1989 Fiscal Year Final Research Report Summary
MECHANISMS OF PROGRESSION OF MYOCARDIAL FAILURE -ROLE OF SYMPATHETIC ACTIVATION DURING EXERCISE-
| Project/Area Number |
63480229
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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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 | OSAKA UNIVERSITY |
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Principal Investigator |
TAKEDA Hiroshi OSAKA UNIVERSITY HOSPITAL MEDICAL INFORMATION SCIENCE ASSOCIATE PROFESSOR, 医学部附属病院, 助教授 (20127252)
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| Co-Investigator(Kenkyū-buntansha) |
MATSUYAMA Taizo OSAKA UNIVERSITY HOSPITAL, 医学部附属病院, 医員
SATO Hideyuki OSAKA UNIVERSITY HOSPITAL, 医学部附属病院, 医員
ISHIDA Yoshio OSAKA UNIVERSITY HEALTH AND SPORT SCIENCE ASSISTANT, 健康体育部, 助手 (80144533)
KITABATAKE Akira OSAKA UNIVERSITY SCHOOL OF MEDICINE LECTURER, 医学部, 講師 (00124769)
INOUE Michitoshi OSAKA UNIVERSITY HOSPITAL MEDICAL INFORMATION SCIENCE PROFESSOR, 医学部附属病院, 教授 (30028401)
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| Project Period (FY) |
1988 – 1989
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| Keywords | HEART FAILURE / beta-BLOCKER / LEFT VENTRICULAR DIASTOLIC PROPERTY / CALCIUM OVERLOAD |
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| Research Abstract |
To investigate a role of exercise and an accompanying aynpathetic activation in progression of chronic myocardial failure, we assessed the effects of dynamic exercise on left ventricular (LV) diastolic properties of failing human heats before and after beta adrenoceptor blockade. Micromanometric LV pressure (p) and LV volume (V) using a digital subtraction cineangiography were simultaneously measured at rest and soon after mild (1/2 maximal oxygen consumption) bicycle exercise before and after a single intravenous administration of 0.1 mg/kg propranolol in 12 patients with dilated cardiomyopathy (DCM). Five patients with aortic regurgitation and normal LV function served as a control group. The LV diastolic P-V relation shifted upward during exercise in DCM patients.
Propranolol attenuated this shift. The similar changes were observed after correction of LV pressure by right atrial pressure reflecting pericardial constraints. In the control group, the diastolic P-V relation was not affected by exercise and, thereby, the effect of propranolol on the diastolic P-V relation was not observed. These results indicate that dynamic exercise increases myocardial stiffness of failing hearts through sympathetic activation. Because the acutely increased myocardial stiffness is likely to be produced by a residual interaction of contractile proteins due to an increased intracellular calcium concentration, the exercise-induced sympathetic activation may be associated with progression of cardiac failure through myocardial calcium overload.
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