| Project/Area Number |
61570684
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Thoracic surgery
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| Research Institution | National Cardiovascular Center |
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Principal Investigator |
TAKAICHI Shigeko National Cardiovascular Center Department of Etiology and Pathology, 病因部, 研究員 (00093930)
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| Co-Investigator(Kenkyū-buntansha) |
KINOSHITA Masayuki National Cardiovascular Center Department of Artifitial Organs, 研究所・人工臓器部, 研究員 (00183301)
NODA Hiroyuki National Cardiovascular Center Department of Artifitial Organs, 研究所・人工臓器部, 研究員 (20183551)
MATSUDA Takehisa National Cardiovascular Center Department of Biomedical Engineering, 研究所・生体工学部, 部長 (60142189)
TAKANO Hisateru National Cardiovascular Center Department of Artifitial Organs, 研究所・人工臓器部, 部長 (60028595)
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| Project Period (FY) |
1986 – 1987
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| Project Status |
Completed (Fiscal Year 1988)
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| Budget Amount *help |
¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 1987: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1986: ¥1,300,000 (Direct Cost: ¥1,300,000)
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| Keywords | Left Ventricular Assist Device / Myocardial High Energy Phosphate / Morphometric Study / Catecholamine / Myocardial Atrophy / 不全心 / 心不全 / 人工心臓 / 心筋微細構造 / 両心補助人工心臓 / 心筋代謝 / 高エネルギーリン酸 / 左心不全 / 両心不全 |
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| Research Abstract |
1. THE EFFECT OF LEFT VENTRICULAR ASSIST DECICE (LVAD) ON THE MYOCARDIAL ENRGY BALANCE High energy phosphate levels did not change in the normal heart group (n=3) with LVAD pumping. The LVAD pumping preserved high energy phosphate concentrations in the ischemic myocardium, and prevented the increase in catecholamine concentrations in the case of profound heart failure (n=6). These results suggest that LVAD preserves myocardial high energy phosphate concentrations with its hemodynamic and metabolic effects, and reduces the infarcted area.
2. MORPHOLOGICAL CHANGES IN MYOCARDIAL TISSUE WITH THE LONG TERM USE OF LEFT VENTRICULAR ASSIST DEVICE (LVAD) -MORPHOMETRIC STUDY- With using an LVAD, the maximum bypass rate ( about 8/% of the total cardiac output) was yielded in 2 goats for 30 days, and the limited bypass rate (around 60%) was maintained in one goat each for 30 days and 90 days. Morphometric studies of these left ventricular myocardium were performed comparing with the control values (n=4). The results were as follows. 1. Relative tissue volume densities of myocyte and intersitial tissue were unchanged. 2. Mean cross-sectional area of the myocyte in the maximum bypass cases was 327.4 um, while the control value was 451.0 um.
3. Relative myocyte volume dencities of myofibrils reduced to 49.7% in the maximum bypass cases and to 48.0% in the 90 days bypass case from the control value of 56.5%, and that of mitochondria decreased to 18.2% from 23.6% only in the 90 days bypass case. The LVAD induces cardiac disuse atrophy in accordance with both the bypass rate and the duration of assistance. These two types of experiments indicate that LVAD saves the reversely injured myocardium, but the long term assistance with LVAD induces cardial atrophy in the normal myocardium. The long term assistance with LVAD induces cardiac atrophy in the normal myocardium. It is the problem awaiting solution how these results influence the contractile recovery of failed hearts.
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