| Co-Investigator(Kenkyū-buntansha) |
MUTO Shigeaki M.D., Jichi Medical School, 医学部, 助手 (40190855)
IINO Tomoya M.D., Jichi Medical School, 医学部, 助手 (40176053)
TAKEDA Katsuji M.D., Jichi Medical School, 医学部, 助手 (10102253)
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| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1987: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1986: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Research Abstract |
Since the pathophysiology of congestive heart failure in hypertensive heart is so complexed, the causes are difficult to be concluded only from the pressure overload. Although discussed the relations between humoral factors or autonomic nervous system, and hypertensive hypertrophy, regression or heart failure, the definite evidences were to be determined. So we investigated 1) the regression of hypertensive cardiac hypertrophy with antihypertensive agents, 2) the pumping ability of hypertensive hypertrophied heart, regressed heart and normal heart.
Study 1): <alph>-blocker; prazosin (PR), Ca-antagonists; diltiazem (DT) and converting enzyme inhibitor; captopril (CP) were administered for 3 weeks in spontaneously hypertensive rats (SHR) and blood pressure and cardiac weight were evaluated. Significant depressor effects were determined in PR, DT and CP, but the decrease of cardiac weight (regression) resulted only from CP treatment. Study 2) Captopril and vehicle were administered for 3 weeks in SHR (SHR-T, SHR-C) and WKY (WKY-T,WKY-C). Under the conditions of ether anesthesia and open chest, electromagnetic flowmeter was put on the ascending aorta and cannulation was performed into LV through left afrium to measure cardiac output and LV end-diastolic pressure (EDP), respectively. 40 ml/kg/min of whole blood was infused to give the rapid volume overload, then stroke volume (SB) and EDP were measured to obtain the ventricular function curve (VFC). VFCs were not different significantly among four groups (SHR-C,T, WKY-C, T). However in pressure-overloaded SHR-T, VFCs shifted to the right significantly to indicate the decrease of pumping ability in regressed heart.
From these results it was concluded that (1) hypertensive cardiac hypertrophy and regression were induced not only by pressure overload but also by other factors, (2) the pumping ability and potentiality of regressed heart might possibly attenuate against pressure or volume overload.
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