Radio frequency transmyocardial revascularization enhances angiogenesis and causes myocardial denervation in canine model
Background and Objective Transmyocardial revascularization (TMR) relieves angina and improves exercise tolerance in patients. Angiogenesis and myocardial denervation have been proposed as factors contributing to these benefits. To test whether radio frequency transmyocardial revascularization (RF‐TM...
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Published in | Lasers in surgery and medicine Vol. 27; no. 1; pp. 18 - 28 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
New York
John Wiley & Sons, Inc
2000
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Subjects | |
Online Access | Get full text |
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Summary: | Background and Objective
Transmyocardial revascularization (TMR) relieves angina and improves exercise tolerance in patients. Angiogenesis and myocardial denervation have been proposed as factors contributing to these benefits. To test whether radio frequency transmyocardial revascularization (RF‐TMR) enhances angiogenesis and causes myocardial denervation.
Study Design/Materials and Methods
RF‐TMR channels were created in 12 dogs which survived up to 4 weeks. Bromodeoxyuridine was administered subcutaneously to mark proliferating cells as an assay of angiogenesis. Western blot analysis of tyrosine hydroxylase and blood pressure response to topical bradykinin were used as indices of myocardial denervation.
Results
RF‐TMR increased local vascularity by an average of 50%, whereas the rate of vascular cell proliferation was tripled over that of the untreated region. Changes in mean arterial pressure with bradykinin and tyrosine hydroxylase content were significantly decreased in RF‐TMR regions as compared with normal myocardium in the same hearts.
Conclusion
RF‐TMR enhances angiogenesis and causes myocardial denervation in canine myocardium as with laser TMR. Lasers Surg. Med. 27:18–28, 2000. © 2000 Wiley‐Liss, Inc. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0196-8092 1096-9101 |
DOI: | 10.1002/1096-9101(2000)27:1<18::AID-LSM3>3.0.CO;2-F |