Alcohol and heart disease:
Gespeichert in:
Format: | Buch |
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Sprache: | English |
Veröffentlicht: |
London [u.a.]
Taylor & Francis
2002
|
Ausgabe: | 1. publ. |
Schlagworte: | |
Online-Zugang: | Inhaltsverzeichnis |
Beschreibung: | XVII, 261 S. Ill., graph. Darst. |
ISBN: | 0415273471 |
Internformat
MARC
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245 | 1 | 0 | |a Alcohol and heart disease |c ed. by Ronald R. Watson ... |
250 | |a 1. publ. | ||
264 | 1 | |a London [u.a.] |b Taylor & Francis |c 2002 | |
300 | |a XVII, 261 S. |b Ill., graph. Darst. | ||
336 | |b txt |2 rdacontent | ||
337 | |b n |2 rdamedia | ||
338 | |b nc |2 rdacarrier | ||
650 | 7 | |a Alcohol |2 gtt | |
650 | 7 | |a Alcoholgebruik |2 gtt | |
650 | 7 | |a Hart- en vaatziekten |2 gtt | |
650 | 4 | |a Alcohol Drinking |x adverse effects | |
650 | 4 | |a Alcohol |x Physiological effect | |
650 | 4 | |a Heart Diseases |x etiology | |
650 | 4 | |a Heart |x Diseases | |
650 | 4 | |a Heart |x drug effects | |
650 | 0 | 7 | |a Alkoholismus |0 (DE-588)4001220-7 |2 gnd |9 rswk-swf |
650 | 0 | 7 | |a Herzkrankheit |0 (DE-588)4024663-2 |2 gnd |9 rswk-swf |
689 | 0 | 0 | |a Alkoholismus |0 (DE-588)4001220-7 |D s |
689 | 0 | 1 | |a Herzkrankheit |0 (DE-588)4024663-2 |D s |
689 | 0 | |5 DE-604 | |
700 | 1 | |a Watson, Ronald R. |e Sonstige |4 oth | |
856 | 4 | 2 | |m HBZ Datenaustausch |q application/pdf |u http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&local_base=BVB01&doc_number=010449539&sequence=000002&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA |3 Inhaltsverzeichnis |
999 | |a oai:aleph.bib-bvb.de:BVB01-010449539 |
Datensatz im Suchindex
_version_ | 1804130171541782528 |
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adam_text | Contents
List of tables vii
List of figures viii
List of contributors x i i
Preface xv
The editors xvii
1 Alcohol and cardiovascular disease: large population studies 1
YOULIAN L1AO, DANIEL McGEE AND RICHARD CCX1PER
2 The alcoholic cardiomyopathies: genuine and pseudo 15
JULES CONSTANT
3 Wine and lifestyle: role in cardiovascular disease and premature death 21
S. GOYA WANNAMETHEE AND A. GERALD SHAPER
4 Effects of gender on alcohol s heart dysfunction 28
MARIANN R. PIANO
5 Alcohol and cardiac medications: interactions 48
SIMON K.K. CHEUNG AND TIMOTHY ]. REGAN
6 Alcohol abuse and hemorrhagic stroke 58
SEPPO JUVELA
7 Alcohol abuse and ischemic stroke 72
MATTI II1LLBOM
8 Alcohol consumption and the risk of stroke: the role of tobacco? 83
JAANA M. LEPPALA
9 Alcohol, vascular cells and hemodynamic forces 91
EILEEN M. REDMOND AND PAL L A. CAHILL
10 Moderate alcohol exposure protects cardiac myocytes from
ischemia reperfusion injury 104
MARY O. GRAY AND DARIA MOCHLY ROSEN
j
vi Contents
11 Alcohol and smoking: synergism in heart disease? 114
JIN ZHANG AND RONALD WATSON
12 Oxidative stress, cell damage and its possible prevention by
alpha tocopherol: cardiovascular and other cells 120
VICTOR R. PREEDY AND HELMUT SEITZ
13 Alcohol and platelet function 146
ADAM K. MYERS, KABITA DAS AND QING HUI ZHANG
14 Fatty acid ethyl esters: role in alcohol cardiotoxicity 157
LEO HSU, MARY E. BECKEMEIER AND PURAN S. BORA
15 Alcohol and apolipoproteins 169
MARK DEEG
16 Alcohol and polyunsaturated fatty acid metabolism in the
cardiovascular system 180
JOHN W. KARANIAN AND NORMAN SALEM
17 Alcohol and heart muscle proteins: with special reference
to measurement of protein synthesis in vivo 197
V.R. PREEDY, M.J. DUNN, R. HUNTER, D. MANTLE, S. WORRALL, P.J. RICHARDSON
18 Cocaethylene: immunologic, hepatic and cardiac effects 212
ALBERT 13. ARVALLO AND RONALD R. WATSON
19 Cardiotoxicity of cocaine use by humans and rodents:
synergisms of concomitant cocaine plus alcohol exposure 218
DAVID SOLKOFF AND RONALD R. WATSON
20 Mechanisms of cocaine cardiotoxicity 228
DAVID SOLKOFF AND RONALD R. WATSON
21 Alcohol and reflex regulation of the cardiovascular system 235
ABDEL A. ABDEL RAHMAN
22 Alcohol s accentuation of AIDS nutritional and immune damage,
a cofactor in heart disease 250
R. TOM AS SEI ULVEHA AND RONALD R. WATSON
Index 259
Tables
1.1 Large population studies examining alcohol intake and cardiovascular
disease 2
3.1 Age adjusted rates and fully adjusted ( + ) relative risks for major CHD
events and all cause mortality for all men who drink and by type of drink in
