dx.doi.org/10.1007/s003900050314

    Articles: DFG German National Licenses