Increased myocardial gene expression of tumor necrosis factor-α and nitric oxide synthase-2: A potential mechanism for depressed myocardial function in hibernating myocardium in humans

Whether cardioinhibitory cytokines are elevated in regions of hibernating myocardium and account in part for the depression in resting function is currently not known. Methods and Results- Thirteen patients with stable ischemic ventricular dysfunction scheduled for bypass surgery underwent preoperat...

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Published in:Circulation (New York, N.Y.) N.Y.), 2002-04, Vol.105 (13), p.1537-1540
Main Authors: KALRA, Dinesh K, XI ZHU, RAMCHANDANI, Mahesh K, LAWRIE, Gerald, REARDON, Michael J, LEE-JACKSON, Dorellyn, WINTERS, William L, SIVASUBRAMANIAN, Natarajan, MANN, Douglas L, ZOGHBI, William A
Format: Article
Language:English
Subjects:
Biological and medical sciences
Cardiology. Vascular system
Coronary heart disease
Female
Heart
Heart - physiopathology
Humans
Male
Medical sciences
Middle Aged
Myocardial Stunning - diagnostic imaging
Myocardial Stunning - metabolism
Myocardial Stunning - physiopathology
Myocardium - metabolism
Nitric Oxide Synthase - biosynthesis
Nitric Oxide Synthase - genetics
Nitric Oxide Synthase Type II
Nitrites - blood
Receptors, Adrenergic, beta - metabolism
RNA, Messenger - biosynthesis
Transcriptional Activation
Tumor Necrosis Factor-alpha - biosynthesis
Tumor Necrosis Factor-alpha - genetics
Ultrasonography
Ventricular Dysfunction, Left - metabolism
Ventricular Dysfunction, Left - physiopathology
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Summary:Whether cardioinhibitory cytokines are elevated in regions of hibernating myocardium and account in part for the depression in resting function is currently not known. Methods and Results- Thirteen patients with stable ischemic ventricular dysfunction scheduled for bypass surgery underwent preoperative dobutamine echocardiography (DE) and intraoperative myocardial biopsies. The numbers of copies of mRNA for the negatively inotropic cytokines tumor necrosis factor-alpha (TNF-alpha) and inducible nitric oxide synthase (NOS2) were quantified by reverse transcription-polymerase chain reaction. In normal segments, myocardial TNF-alpha was barely detectable (1.2+/-0.4 copies per 10(6) copies of beta-actin). A 13.7-fold increase in myocardial TNF-alpha was observed in dysfunctional segments with a biphasic response to DE (contractile reserve and ischemia) and was highest (45.5-fold) in segments with ischemia and without contractile reserve (P
ISSN:0009-7322
1524-4539
DOI:10.1161/01.CIR.0000013846.72805.7E