The relationship of the presence or absence and the severity of tricuspid insufficiency with the data of preoperative clinical and hemodynamic examinations were investigated in 50 patients with tricuspid insufficiency and in 40 patients without tricuspid insufficiency who underwent open mitral valve surgery. The presence or absence of the tricuspid insufficiency correlated well with the data of preoperative clinical and hemodynamic examinations. The correlation between the severity of tricuspid insufficiency estimated by the surgeons at the time of surgery and the preoperative data were variable. Pulmonary arterial hypertension was considered to be one of the cause for tricuspid insufficiency in patients with mitral stenosis but was not in patients with mitral insufficiency. The utilization of thermodilution technique as the preoperative quantitative means for the tricuspid insufficiency was reported.

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A review was made of 69 cases manifesting congestive right-side heart failure among 1, 910 cases who had undergone cardiac catheterization at the Department of Pediatrics, Tenri Hospital. Hemodynamic and angiographic studies were made in 32 cases which had undergone corrective surgery of tetralogy of Fallot at ages between l to 14 more than 2 years earlier. The circulatory responses to exercise were also studied in 21 patients to evaluate the pumping performance of the heart. Although all patients but 2 with operatively corrected tetralogy of Follot are quite asymptomatic, there were elevations of RVEDP noted despite the absence significant residual pulmonary stenosis at rest. In addition, patients revealed abnormal hemodynamic response to exercise. It was also noted that among patients with residual pulmonary stenosis a large systolic pressure gradient across the right ventricular outflow tract appeared during exercise. In addition to the evaluation of residual pulmonary stenosis by routine catheterization, the clinical importance of the evaluation of right ventricular performance in response to exercise following operative correction of tetralogy of Fallot was identified as an essential feature in long-term medical management.

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The postnatal maturation of pulmonary vasculature which occurs early neonatal stage brings a decrease of pulmonary artery pressure and of pulmonary vascular resistance as shown in our study on the normal subjects. The presence of small ventricular septal defect (VSD) did not affect the normal maturation pattern. In some severe congenital heart diseases the maturation also occurs but is modified to some extent. The maturation occurred in a case of large VSD causes transient increase of pulmonary blood flow as seen in our data and the latter may act as a precipitating factor for the onset of congestive heart failure. However, we showed that there are a number of cases which have heart failure prior to the increase of pulmonary blood flow. The traditional concept of maturation cannot be applicable, for such cases to explain the development of heart failure. We proposed a broader concept of the maturation of the right heart containing the maturation of right ventricular musculature, and showed that it is effectively applicable for the explanation of the hemodynamic transition and the onset of heart failure in large VSD, transposition of great vessels (TGA) and pure pulmonary stenosis (PPS). A transient postnatal decrease of right ventricular pressure in TGA and a discrepancy existing between the hemodynamic severity and the grade of ECG findings in young children with PPS were found and discussed. The pathologic physiology of maturation containing the re-activity of pulmonary vasculature, the right ventricular function and the heart failure was discussed on the ground of the above mentioned data and the added cases of primary pulmonary hypertension and cor pulmonale.

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Studies were made on the hemodynamics in the liver of dogs during hypoxic conditions. Dogs were divided into two groups: Group A in which the periarterial nerve plexus was intact and Group B in which it was neurectomized. Dogs were anesthetized with sodium pentobarbital and given a mixture of 5% O₂ and 95% N₂ . Resultant changes in the blood pressure. and blood flow of the hepatic artery and portal vein were observed. (1) In the control period, the resistance in the hepatic artery and portal vein were lower in Group B than in Group A. (2) In both groups, the abdominal aortic pressure and hepatic arterial flow increased during hypoxia, but the hepatic arterial resistance did not change. (3) During hypoxia the portal venous pressure, flow and resistance did not change significantly. From the results, the change in the hepatic arterial circulation during systemic hypoxia seems to be passive, resulting mainly from change in the systemic circulation, and neurogenic control of the hepatic artery through the periarterial nerve plexus seems to be extremely slight. In the portal circulation, the influence of the increase in systemic blood pressure during hypoxia seems to be offset by increase in splanchnic vascular resistance, so that there is no apparent change in portal hemodynamics. The reason for the low portal venous resistance during the control period after section of the periarterial nerve plexus requires study.

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Micronephelometric procedure of an intravenous fat tolerance test was studied. 'An elimination graph of exogenous plasma triglyceride was accurately determined by the micronephelometric technique, instead of chemical triglyceride analysis, and the obtained exponential elimination curve had a high regression coefficient. No significant difference in the values obtained for the elimination constant K₂ by either the original PVP gradient method or the micronephelometric procedure was observed. Also, the micronephelometric method had good reproducibility and good repeatability. By this technique, the fat tolerance test was completed rapidly and with reliable results, and the test utilizing a micronephelometer is suitable for clinical purposes.

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The renin-angiotensin system in chronic hepatitis and liver cirrhosis was studied functionally and morphologically. PRA, PRC and Ang 11 tended to increase in the non-ascitic stage of liver cirrhosis, and in the ascitic stage of liver cirrhosis those levels futher increased, although PRS gradually decreased. Even in chronic hepatitis these values were slightly higher than control levels, but the differences were statistically not significant. There was no significant relationship between serum creatinine levels and PRA. JGI was, however, significantly increased in all 6 patients with liver cirrhosis, in whom JGA was Observed. Even in a cirrhotic patient without ascites, JGI was slightly increased. From these results it is concluded that the renin-angiotensin system is Stimulated even in liver cirrhosis before ascites develops, and that the most parts of the increases in renin and angiotensin depend on renin production in the kidney.

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