Two series of experiments were performed to investigate the effects of altered dietary sodium, of sodium-retaining steroids, and of increased blood pressure on rat plasma prekallikrein. Plasma prekallikrein increased with age in all groups of rats; thus all comparisons are made with age-metched controls. In the NIH strain of Wistar Kyoto spontaneously hypertensive rats (SHR/N), normotensive at 4 weeks of age, a significant and sustained elevation of blood pressure was apparent by 6-8 weeks of age. Mean plasma prekallikrein, which rose with advancing age, did not differ from that of control Wistar Kyoto NIH (WKY/N) rats during the prehypertensive (0-6 weeks of age), the early hypertensive (8 weeks) or the advanced hypertensive (13 weeks) stages. In the stage of severe hypertension (19-29 weeks), however, SHR/N rats showed significantly lower plasma prekallikrein (p < 0.05-0.005) than agematched WKY/N rats. Plasma prekallikrein was higher in SHR/N in the severe-hypertension stage given a low-sodium diet than in those given an average-sodium diet (p < 0.0 1 ), and this was also the case for the age-matched WKY/N rats on a low-sodium diet, in which plasma prekallikrein was higher (p < 0.05) than in those on average-sodium diet . In young Wistar NIH (W/N) rats given average-sodium diet, desoxycorticosterone (DOC) (27.5 mg/100 gm body weight in 2 doses) increased plasma prekallikrein (p < 0.05-0.005). When DOC was given with a high-sodium diet, however, hypertension developed (p < 0.005) and plasma prekallikrein remained normal. With a low-sodium diet alone, plasma prekallikrein in W/N rats was increased by the 10th day (p < 0.05), but had returned to normal by the 30th day. Thus plasma prekallikrein increases with age and with (exogenous or endogenous) sodium-retaining steroid, and decreases with severe hypertension.

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We observed previously that allopurinol, which was used for the treatment of gout, had a life saving effect after experiment on traumatic shock rats and hemorrhagic shock rabbits. To evaluate the effect of allopurinol fifteen patients undergoing open heart surgery who were considered to have similar metabolic derangement in shock patient were examined. Allopurinol was given orally 2 mg per kg body weight twice before the start of nitrous oxide, oxygen and halothane anesthesia. In the control group of ten patients who were not treated with allopurinol, serum uric acid increased, the lactate/ pyruvate ratio rose and β-glucuronidase activity increased respectively after open heart surgery as in shock. But the metabolic changes of the fifteen patients pretreated with allopurinol were less significant, although same tendency was observed. The heart beat of all patients except one case in the allopurinol group, started spontaneously after extracorporeal circulation without using DC counter shock. In the control group all patients needed DC counter shock. We concluded that allopurinol was effective in preventing damage of cellular structures and derangements of metabolism of patients undergoing open heart surgery.

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In order to investigate the pathophysiology of tachycardia and bradycardia dependent block in the His-Purkinje system, anterior septal artery was ligated and the effects of vagal stimulation and atrial pacing were serially checked in 26 dogs. Tachycardia dependent intra-His bundle block or H-V blocks developed in all cases following ligation of the anterior septal artery and bradycardia dependent block ensued in 3 cases. The latter appeared only in the form of split His bundle or lengthening of the H-V intervals. Spontaneous second or third degree AV block appeared thereafter. Bundle branch block appeared in 19 cases after ligation of the artery. Rate dependent bundle branch block was observed before the development of stable bundle branch block. Frequently, a very long pause was necessary to produce bradycardia dependent block. On the other hand, bradycardia dependent H-V blocks by vagal stimulation were not necessarily dependent upon cardiac cycle length alone. Tachycardia dependent paroxysmal A-V blocks were induced in 7 cases by atrial pacing, soon before or after the onset of spontaneous second degree A-V block. In addition, this block was induced in the very early phase after ligation of the artery in one case. This repetitive intra-His bundle block or H-V block was induced not only by progressive increase in pacing rate but also by gradual decrease in pacing rate after a Wenckebach type of second degree A-H block.

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Our data indicate that the resistant strains isolated from Japan show cross-resistance between EM, LCM, TC, and CP. In 1975, there were a few EM-resistant strains isolated from New Zealand and Australia at a low MIC. In 1977, no EM-resistant strains were found outside of Japan. Almost all of the EM-resistant strains were type T-12 in Japan and were not typable in New Zealand and Australia. It was suggested that the serotypes of group A streptococci are related to their antibiotic resistance pattern.

