Verlag: Perimed Fachbuch Verlag, Erlangen, 1982
Anbieter: Antiquariat am Soonwald, Sponheim, Deutschland
ISBN 3-88429-043-6 143 S 24,1x17cm, OPpd, Tabellen und Abbildungen im Text, leichte Gebrauchsspuren.
Sprache: Deutsch
Verlag: perimed Fachbuch-Verlagsgesellschaft Erlangen, 1982
ISBN 10: 3884290436 ISBN 13: 9783884290439
Anbieter: Antiquariat Armebooks, Frankfurt am Main, Deutschland
perfect. Zustand: Gut. Seiten; Peri med 6 - 1. Auf. 1982 : W. Kupper - tb - 9-27-2-L2 5A-R7T5-P0IA Sprache: Deutsch Gewicht in Gramm: 500.
Sprache: Deutsch
Verlag: perimed Fachbuch-Verlagsgesellschaft Erlangen,, 1982
Anbieter: Clerc Fremin, Steingaden, Deutschland
Softcover Gut. 142 S / 310 gr / Sprache: Deutsch Gewicht in Gramm: 250.
Sprache: Deutsch
Verlag: Erlangen, perimed fachbuch Verlagsgesellschaft, 1982
ISBN 10: 3884290436 ISBN 13: 9783884290439
Anbieter: Antiquariat Liber Antiqua, Krems an der Donau, Österreich
Abbildungen, Tabellen, 143 Seiten ISBN 3884290436, ISBN13: 9783884290439, 1982 (Copyright), Softcover, abgegriffen, verschmutzt, fleckig, Kanten und Ecken bestossen, schiefgelesen, Seiten leicht gebräunt, wellig, mittlerer und eher guter Zustand 9783884290439 Sprache: Deutsch Aus der Reihe "Koronar Bibliothek Sandoz",.
Verlag: perimed Fachbuch-Verlagsgesellschaft, 1982
Anbieter: Antiquariat Wortschatz, Markt Hartmannsdorf, Österreich
Softcover/Taschenbuch. Zustand: Gut. zahlreiche (illustrator). kA. Auflage. Anzahl Bände: 1 - Bd.Nr.: kA - Sprache: de - Einband: Paperback - Gewicht: 292 - Illust.: zahlreiche - Zustand: Gut -.
Anbieter: Revaluation Books, Exeter, Vereinigtes Königreich
EUR 147,37
Anzahl: 2 verfügbar
In den WarenkorbPaperback. Zustand: Brand New. 144 pages. 9.25x6.10x0.33 inches. In Stock.
Sprache: Englisch
Verlag: Kluwer Academic Publishers, 1984
ISBN 10: 0898386462 ISBN 13: 9780898386462
Anbieter: Kennys Bookstore, Olney, MD, USA
Zustand: New. Editor(s): Kupper, W.; Bleifeld, Walter; MacAlpin, R.N. Series: Developments in Cardiovascular Medicine. Num Pages: 130 pages, 17 black & white illustrations, biography. BIC Classification: MJD. Category: (P) Professional & Vocational; (UP) Postgraduate, Research & Scholarly. Dimension: 234 x 156 x 9. Weight in Grams: 870. . 1984. Hardback. . . . . Books ship from the US and Ireland.
Anbieter: moluna, Greven, Deutschland
EUR 124,02
Anzahl: Mehr als 20 verfügbar
In den WarenkorbGebunden. Zustand: New. 1. Introduction.- 2. Relation of coronary arterial spasm to sites of organic stenosis.- 3. The concept of dynamic coronary stenoses.- 4. Contribution of dynamic vascular wall thickening to luminal narrowing during coronary arterial vasomotion.- 5. Alteratio.
Anbieter: AHA-BUCH GmbH, Einbeck, Deutschland
Taschenbuch. Zustand: Neu. Druck auf Anfrage Neuware - Printed after ordering - W. KUPPER Coronary artery vasoconstriction is not only the mechanism responsible for Prinzmetal's variant angina, but may also be involved in stable angina pectoris and myocardial infarction. However, the underlying patho-physiological mecha nisms and the importance of coronary vasoconstriction in these syndromes is still largely unknown. Several hypotheses have been proposed. Sympathetic nervous activity plays a key role in the regulation of coronary blood flow, but mechanical or humoral constrictive factors may be active as well. a-adrenergic tone Adrenergic nerve fibers accompany coronary vessels of any size. The stimulation of cardiac sympathetic nerves causes an increase in coronary blood flow. If, however, chronotropic and inotropic effects of adrenergic stimulation are sup pressed pharmacologically by beta-adrenoceptor blockade, a reduction in flow is observed. Thus, the primary effect of sympathetic stimulation on the coronary arteries is the alpha-adrenergic mediated vasoconstriction. Functionally inner vated alpha-adrenoceptors have been documented both in large coronary con ductance arteries and in the small resistance vessels. Animal studies and a human study have documented that a permanent constrictor tone is present on the coronary circulation both at rest and during exercise; this condition could be prevented with alpha-adrenoceptor blockade or was absent after heart transplan tation. Therefore, alpha-adrenoceptor mediated coronary constriction is an at tractive hypothesis as a possible pathophysiological mechanism of inappropriate coronary vasoconstriction and cororiary vasospasm.
Anbieter: AHA-BUCH GmbH, Einbeck, Deutschland
Buch. Zustand: Neu. Neuware - W. KUPPER Coronary artery vasoconstriction is not only the mechanism responsible for Prinzmetal's variant angina, but may also be involved in stable angina pectoris and myocardial infarction. However, the underlying patho-physiological mecha nisms and the importance of coronary vasoconstriction in these syndromes is still largely unknown. Several hypotheses have been proposed. Sympathetic nervous activity plays a key role in the regulation of coronary blood flow, but mechanical or humoral constrictive factors may be active as well. a-adrenergic tone Adrenergic nerve fibers accompany coronary vessels of any size. The stimulation of cardiac sympathetic nerves causes an increase in coronary blood flow. If, however, chronotropic and inotropic effects of adrenergic stimulation are sup pressed pharmacologically by beta-adrenoceptor blockade, a reduction in flow is observed. Thus, the primary effect of sympathetic stimulation on the coronary arteries is the alpha-adrenergic mediated vasoconstriction. Functionally inner vated alpha-adrenoceptors have been documented both in large coronary con ductance arteries and in the small resistance vessels. Animal studies and a human study have documented that a permanent constrictor tone is present on the coronary circulation both at rest and during exercise; this condition could be prevented with alpha-adrenoceptor blockade or was absent after heart transplan tation. Therefore, alpha-adrenoceptor mediated coronary constriction is an at tractive hypothesis as a possible pathophysiological mechanism of inappropriate coronary vasoconstriction and cororiary vasospasm.