Yoshio Ito

Hemodynamic effects of nifedipine in congestive heart failure

Nifedipine, a potent coronary vasodilator, was administered in a single sublingual dose of 20 mg to eight patients with mild to moderate congestive heart failure. Nifedipine produced a slight increase in heart rate (mean +/- standard error of the mean 73.3 +/- 3.2 versus 80.9 +/- 2.1 beats/min, p < 0.025) and an increase in cardiac index (from a control value of 3.51 +/- 0.22 to 4.06 +/- 0.31 liters/min per m2, p < 0.01). Arterial blood pressure decreased from 112.9 +/- 6.2/67.7 +/- 4.2 (mean 84.9 +/- 4.0) to 100.8 +/- 4.4/56.4 +/- 11.0 (mean 76.1 +/- 4.3) mm Hg (p < 0.01) and total systemic vascular resistance also decreased from a control value of 15.6 +/- 1.0 to 12.4 +/- 0.8 units (p < 0.01) after administration of nifedipine. These data suggest that nifedipine may be useful for vasodilation in congestive heart failure.

CONGENITAL HEART DISEASE IN FORTY YEARS OF AGE AND OVER : Prevalence, relative incidence and clinical features

The number of patients of C.H.D. over 40 years old was 40 (male 26, female 14) among 43285 (male 30320, female 12965). Its item: ASD 24, VSD 6, PDA 3, PS 3, ECD 2, Coarctation of the Aorta 1, Eisenmenger whose shunt site was unclear 1. The total prevalence rate was 0.92 per 1000 and female showed slightly higher rate than male (male 0.86 per 1000, female 1.08 per 1000). When it was compared with rheumatic valvular diseases, the ratio of both male and female was about 1/3. C.H.D. is assumed to decrease to about 1/3 or less between the period of school age and the middle age, but the prevalence rate over 60 years old was never lower than the overall prevalence investigated. C.H.D. in the middle and old aged should be kept in mind while examination.

Evidence for a humoral factor mediating the effect of a pressure load on lysine incorporation in rabbit heart

Abstract Mechanisms of an increase in protein synthesis in pressure-loaded heart were studied by measuring rates of 3 H-lysine incorporation into cardiac myosin B in a perfused rabbit heart. When a pressure load had been applied to the right ventricle, a significant increase in the incorporation was found not only in the right but also in the left ventricle where pressure load was not applied. Rates of the incorporation in hearts without pressure load increased significantly in both ventricles when they were co-perfused with a heart with a pressure load on the right ventricle. These results suggest that humoral factor(s) is released from the pressure-loaded ventricle which accelerate amino acid incorporation in unloaded ventricles.