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The number of patients with the first attack of rheumatic fever reached a peak in 1960, decreased remarkably until 1968, then has remained unchanged for the last nine years. Approximately 10% of rheumatic patients still develop recurrences. we would like to express our thanks for the cooperation of the seven pediatric departments which made this report possible.

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Sixty-eight patients of clinically diagnosed myocarditis, 0-15 years of age, were followed up and analyzed. Forty (58.8%) were males. The majority were older than 5 years. Clinical courses were rather mild, chronic and self-limiting at large. Only 1 case had a relation to chronic cardiomyopathy. Exertional symptoms (chest pain, chest distress, syncope) were seen in 25 (36.8%). ECG changes or both, mainly in leads II, III V5 and V6. Positive Master' test, prolonged QTc, widened mean spatial QRS-T angle and various arrhythmias were also observed. Cardiac performance, estimated by echocardiogram and phono-mechanocardiogram was lowered in 41 (60.3%). Large IV sound and large A wave in apexcardiogram were also frequently found. All but 3 patients showed continuous elevation of serum enzymes, namely, LDH, LDH-1/LDH-2, CPK, CPK-MB, HBD and GOT. Etiological evidences were obtained by serological study in 11 cases (16.2%) : 2 of Coxsackie B-1, 3 of Coxsackie B-2, 1 of Coxsackie B-4, 2 of mycoplasma pneumoniae, 1 of cytomegalovirus, 1 of ECHO-7 and 1 of rubella. We proposed a criteria for diagnosis of myocarditis as follows : (1) Exertional symptoms. (2) ECG findings. (3) Serum enzyme abnormality. (4) Lowered cardiac performance. (5) Cardiomegaly. (6) Changing character of all signs and symptoms.

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Clinical features of 11 patients of acute Coxsackie B viral myocarditis diagnosed by neutralizing antibody titers were reported. All patients had a flu-like symptom and 8 patients had fever. Initial cardiac manifestations were congestive heart failure in 9 patients, and syncopal attack in 4 patients. Electrocardiographic abnormalities frequently observed were non-specific ST-T changes, low voltage, and intraventricular conduction disturbances including 4 patients of complete A-V block due to trifascicular block. Ten patients had a rise of serum enzymes. It seemed that in severe patients the serum enzymes rose markedly. From the analysis of laboratory and histological findings, Coxsackie B viral myocarditis were often complicated by hepatitis.

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1. HLA antigens were determined in 30 Japanese patients with hypertrophic cardiomyopathy. Several antigens were more common in patients compared with controls, but statistically significant differences were not evidenced. In families one and two, six of seven kindred who inherited HLA-A9 and B7 had the disease. None of five kindred lacking HLA-B7 showed evidence of the disease. In families three and four, affected family members had HLA-A2 and BW-35. Our finding suggest that the HLA system may play some role in the pathogenesis of hypertrophic cardiomyopathy with familial occurrence. 2. Twenty patients with rheumatic valvular heart disease were also studied. There was no significant difference in frequencies of HLA antigens between patients and controls.

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Rabbits and rats developed myocarditis on the 16th, 30th, and 60th day after intrarenal inoculation with Cryptococcus neoformans. The cardiac lesions consist of focal necrosis with infiltrations of small round cells in the myocardium. Cryptococcal antigens were demonstrated by a direct immunofluorescent antibody method in the damaged myocardial lesions. Cryptococcus neoformans itself was found by periodic acid-Schiff stain in the damaged myocardial lesions.

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The human heart antigens demonstrated in citric acid extracts by immunodiffusion were submitted to further analysis. Heart antigens were precipitated at 30% to 70% saturated ammonium sulphate. These fractions contained antigens reactive with rabbit antisera to human heart. The third fraction out of four proteins which were separated by Sephadex G-150 gel filtration, was reactive against rabbit antisera to human heart. The intensely stained proteins of both heart antigens were located at the nineth protein band out of proteins separated by polyacrylamide gel electrophoresis. This protein exhibited precipitin line against rabbit antisera to human heart by two-dimensional electrophoresis, and had mobility between that of serum α₂ and β₁ globulin in immunoelectrophoresis.

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This report showed the comparative study of the rheumatic fever and rheumatic heart disease in Japan and Thailand. At first there is remarkable difference about the incidence of the rheumatic heart disease. The incidence of the rheumatic heart desease in Thailand was one hundred times that in Japan. Secondly, there is particular difference about the course of mitral stenosis in childhood. In Japan common pattern of rheumatic heart disease was slight mitral insufficiency and mitral stenosis was seldom. In Thailand mitral stenosis was observed in 5% on rheumatic heart disease, and mitral stenosis developed early following an attack of rheumatic fever. These differences were supposed due to the socio-economic state in each country.

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