| Budget Amount *help |
¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 1986: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1985: ¥1,000,000 (Direct Cost: ¥1,000,000)
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| Research Abstract |
We investigated how changes in ventricular contractility associated with exercise and experimental heart failure influence the transmission of mechanical energy from the ventricle to the arterial system in 14 conscious dogs.
We instrumented a high fidelity pressure transducer in the left ventricle (LV) and an electromagnetic flow probe around the ascending aorta. After complete recovery from the surgery (usually about 10 days), we let dogs run on a treadmill, while measuring hemodynamic variables (control study). We then created LV failure by injecting microspheres to the left main coronary artery under fluoroscopic guidance. After recovery from this procedure, we measured hemodynamic variables at rest.
With exercise, heart rate, cardiac output and end-systolic elastance (Ees) of LV nearly or more than doubled, while decreasing arterial resistance (R). Estimated ratio of Ees to the effective arterial elastance (as approximated by R/T where T is a cardiac cycle length) was nearly unity at rest and remained almost unity during exercise. On the basis of our previous study (Sunagawa et al., Circ Res 56: 586, 86), this is to say that stroke work (SW) of LV is always maximum or nearly maximum during exercise as well as at rest in healthy dogs. Indeed average SW for normal heart during exercise was more than 95% of maximal SW which is theoretically derived for each heart. In dogs with heart failure, however, SW decreased to 50% of the maximal SW.
We conclude that the regulatory mechanism adjusts LV contractility, heart rate and arterial resistance so that SW of LV becomes maximal at rest and during exercise as long as the cardiovascular system is in good shape. Once cardiac function is deteriorated, however, the regulatory response of the system is no longer teleologically sound. It rather worsens the efficiency of mechanical energy transmission of failing LV to the arterial system.
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