6860 men. Occasional drinkers are used as the reference group within each
alcohol type category [20] 22
3.2 Type of alcoholic drink and risk of major CHD events and of all cause and
cardiovascular and non cardiovascular mortality in occasional or regular
drinkers (N = 6860 men). Beer drinkers used as the reference group [20] 23
3.3 Personal, lifestyle and biological characteristics at screening by
different types of drinking [20] 24
4.1 Summary of clinical studies of AHMD in women 30
4 2 Clinical characteristics of men and women with AHMD 34
4.3 Echocardiographic parameters in men and women with AHMD
compared to healthy controls 34
4.4 Acute effects of ethanol in male and female papillary muscles 38
4 5 Echocardiographic parameters in male and female control
and ethanol fed animals 39
4.6 Comparison of male and female body weight and Lieber
DeCarli diet consumption 43
7.1 Previously published and new case histories illustrating several
different mechanisms that could link alcohol abuse to an increased
risk of ischemic brain infarct 7 3
12.1 Reactive oxygen species 121
12.2 Cardiac muscle protein synthesis in vehicle injected and
n tocopherol supplemented rats injected with either saline or ethanol 1 M
17.1 Rate of protein synthesis in various fractions of the rat heart 202
17.2 The chronic effect of amlodipine treatment and alcohol on LV
total and protein fraction synthesis rates 204
17.3 The acute effect of alcohol and propranolol on protein synthesis rates 206
18.1 Symptoms reported by cocaine and alcohol concomitantly using patients 213
Figures
4 1 Survival curves of cardiac deaths in male patients with alcoholic
dilated cardiomyopathy (DCM). Solid line indicates patients with
alcoholic DCM and alcohol abstinence, large dashed line indicates patients
with alcoholic DCM without abstinence and small dashed line indicates
idiopathic DCM. Used with permission from Fauchier eta!. European
Heart J. 2000; 21: 306 314 37
4 2 Representative echocardiograms from control and ethanol fed female rat 40
4 3 Representative echocardiograms from control and ethanol fed male rat 40
4 4 Lieber DeCarli diet consumption for two different female cohorts 42
4 5 Lieber DeCarli diet consumption for two different male cohorts 42
9.1 Hemodynamic forces directly influence vascular cell biology. Fluid shear
stress and/or pressure (cyclic stretch) can modulate the production of
vasoactive mediators such as nitric oxide (NO), prostacyclin (PGI2) and
endothelin (ET) from the endothelium, which in turn influence smooth
muscle cell structure and function 92
9.2 Shear stress stimulates nitric oxide (NO) production by endothelial
cells. By a mechanism thought to involve a pertussis toxin sensitive
G protein (G) and a K+ channel, shear stress stimulates nitric
oxide synthase (NOS) activity in endothelial cells. The resulting NO
can stimulate soluble guanylyl cyclase (GC) in adjacent smooth muscle
cells, leading to increased levels of cGMP and subsequent vasorelaxation
and inhibition of proliferation 93
9.3 The fihrinolytic plasminogen activator system. The inactive proenzyme
plasminogen is converted to the proteolytic enzyme plasmin by
urokinase type plasminogen activator (uPA) or tissue type plasminogen
activator (tPA). The system is regulated by a series of plasminogen
activator inhibitors (PA1), of which PAI 1 is believed to be the most
physiologically important. (* modulated by hemodynamic forces) 96
9.4 The effect of ethanol on pulse pressure induced smooth muscle cell
migration. Human smooth muscle cells (HuSMC) in perfused transcapillary
cultures were exposed to low or high pulsatile flow conditions, in the absence
or presence of ethanol (20 mM). Cells were then harvested and their
migration assessed by Transwell assay. Ethanol inhibited the flow induced
Figures ix
increase in HuSMC migration. (Reproduced by permission of Academic
Press from Hendrickson etal. (1999), [46] 97
9.5 The effect of ethanol on smooth muscle cell proliferation. Ethanol
(24 h exposure) dose dependently inhibits (a) SMC 3H Thymidine
incorporation, and (b) MAPK activity, determined by measuring
phosphorylated ERK 1 and ERK 2. (Reproduced by permission of
Elsevier Science from Hendrickson etal. (1998), [59]) 99
14 1 Fatty acids (FA) are found linked to fatty acid binding proteins (FABP)
and are therefore prevented from entering the mitochondria.
