| Co-Investigator(Kenkyū-buntansha) |
MATSUKAWA Kanji National Cardiovascular Center Research Institute, Dept. of Cardiac Physiology, 研究所心臓生理部, 室員 (90165788)
HONDA Toshihiro National Cardiovascular Center Research Institute, Dept. of Cardiac Physiology, 研究所心臓生理部, 室員 (70173664)
NISHIURA Naoki National Cardiovascular Center Research Institute, Dept. of Cardiac Physiology, 研究所心臓生理部, 室員 (70132933)
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| Budget Amount *help |
¥1,600,000 (Direct Cost: ¥1,600,000)
Fiscal Year 1986: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1985: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Research Abstract |
Responses in efferent cardiac sympathetic nerve activity (CSNA) and heart rate (HR) to a 100-s anterior descending coronary artery occlusion were measured in cats under awake, atropinized, anesthetized, or anesthetized and atropinized states. In the conscious state,at 20 and 90s of occlusion, CSNA increased by 23% and then decreased by 7%, respectively, whereas HR decreased by 5 and 17% , respectively. With atropinization and/or anesthesia, the initial increas in CSNA was inhibited and the later decreas in CSNA was enhanced whereas the bradycardia was diminished. HR changed in proportion to CSNA responses with high correlations, i.e.,r =+0.89, +0.90, +0.96, and +0.91 for the four states, respectively. In the conscious state, the CSNA-HR relation line shifted toward bradycardia, but this shift was blocked by atropinization and anesthesia. This finding suggested that, in the conscious state, cardiac vagal nerve activity (CVNA) increased immediately and did not decrease during occlusion. At the early stage of occlusion, HR response (bradycardia or tachycardia) was determined by the relative contribution of enhanced CSNA and CVNA. At the later stage of occlusion, bradycardia was induced by a combination of decreased CSNA and enhanced CVNA. IN anesthesia and/or atropinization it was induced mainly by the decreased CSNA.
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