Abstract | BACKGROUND: Abnormalities in the beta- adrenergic control of cardiac function play a role in the pathogenesis of several disease states. Because circulatory failure in patients with septic shock is known to be less responsive to catecholamines, we investigated whether the beta- adrenoceptor-linked signal transduction mechanisms are altered in the heart of a septic animal model METHODS: RESULTS: CONCLUSIONS: Impairment of myocardial functional responsiveness to beta- adrenoceptor stimulation appears in the early stage of sepsis. The impaired response to beta- adrenoceptor stimulation in the heart in this pathologic state may result in part from a decreased level of G(s alpha) protein which occurs at the level of gene expression.
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Authors | N Matsuda, Y Hattori, Y Akaishi, Y Suzuki, O Kemmotsu, S Gando |
Journal | Anesthesiology
(Anesthesiology)
Vol. 93
Issue 6
Pg. 1465-73
(Dec 2000)
ISSN: 0003-3022 [Print] United States |
PMID | 11149442
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Adrenergic beta-Antagonists
- Lipopolysaccharides
- RNA, Messenger
- Receptors, Adrenergic, beta
- Iodocyanopindolol
- GTP-Binding Proteins
- Adenylyl Cyclases
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Topics |
- Adenylyl Cyclases
(metabolism)
- Adrenergic beta-Antagonists
(metabolism)
- Animals
- Blood Pressure
(physiology)
- Escherichia coli
- GTP-Binding Proteins
(genetics, metabolism)
- Gene Expression Regulation
- Heart Rate
(physiology)
- Iodocyanopindolol
(metabolism)
- Lipopolysaccharides
- Models, Animal
- Myocardial Contraction
(physiology)
- RNA, Messenger
(metabolism)
- Rabbits
- Receptors, Adrenergic, beta
(physiology)
- Shock, Septic
(physiopathology)
- Signal Transduction
(physiology)
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