The left ventricular myocardial function in the ejection phase of auxotonic contraction was investigated in direct relation to aortic distensibility in twenty-five patients with varying heart lesions. Analysis of the aortic pressure curve and the ascending aorta volume obtained by routine left heart catheterization and biplane angiocardiography provided an approach to compute aortic distensibility. The mean value of the aortic distensibility in all patients was 0.847 ± 0.430 S.D. percent per mmHg pulse pressure. In patients with normal left ventricular (LV) function, the aortic distensibility demonstrated a significant inverse relationship to the duration of the LV wall stress at top 20 percentile of its peak (r=-0.71), and also a positive one to the contractile element velocity at the peak stress (r=0.70). Patients with LV dysfunction defined by ejection fraction of below 50% showed an increase in duration of higher stress with relatively low aortic distensibility. This characteristic feature of the aortic property and stress-time relation in the ejection phase observed in LV dysfunction were not always found to concur with low maximal contractile element velocity (V_max) which was computed in the isovolumic phase. These results suggest that the aortic distensibility is one of the major determinants on LV myocardial force and velocity development, and that evaluation of myocardial functions in the ejection phase should be made as well as in the isovolumic phase.

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To 10 hypertensive patients fusaric acid, a dopamine-β-hydroxylase inhibitor, was administered orally in daily dose of 300-600 mg for 4 weeks, and the change of urinary catecholamines was examined almost every day. The results obtained were as follows. (1) There were three patterns of the time-course change in the urinary excretion of noradrenaline during the fusaric acid therapy, i.e., (i) that of "initial spike-like increase followed by a continuous increase throughout the later stage", found in 3 cases receiving 300 mg/day dose and I case receiving 600 mg/day, (ii) that of "late rise", i.e. a continuous rise throughout the later stage, seen in 4 cases receiving 300 mg/day, and (iii) that of "minimal change", seen in 2 cases receiving 600 mg/day. These observations formed a sharp contrast with the fact that, during the administration of reserpine, urinary noradrenaline excretion was moderately to severely decreased. (2) Urinary adrenaline excretion did not change with the administration of fusaric acid. (3) No definite relation was found between the cnages in urinary noradrenaline excretion and changes in blood pressure during the fusaric acid therapy . In conclusion, it is suggested that a small amount of fusaric acid (300 mg/day for adults), administered orally, causes noradrenaline to be released and noradrenaline biosynthesis to be accelerated later. With larger doses (600 mg/day), ho*Never, this trend was not conspicuous.

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