1998 Fiscal Year Final Research Report Summary
Chronic Animal Experimant Using Transmycardial Laser Revascularization (TMLR)
| Project/Area Number |
09671376
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Thoracic surgery
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| Research Institution | KYOTO UNIVERSITY |
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Principal Investigator |
NISHIMURA Kazunobu Kyoto University, Faculty of Medicine, Associate Professor, 医学研究科, 助教授 (70252450)
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| Project Period (FY) |
1997 – 1998
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| Keywords | TMLR / late results / sympathetic nerve / tissue blood flow / Bradykinin |
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| Research Abstract |
Transmyocardial laser revascularization (TMLR) enables myocardium to increase blood supply by creation of micropores. Although the clinical symptom of angina pectoris was improved by TMLR, the precise mechanism as well as long term results are unclear. The purpose of this study is to investigate chronic effects of TMLR on tissue blood flow (TBF) and destruction of neuroreceptors.
<Methods> Fourteen swine were used in this study. In all animals, 30 microchannels by TMLR were created around the left anterior descending artery and the first diagonal artery (D1). Then, D1 was ligated in group 1 (n=7), and was intact in group 2 (n=7). Twelve months after operation, D1 of group 2 animals was also ligated. Regional wall motion (RWM) and TBF was measured in both groups. Furthermore, Bradykinin was injected into the myocardium around TMLR area to evaluate response to sympathetic neuroreceptors, which were confirmed by immunohistochemistry. <Results> In group 1, RWM of TMLR area was severely reduced or akinetic in association with poor TBF, and histology revealed marked fibrosis. In group 2, RWM was also reduced, but was better than in group 1 with substantially restored TBF. The response to Bradykinin was maintained in group 2, while it was poor in group 1. Tyrosine hydroxylase was observed around epicardium in both groups. <Conclusion> TMLR increased TBF, but failed to improve RWM. Since neuroreceptors were not destroyed by TMLR, it was speculated that angina pectoris was predominantly relieved after TMLR due to improvement of TBF rather than destruction of neuroreceptors.
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