However, FA can react with ethanol (ETOH) to produce fatty
acid ethyl esters (FAEE) via fatty acid ethyl ester synthase.
Once inside the mitochondria, FAEE can cause direct damage, but
also their hydrolysis to fatty acids can lead to uncoupling of oxidative
phosphorylation. 159
14.2 (A) Histopathological analyses of control rat myocardium with 30 (ll
phosphate buffered saline (PBS)+ 0.01% dimethylsulfoxide. Sections
stained with Mason trichrome. No cell damage is observed (original
magnification X300). (B) Histopathological analyses of rat myocardium
injected with 30(xl of 50 (iM FAEE. Sections stained with Mason
trichrome. The significant cell damage was observed after 30 days.
The cells were enlarged and irregular in shape (original magnification
X300) 160
16.1 The structures of some essential and non essential fatty acids
commonly found in mammalian cells 181
16.2 Metabolism of the n 3 and n 6 families of essential fatty acids 184
16.3 Schematic of arachidonic acid (AA) mobilization from membrane
phospholipids and metabolism via cyclooxygenase (CO) enzymes to
form prostaglandins (PG) and lipoxygenase (LO) enzymes to form
leukotrienes (LT) 187
17.1 Changes in precursor specific radioactivities in different methods
for measuring protein synthesis m vivo. The three methods of measuring
protein synthesis are (top) pulse injection of a tracer amount of amino acid,
(middle) constant infusion of a tracer amino acids and (bottom) injection
of a flooding dose of amino acid. Phase (a) and (b) are arbitrary assigned
periods of each method. For a fuller explanation see text.
Adapted from works of P.]. Garlick 200
17.2 Cardiac protein synthesis in response to acute alcohol. Rats were
injected i.p. with 0.15 mol/1 saline (NaCl); or ethanol
(75 mmol/kg body weight, i.p). All data are means+ SEM of 6 8
observations. From [73] 201
17.3 Cardiac protein synthesis, ATP and plasma troponin T in rats
treated with alcohol. Data are mean±SEM of 4 9 observations in
each group. Ethanol (75 mmol/kg body weight; i.p) was given with or
without cyanamide pretreatment (0.5 mmol/kg body weight; i.p.).
Rats were killed 2.5 hours after ethanol dosing, p values over histograms
x Figures
pertain to differences from saline plus saline controls. (#) Difference
in ks between saline plus ethanol and cyanamide plus ethanol,
p 0.01. Data from various studies of the authors and [73] 203
21.1 Bar graphs showing that ethanol (0.1,0.5 and 1.0 g/kg) produces graded
decreases in regression coefficient (baroreflex slopes; beats/min/mmHg) in
SO but not in aortic barodenervated (ABD) rats. Values are
expressed as mean+S.E.M.; *p 0.05 compared to base line value.
Number of rats in each group is shown in parentheses; with permission [28] 237
21.2 Baroreflex curves relating decreases in HR to PE induced elevations in
BP obtained in conscious freely moving ABD or SO rats before and after
i.v. administration of an anesthetizing dose of pentobarbital (30mg/kg).
In either group, pentobarbital produced a downward shift in the curve as
evident by a reduction in the regression coefficient (baroreflex slope; inset).
Values are expressed as mean±S.E.M; *p 0.05 compared to
prepentobarbital values (ANOVA). Number of rats in each group is
shown in parentheses; with permission [28] 237
21.3 The effect of ethanol (1 g/kg) on baroreflex curves relating changes
in HR to rises in BP evoked by PE in conscious unrestrained CBD and
SO rats. Note that ethanol, but not saline, causes a significant (*f 0.05,
ANOVA) downward shift in the baroreflex curves in both groups of rats as
compared to pre ethanol values. Values shown are the regression
coefficients of baroreflex curves in beats per minute per millimeter
of mercury; the number of rats in each group is shown in parentheses;
with permission [29] 238
21.4 Bar graphs showing the capacity of ethanol (1 g/kg) to produce
a significant reduction in the regression coefficient (baroreflex slopes; beats/
min/mmHg) of PE baroreflex curves. Values are expressed as mean±S.E.M.;
