Linked Life Data

16387787

Source:http://linkedlifedata.com/resource/pubmed/id/16387787

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2006-5-11
pubmed:abstractText
Enhanced cardiac beta(2)-adrenoceptor (beta(2)-AR) responsiveness can increase susceptibility to ventricular fibrillation (VF). Exercise training can decrease cardiac sympathetic activity and could, thereby, reduce beta(2)-AR responsiveness and decrease the risk for VF. Therefore, dogs with healed myocardial infarctions were subjected to 2 min of coronary occlusion during the last minute of a submaximal exercise test; VF was observed in 20 susceptible, but not in 13 resistant, dogs. The dogs were then subjected to a 10-wk exercise-training program (n = 9 susceptible and 8 resistant) or an equivalent sedentary period (n = 11 susceptible and 5 resistant). Before training, the beta(2)-AR antagonist ICI-118551 (0.2 mg/kg) significantly reduced the peak contractile (by echocardiography) response to isoproterenol more in the susceptible than in the resistant dogs: -45.5 +/- 6.5 vs. -19.2 +/- 6.3%. After training, the susceptible and resistant dogs exhibited similar responses to the beta(2)-AR antagonist: -12.1 +/- 5.7 and -16.2 +/- 6.4%, respectively. In contrast, ICI-118551 provoked even greater reductions in the isoproterenol response in the sedentary susceptible dogs: -62.3 +/- 4.6%. The beta(2)-AR agonist zinterol (1 microM) elicited significantly smaller increases in isotonic shortening in ventricular myocytes from susceptible dogs after training (n = 8, +7.2 +/- 4.8%) than in those from sedentary dogs (n = 7, +42.8 +/- 5.8%), a response similar to that of the resistant dogs: +3.0 +/- 1.4% (n = 6) and +3.2 +/- 1.8% (n = 5) for trained and sedentary, respectively. After training, VF could no longer be induced in the susceptible dogs, whereas four sedentary susceptible dogs died during the 10-wk control period and VF could still be induced in the remaining seven animals. Thus exercise training can restore cardiac beta-AR balance (by reducing beta(2)-AR responsiveness) and could, thereby, prevent VF.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0363-6135
pubmed:author
pubmed:issnType
Print
pubmed:volume
290
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
H2590-9
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:16387787-Adrenergic beta-Agonists, pubmed-meshheading:16387787-Adrenergic beta-Antagonists, pubmed-meshheading:16387787-Animals, pubmed-meshheading:16387787-Citrate (si)-Synthase, pubmed-meshheading:16387787-Death, Sudden, pubmed-meshheading:16387787-Dogs, pubmed-meshheading:16387787-Electrocardiography, pubmed-meshheading:16387787-Ethanolamines, pubmed-meshheading:16387787-Heart Rate, pubmed-meshheading:16387787-Isoproterenol, pubmed-meshheading:16387787-Myocardial Contraction, pubmed-meshheading:16387787-Myocardial Ischemia, pubmed-meshheading:16387787-Myocytes, Cardiac, pubmed-meshheading:16387787-Physical Conditioning, Animal, pubmed-meshheading:16387787-Physical Endurance, pubmed-meshheading:16387787-Receptors, Adrenergic, beta-2, pubmed-meshheading:16387787-Ventricular Fibrillation
pubmed:year
2006
pubmed:articleTitle
Endurance exercise training attenuates cardiac beta2-adrenoceptor responsiveness and prevents ventricular fibrillation in animals susceptible to sudden death.
pubmed:affiliation
Department of Physiology and Cell Biology, The Ohio State University, 1645 Neil Avenue, Columbus, OH 43210-1218, USA. billman.1@osu.edu
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural