2005 Fiscal Year Final Research Report Summary
Cardiomechanical and biophysical effects of left ventricular assist device upon profoundly depressed heart.
| Project/Area Number |
16390390
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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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 | Tokyo Medical and Dental University |
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Principal Investigator |
SAKAMOTO Tohru Tokyo Medical and Dental University, Postgraduate school of medicine, Professor, 大学院・医歯学総合研究科, 教授 (10101875)
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| Project Period (FY) |
2004 – 2005
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| Keywords | left ventricular assist device / profound heart failure / pressure-volume relationship / left ventricular drainage / apoptosis |
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| Research Abstract |
Left ventricular (IV) assist using IV drainage showed sufficient unloading effects on profoundly depressed heart, without coupled ejection to the native LV. On the volume study, end-diastolic IV volume was mildly increased and end-systolic LV volume was decreased with the increase of assisted ratio, showing the triangle loop as a whole. This volume change was large with obtaining, enough afterload reduction, and erectronmicroscopic myocardial configuration showed same results as control findings. On cell biochemical analysis in myocardium, the mRNA level in Angiotensin II type 1 receptor rose mildly, but the mRNA level in β-1 adrenergic receptor approximately showed equivalent value with "a control state". In addition, it increased to about 3 times comparing the mean value to LA drainage group, resulted in significant statistical difference between LA and IV drainage groups. Angiotensin II type 1 receptor and β-1 adrenergic receptor is the same factor as a G albuminoidal conjugation type acceptor, but this phenomenon is different from Gs, Gq in acceptor coupling factor (a transducer). It is thought that the elevation of the mRNA level of β-1 adrenergic receptor in myocardium increases during left ventricular assist is evidence indicating enough inotropic potentiality after myocardial recovery, and it is thought to be advantageous as a clinical program to achieve "Bridge to Recovery". On the other hand, IV assist with LA drainage did not showed enough afterload reduction, and resulted in persistent occurrence of intracellular edema, mitochondrial size discrepancy and myocardial disarray.
In addition, the mRNA level of Angiotensin II type 1 receptor in myocardium increased, showing that afterload for left ventricle was present during IV support.
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