# and *p 0.05 compared to base line and after saline values, respectively.
CBD, carotid barodenervation. The number of rats in each group is shown
in parentheses; with permission [29] 239
21.5 Effect of ethanol on depressor and bradycardic responses elicited by
unilateral microinjection of graded doses of NMDA into the NTS of
urethane anesthetized rats. Ethanol was administered either into the NTS
(10|0.g, left panels) or systematically (1 g/kg, right panels). The values
are expressed as the mean±S.E.M. *p 0.05 (ANOVA) compared with
corresponding pre ethanol and after vehicle (ACSF or saline) values,
respectively. The number of rats in each group is shown in parentheses;
with permission [30] 242
21.6 Bar graphs showing the depressant effects of ethanol (i.v., 1 g/kg;
intra NTS, 10(Xg) or respective vehicle (saline, i.v.; ACSF, intra NTS)
treatment on hemodynamic responses elicited by NMDA (25 pmol) and
non NMDA (kainate, 3 pmol and AMPA, 1 pmol (expressed as the percent
reduction in these responses compared with pretreatment responses. The
values are the means ± S.E.M. * and #p 0.05 (ANOVA) compared with
Figures xi
corresponding vehicle and NMDA (after ethanol) values, respectively;
with permission [30] 244
21.7 Bar graphs showing the depressant effect of ethanol on BRS
(A/HR/AMAP) tested by i.v. PE (16 M g/lcg) in urethane anesthetized rats.
Ethanol was administered either unilaterally into the NTS (10|J.g)
or systemically (0.1 or l.Og/kg). The values are expressed as the
mean±S.E.M. * and #p 0.05 (ANOVA) compared with
corresponding pre ethanol and after intra NTS ethanol values,
respectively; with permission [30] 245
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id | DE-604.BV017332785 |
illustrated | Illustrated |
indexdate | 2024-07-09T19:16:48Z |
institution | BVB |
isbn | 0415273471 |
language | English |
oai_aleph_id | oai:aleph.bib-bvb.de:BVB01-010449539 |
oclc_num | 48534051 |
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owner_facet | DE-355 DE-BY-UBR DE-29 |
physical | XVII, 261 S. Ill., graph. Darst. |
publishDate | 2002 |
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publisher | Taylor & Francis |
record_format | marc |
spelling | Alcohol and heart disease ed. by Ronald R. Watson ... 1. publ. London [u.a.] Taylor & Francis 2002 XVII, 261 S. Ill., graph. Darst. txt rdacontent n rdamedia nc rdacarrier Alcohol gtt Alcoholgebruik gtt Hart- en vaatziekten gtt Alcohol Drinking adverse effects Alcohol Physiological effect Heart Diseases etiology Heart Diseases Heart drug effects Alkoholismus (DE-588)4001220-7 gnd rswk-swf Herzkrankheit (DE-588)4024663-2 gnd rswk-swf Alkoholismus (DE-588)4001220-7 s Herzkrankheit (DE-588)4024663-2 s DE-604 Watson, Ronald R. Sonstige oth HBZ Datenaustausch application/pdf http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&local_base=BVB01&doc_number=010449539&sequence=000002&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA Inhaltsverzeichnis |
spellingShingle | Alcohol and heart disease Alcohol gtt Alcoholgebruik gtt Hart- en vaatziekten gtt Alcohol Drinking adverse effects Alcohol Physiological effect Heart Diseases etiology Heart Diseases Heart drug effects Alkoholismus (DE-588)4001220-7 gnd Herzkrankheit (DE-588)4024663-2 gnd |
subject_GND | (DE-588)4001220-7 (DE-588)4024663-2 |
title | Alcohol and heart disease |
title_auth | Alcohol and heart disease |
title_exact_search | Alcohol and heart disease |
title_full | Alcohol and heart disease ed. by Ronald R. Watson ... |
title_fullStr | Alcohol and heart disease ed. by Ronald R. Watson ... |
title_full_unstemmed | Alcohol and heart disease ed. by Ronald R. Watson ... |
title_short | Alcohol and heart disease |
title_sort | alcohol and heart disease |
topic | Alcohol gtt Alcoholgebruik gtt Hart- en vaatziekten gtt Alcohol Drinking adverse effects Alcohol Physiological effect Heart Diseases etiology Heart Diseases Heart drug effects Alkoholismus (DE-588)4001220-7 gnd Herzkrankheit (DE-588)4024663-2 gnd |
topic_facet | Alcohol Alcoholgebruik Hart- en vaatziekten Alcohol Drinking adverse effects Alcohol Physiological effect Heart Diseases etiology Heart Diseases Heart drug effects Alkoholismus Herzkrankheit |
url | http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&local_base=BVB01&doc_number=010449539&sequence=000002&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA |
work_keys_str_mv | AT watsonronaldr alcoholandheartdisease |