A recently developed highly sensitive radioimmunoassay method for detecting plasma kinin was used to re-evaluate the results of previous studies, in which plasma kinin had been measured with a bioassay method. To clarify the mechanism of plasma kinin release in global myocardial ischaemia the left main coronary artery was cannulated using a Griggs type autoperfusing cannula after pentobarbital anaesthesia in open chest dogs. The animals were divided into a non-coronary constricted group (n = 4) and a moderately coronary constricted group (n = 7). Cardiac sympathetic nerve stimulation (10 V, 4 Hz, 2 ms duration) was given to both groups. Haemodynamic recordings and blood samples were taken before and after coronary constriction as well as after sympathetic nerve stimulation. The arterial and coronary sinus plasma kinin concentrations were determined with the new radioimmunoassay method. After sympathetic nerve stimulation apparent myocardial ischaemia occurred and the plasma kinin concentration in coronary sinus blood increased significantly in the constricted group. In the non-constricted group, however, myocardial ischaemia did not appear and no significant change in coronary sinus plasma kinin concentrations was seen. These findings show that there was a pronounced release of plasma kinin from the heart when apparent myocardial ischaemia occurred.

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A highly sensitive and specific radioimmunoassay for kinin (minimal detectable

We describe a rare case of surgical repair of a coronary artery aneurysm with arteriosclerotic changes accompanied by coronary arteriovenous fistula (CAVF) after 26 years of conservative therapy. A 71-year-old woman, diagnosed with CAVF 26 years previously, was admitted to our hospital for general fatigue and dyspnea on exertion. Physical examinations revealed that the CAVF originated from the distal portion of the left circumflex artery (LCX), draining into the coronary sinus (CS); it affected the coronary artery aneurysm with arteriosclerotic changes and was calcified from the left coronary main trunk to the distal portion of the LCX. Treatment without resection of the calcified coronary aneurysm was suggested because of fear of excessive bleeding. The CAVF was closed directly from inside the dilated coronary sinus under cardiopulmonary bypass. The dilated ostium of the left coronary artery was closed using a Xenomedica patch. Coronary artery bypass grafting was performed in the left anterior descending artery (LAD) and posterolateral branch (PL) of the LCX using saphenous vein grafts. Postoperatively, the coronary aneurysm was spontaneously thrombosed for low blood flow. The bleeding might have been uncontrolled if the arteriosclerotic and calcified coronary aneurysm had been incised. Therefore, we successfully thrombosed the calcified coronary aneurysm without resection, after reducing the systemic blood flow to the coronary aneurysm and sustaining the coronary blood flow, performed with CABG.

In order to determine the presence or absence of myocarditis in cases with viral or idiopathic pericarditis, a study was conducted as one of our series on endomyocardial biopsy. There were two groups of patients, pericarditis cases (n = 8), and patients with perimyocarditis (n = 6). In the former group, it was confirmed that cardiac sarcoplasmic enzymes were not released during the acute stage of the disease. In the latter, there was positive evidence of the enzyme release. Also, employing our method of categorizing the possibility of myocarditis at the histopathological level, we found that the category 'highly suggestive' of myocarditis was absent in all eight cases with pericarditis. However, in cases with perimyocarditis, this category was assigned in four out of six cases (67%), indicating a high incidence. The category, 'slightly suggestive', was seen in three cases of the former (38%) and two cases of the latter group (33%). It is concluded that in patients with pericarditis, the release of cardiac sarcoplasmic enzyme is an important diagnostic element in the diagnosis of perimyocarditis even if the clinical features reveal a predominance of pericarditis. In patients with perimyocarditis, progression to residual cardiac disease, such as conduction disturbance or congestive heart failure, is likely.

In four patients with essential hypertension and one patient with renovascular hypertension, decreases in blood pressure and plasma angiotensin II levels, and increases in plasma renin activity and plasma kinin levels were observed during eight days of alacepril treatment. Significant correlations between the changes in mean arterial pressure and those in plasma angiotensin II or kinin levels were observed positively or negatively, respectively, in the essential hypertensives. These findings suggest that the hypotensive effect of alacepril might be caused mainly by a decrease in plasma angiotensin II levels and, at least in part, by an increase in plasma kinin levels.

In order to clarify the mechanismof the hypotensive action of captopril, the acute and chronic effects of this drug on the kallikrein-kinin and renin-angiotensin systems were investigated respectively in 14 and 19 patients with hypertension. To determine the acute effect, a dose of 50 mg of captopril was administered once orally. For the chronic effect, 75-300 mgof the drug was administered daily for 14 days. In observations of the acute effect, blood pressure decreased significantly at 30 min. and maximally at 60-180 min. after administration with no change in heart rate. Significant increases in blood kinin levels and plasma renin activity (PRA), and a decrease in plasma angiotensin II levels were also observed. A marked augmentation was also found in urinary kinin excretion, but not in urinary kallikrein excretion. Moreover, the changes in blood pressure significantly correlated negatively with basal PRA, basal plasma angiotensin II and the changes in blood kinin levels, and positively with the changes in plasma angiotensin II. In our study of the chronic effect of captopril, similar changes in blood kinin levels, PRA, plasma angiotensin II levels, blood pressure and heart rate to the acute effect study were observed. Significant correlations of the changes in blood pressure were found negatively with basal PRA, basal plasma angiotensin II levels and the changes in blood kinin levels and positively with the changes in plasma angiotensin II levels. In addition, significant increases in urine volume and urinary sodium excretion occurred following administration of captopril for 14 days, and both increases negatively correlated with the changes in blood pressure. These findings suggest that the hypotensive effect of captopril might be caused, in part at least, by a decrease in plasma angiotensin II levels and an increase in blood kinin levels, and by augmentation of urine volume and urinary sodium excretion during longterm administration.

We encountered two brothers with a combination of Barlow's disease and bilateral axillary artery aneurysms who were operated on during their third decade of life. A symmetrical form of true bilateral axillary artery aneurysms is uncommon. Recurrent mitral regurgitation was presented in the older brother with an endocardial defect in the left atrium, suggesting connective tissue fragility. A hereditary connective tissue disorder was strongly suspected because of the similar presentation and an unusual cluster of pathologies in siblings. Careful follow-up is required to detect recurrence of mitral regurgitation or aneurysm formation in other vessels.