The mechanism of physiological adaptation for chronic nonpulsatile perfusion.
| Project/Area Number |
07457296
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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 | Kyushu University |
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Principal Investigator |
TOMINAGA Ryuji Kyushu Univ. Faculty of medicine.associate professor, 医学部, 助教授 (70136464)
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| Co-Investigator(Kenkyū-buntansha) |
FUKUMURA Fumio Kyushu Univ. Faculty of medicine.assistant.prof., 医学部, 助手 (80264026)
MORITA Shigeki Kyushu Univ. Faculty of medicine.assistant.prof., 医学部, 講師 (70243938)
YASUI Hisataka Kyushu Univ. Faculty of medicine. professor, 医学部, 教授 (20089923)
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| Project Period (FY) |
1995 – 1996
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| Project Status |
Completed (Fiscal Year 1996)
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| Budget Amount *help |
¥7,400,000 (Direct Cost: ¥7,400,000)
Fiscal Year 1996: ¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1995: ¥5,200,000 (Direct Cost: ¥5,200,000)
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| Keywords | pulsatile / nonpulsatile / artificial circulation / awake study / sympathetic nerve / vascular endothelial cell / aerobic metabolism / 牛 / 血管内皮細胞 / 両心バイパス / Critical flow / 内皮細胞 / 血流分配 |
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| Research Abstract |
1.In acute artificial circulation study, neurohemodynamic control system and local hemodynamic control system were investigated in anesthetized dogs.
1). The directly measured efferent renal sympathetic nerve activity was significantly decreased to 83.5% by initiation of IABP,which is associated with decrease in peripheral vascular resistance. The increase in pulse rate by IABP is suggested to suppress the efferent sympathetic nerve activity through baroreflex mechanism.
2). In left ventricular assist device model, circulatory depulsation significantly increased the renal sympathetic nerve activity. This increase in nerve activity was well correlated with increase in peripheral vascular resistance in nonpulsatile systemic perfusion.
3). In left ventricular assist device model, basal release of endothelium-derived nitric oxide was significantly decreased in nonpulsatile perfusion compared with pulsatile perfusion. Flow-mediated, endothelium-dependent vasodilation was also impaired in nonpu
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lsatile perfusion, which suggested that flow-stimulated release of endothelium-derived nitric oxide was decreased in nonpulsatile perfusion. Thus impaired basal and flow-stimulated release of endothelium-derived nitric oxide may at least partly contributes to increased peripheral vascular resistance in nonpulsatile perfusion.
2.In chronic artificial circulation study, hemodynamic changes and critical flow rate were investigated in pulsatile and nonpulsatile perfusion in awake calves.
1). Mean blood pressure and systemic vascular resistance were higher in nonpulsatile perfusion and the difference was larger at low systemic flow rates.
2). Serum nitrite/nitate level, stable metabolites of nitric oxide, were high in pulsatile perfusion, which suggested that larger amount of nitric oxide release in pulsatile perfusion.
3). Critical flow rate, determined by O2 consumption and serum lactate level, was around 80 ml/kg/min in nonpulsatile perfusion and even lower in pulsatile perfusion.
Thus pulsatile perfusion has an advantage in maintaining the peripheral circulation in lower systemic flow rates. Less
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Report
(3 results)
Research Products
(6 results)
