| Project/Area Number |
10670637
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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 |
Circulatory organs internal medicine
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| Research Institution | TOYAMA MEDICAL AND PHARMACEUTICAL UNIVERSITY |
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Principal Investigator |
INOUE Hiroshi Toyama Medical & Pharmaceutical University, Faculty of Medicine, Professor, 医学部, 教授 (60151619)
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| Co-Investigator(Kenkyū-buntansha) |
HIRAI Tadakazu Toyama Medical & Pharmaceutical University, Hospital, Assistant Professor, 附属病院, 助手 (10303215)
NOZAWA Takashi Toyama Medical & Pharmaceutical University, Faculty of Medicine, Assistant Professor, 医学部, 助手 (00180737)
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| Project Period (FY) |
1998 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 1999: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 1998: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | Myocardial infarction / Sympathetic nerve / Kidney / Heart failure / Rat |
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| Research Abstract |
Renal sympathetic activation after myocardial infarction (MI) increases renal sodium and water reabsorption and therefore may contribute to worsening heart failure. However, it remains. unknown whether a long-term suppression of renal sympathetic activity could modify ventricular remodeling after MI. Accordingly, we investigated effects of chronic renal sympathetic denervation (RD) on ventricular function after MI in rats.
[Methods] Two days before MI induction by a left coronary artery ligation, bilateral RD was performed by surgically cutting the nerve bundles and coating with 10% phenol solution in Wistar rats. Ventricular function, urinary volume, and sodium excretion were determined 4 weeks afar MI.
[Results] RD at 4weeks after the operation was confirmed by depleted renal norepinephrine (14±7 vs 242±58 ng/g). MI size was similar between rats with RD and without RD. Rats with RD had significantly smaller right ventricular and lung weights, smaller LV end-diastolic pressure (8±5 vs 16±7 mmHg), smaller LV end-diastolic dimension (10.3±0.7 vs 11.0±0.8 mm), greater LV fractional shortening (20.9±3.2 vs 14.9±3.0 %), and greater minimum LVdP/dt (8.3±1.9 vs 6.5±0.8×x10ィイD13ィエD1mmHg/s). Urine volume was not different between the two groups but sodium excretion was greater in rats with RD (1.89±0.81 vs 1.12±0.77 mmol/day). RD in rats without MI did not affect any of above variables.
[Conclusions] The present study suggests that the renal sympathetic activation after MI significantly contributes to worsening heart failure and a chronic RD prevents ventricular remodeling after MI at least in part due to inhibition of renal sodium reabsorption.
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