1992 Fiscal Year Final Research Report Summary
Pathophysiology and management of dilated cardiomyopathy
| Project/Area Number |
02670412
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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 | Kanazawa Medical University |
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Principal Investigator |
MATSUI Shinobu Kanazawa Medical University professor, 医学部, 教授 (00064600)
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| Co-Investigator(Kenkyū-buntansha) |
HIRAKAWA Tomoyuki Kanazawa Medical University research associate, 医学部, 助手 (50199048)
FUKUOKA Takumi Kanazawa Medical University research associate, 医学部, 助手 (10199193)
ASAJI Takayoshi Kanazawa Medical University research associate, 医学部, 助手 (00183137)
MATOBA Munetoshi Kanazawa Medical University assistant professor, 医学部, 講師 (10199903)
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| Project Period (FY) |
1990 – 1992
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| Keywords | dilated cardiomyopathy / heart failure / receptor / anti-receptor antibody / exercise capacity / fatty acid metabolism / adenosine |
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| Research Abstract |
Basic Research : (1)In Syrian hamster, elevation of plasma norepinephrine concentrations and increased numbers of myocardial beta receptors were observed after administration of beta-blocking agent. (2)Characteristics of beta1-, beta2-and Muscarine-2 receptors was examined by monoclonal antibodies. (3)Na・K・ATPase activity and its alpha-subunit of human red cell membrane were measured by inorganic phosphate assay. Clinical research : (1)After administrations of beta-blockade or Ca^<++>antagonist, patients with dilated cardiomyopathy experienced an improvement in exercise tolerance and cardiac function. It was presumed that the mechanism of these clinical improvements in beta-blockade might be an up-regulation of beta receptor function. (2)In patients with dilated cardiomyopathy and/or heart failure, a decreased response of lymphocyte beta-receptor system to dynamic exercise was observed. It is assumed that this phenomenon might be one of the factors which decrease exercise capacity in heart failure. (3)We could not find any abnormalities in fatty acid metabolism in the patients with dilated cardiomyopathy and/or congestive heart failure, but it is suspected that the patients who excrete large amount of free carnitine into the urine, namely the patients with severe heart failure, have some possibility of carnitine deficiency.
(4)In the elderly, neurohumoral factors were already activated in mild or moderate heart failure, but in severe heart failure, neurohumoral activation was not proportional to the severity.
(5)In patients with chronic heart failure, production of adenosine was decreased and vasodilation of exercising muscle induced by adenosine might be impaired during exercise. Therefore, it is assumed that adenosine is one of the important factors which regulate exercise capacity in patients with chronic heart failure.
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