| Project/Area Number |
63570387
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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 |
Circulatory organs internal medicine
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| Research Institution | University of Tokyo, Faculty of Medicine |
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Principal Investigator |
INOUE Hiroshi University of Tokyo, Faculty of Medicine, Instructor, 医学部(病), 助手 (60151619)
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| Co-Investigator(Kenkyū-buntansha) |
KAWAKUBO Kiyoshi University of Tokyo, Faculty of Medicine, Instructor, 医学部(病), 助手 (30152929)
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| Project Period (FY) |
1988 – 1989
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| Project Status |
Completed (Fiscal Year 1989)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1989: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1988: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Keywords | Sympathetic nerve / Vagus / myocardial infarction / Refractory period / Ventricular arrhythmia / 心筋硬塞 / 心筋虚血 |
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| Research Abstract |
Purpose of the study was to determine the time course and spatial distribution of efferent sympathetic and vagal denervation after myocardial infarction. Acute myocardial ischemia was induced by legation of diagonal branch or branches in anesthetized, open chest dogs. Refractory period shortening induced by ansae subclaviae stimulation and refractory period lengthening by vagal stimulation were determined at test sites basal to and epical to the myocardial ischemic area before and after coronary occlusion. Transmural myocardial ischemia was produced in 6 dogs, in which 10 of 24 apical sites lost refractory period response to ansae subclaviae stimulation 30-180 minutes after coronary occlusion. At the remaining, 14 epical sites and basal sites, refractory period shortening in response to ansae subclaviae stimulation was not attenuated by myocardial ischemia. In another 9 dogs, refractory period lengthening in response to vagal stimulation was determined. Vagal response was eliminated at 8 of 15 apicil sites 30-180 minutis after coronary occlusion. At the remaining 27 apical sites and 17 basal sites, vagal response was not affected by myocardial ischemia. Loss of efferent sympathetic innervation and of vagal innervation in noninfarcted apical sites occurred heterogeneously as early as 30 minutes after coronary occlusion with more complete denervation occurring over time. It is quite possible that the heterogeneous development of sympathetic and vagal denervation following myocardial infarction might contribute development of ventricular arrhythmias that occur early after coronary occlusion.
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