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Adrenergic Mechanisms in Myocardial Ischemia (Paperback, Softcover reprint of the original 1st ed. 1991)
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Discovery Miles 16 410
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Adrenergic Mechanisms in Myocardial Ischemia (Paperback, Softcover reprint of the original 1st ed. 1991)
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Stress-induced myocardial ischemia is a frequent manifestation of
coronary heart disease, and sympathetic activation is an important
precipitating and aggravating factor in such stress- induced
ischemia. However, the complex interplay between the sympathetic
initiation of myocardial ischemia, ischemia-induced alterations in
sympathetic neurotransmission, as well as changes in adrenoceptor
density and post-receptor signal transduction that can occur during
ischemia remains incompletely understood. Not only the activation
of myocardial fJ- adrenoceptors, but also the activation of
coronary IX-adrenoceptors can contribute to myocar- dial ischemia.
However, the role of fJ-adrenoceptor-mediated increases in
contractility relative to heart rate in the initiation of ischemia
is not clear, and the significance of IX-adrenoceptor- mediated
changes in coronary vasomotor tone, as well as the responsible
IX-adrenoceptor subtypes are highly controversial. Malignant
arrhythmias may be triggered by both IX- and fJ-adrenergic
mechanisms. Current research in this field is focussed not only on
the underlying physiological and pathophysiological mechanisms, but
also on clinical treatment strategies, e. g. , by fJ-blockade,
IX-blockade, bradycardic agents and calcium antagonists. Recent
findings were presented and future research directions discussed
during the 61" International Titisee Conference, held at the
Schwarzwald-Hotel, Titisee, March 29-31, 1990 under the sponsorship
of the Boehringer Ingelheim Foundation. Dr. Hasso Schroeder and Dr.
Hermann Frohlich deserve special thanks for their generous support
and pleasant organization of the meeting. The publication of the
proceedings has been made possible by grants from Astra Chemicals,
Bayer, ICI, Dr. Karl Thomae, and Upjohn.
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