Two kinds of filaments in parallel arrangement have been observed in the basal part of the cytoplasm in the epithelial cells of a Bowman's capsule and in the epithelial cells of a proximal tubule of a glycerinated rat kidney. The first was thin an linear in shape, 55-70Åin diameter and exhibited arrow-head structures upon treatment with heavy meromyosin (HMM). The other was rod shaped, with thick filaments, 110-130Å in diameter, 0.14-0.16μm in length, few in number scattered among the thin filaments. From the non-glycerinated kidney, bundles of fibers were attached to some electron-dense regions inside the cell membrane. In highly magnified pictures, two kinds of filaments could be observed. One kind was thin, attached to dense regions, and the other thick, and not attached to dense regions. It is conceivable that these filaments correspond to myofibrils from their characteristic electron microscopical features. An electron microscopical analogy detected in both smooth muscle cells and renal cells leads us to speculate than these thin and thick filaments consisted of actin and myosin respectively.

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The activity of lysyl oxidase which catalyzes the initial step of cross-linking of collagen and elastin polypeptides was measured in blood vessels of the hypertensive rat. The enzyme activity was increased in the aorta and mesenteric artery when hypertension was induced in 8-week-old rats with administration of deoxycorticosterone acetate (DOCA) and 1% saline. Reserpine diminished this increase in vascular lysyl oxidase activity concomitant with reduction in blood pressure. When β-aminopropionitrile, a specific inhibitor of lysyl oxidase, was administered before the onset of DOCA-salt hypertension, the aortic collagen content was reduced markedly. Concomitant with reduction in the aortic collagen content, the development of hypertension and arteriosclerotic changes in the kidney was partially prevented. These results would indicate that hypertension increases the amount and the degree of cross-linking of vascular collagen and that the deposition of excess collagen in the vascular wall contributes to the development of hypertension and arteriosclerosis.

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The medullary 'heart area', origins of the vagal preganglionic fibers innervating the heart, were identified in 19 cats with the use of horseradish peroxidase (HRP) as a retrograde axonal tracer. When HRP was infected in the A-V node area, S-A node area, right atrial wall and right ventricular wall, the labeled neurons were principally found in the lateral half of the dorsal motor nucleus (DMN) and in the medial solitary nucleus (MSN), were almost the same in number bilaterally, and were chiefly from the calamus scriptorius to the upper cervical cord. They showed no anatomical proof for asymmetric distribution. When HRP was injected in the left ventricular wall or the apex, few labeled neurons were identified in the DMN. Labeled neurons were not found in the nucleus ambiguus. This study suggests the labeled neurons in the DMN and MSN are origins of the dually innervating vagal preganglionic fibers to the heart.

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A relation ship between the upstroke pattern of LV dP/dt and LV myocardial function was investigated in 37 patients with various cardiovascular diseases. A Millar's catheter-tip micromanometer was used to attain high fidelity of LV pressure pulse. The parameter t[(dP/dt)+(dP/dt)₀]/P was measured at each 5 mmHg increments of LV developed pressure (total pressure minus LV end-diastolic pressure). Where the (dP/dt)₀ is a value of dP/dt at the corresponding point to LVEDP and is usually zero. The values of t[(dP/dt)+(dP/dt)₀]/P varied with time during the pre-ejection phase, having the tendency to increase to a miximum and then to decrease. D(t₅₀), which is the value of t[(dP/dt)+(dP/dt)₀]/P calculated at the LV developed pressure of 50 mmHg, correlated well with SV/mass (r=-0.70) and SW/mass (r=0.69). There was no significant relationship between D(t₅₀) between the normal and the abnormal LV function groups (2.20±0.21, and 1.78±0.10, respectively: p < 0.001), and also between the normal and cardiomyopathy (CM) groups (1.76±0.11: p < 0.001). Two patients with CM whose LV biopsy findings showed severe myocardial fibrosis had low D(t₅₀) values of 1.58 and 1.66, respectively, while a patient diagnosed as having post-myocarditis had a significantly higher value of D(t₅₀), 2.25. He was shown to have a minimal myocardial damage on LV biopsy, and his clinical course was excellent. D(t₅₀) in a patient who had myocardial infarction was also significantly low. The theoretical base of t[(dP/dt)+(dP/dt)₀]/P was also discussed. From these, it is suggested that t[(dP/dt)+(dP/dt)₀]/P, termed as a "dominance index", which indicates the degree of dominance of the upward or downward convexes of the dP/dt curve, assesses the myocardial function and reflects the myocardial property. Hence, the importance of the accelerative phenomena of the LV pressure during the pre-ejection phase was stressed.

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A relation ship between the upstroke pattern of LV dP/dt and LV myocardial function was investigated in 37 patients with various cardiovascular diseases. A Millar's catheter-tip micromanometer was used to attain high fidelity of LV pressure pulse. The parameter t[(dP/dt)+(dP/dt)₀]/P was measured at each 5 mmHg increments of LV developed pressure (total pressure minus LV end-diastolic pressure). Where the (dP/dt)₀ is a value of dP/dt at the corresponding point to LVEDP and is usually zero. The values of t[(dP/dt)+(dP/dt)₀]/P varied with time during the pre-ejection phase, having the tendency to increase to a miximum and then to decrease. D(t₅₀), which is the value of t[(dP/dt)+(dP/dt)₀]/P calculated at the LV developed pressure of 50 mmHg, correlated well with SV/mass (r=-0.70) and SW/mass (r=0.69). There was no significant relationship between D(t₅₀) between the normal and the abnormal LV function groups (2.20±0.21, and 1.78±0.10, respectively: p<0.001), and also between the normal and cardiomyopathy (CM) groups (1.76±0.11: p<0.001). Two patients with CM whose LV biopsy findings showed severe myocardial fibrosis had low D(t₅₀) values of 1.58 and 1.66, respectively, while a patient diagnosed as having post-myocarditis had a significantly higher value of D(t₅₀), 2.25. He was shown to have a minimal myocardial damage on LV biopsy, and his clinical course was excellent. D(t₅₀) in a patient who had myocardial infarction was also significantly low. The theoretical base of t[(dP/dt)+(dP/dt)₀]/P was also discussed. From these, it is suggested that t[(dP/dt)+(dP/dt)₀]/P, termed as a "dominance index", which indicates the degree of dominance of the upward or downward convexes of the dP/dt curve, assesses the myocardial function and reflects the myocardial property. Hence, the importance of the accelerative phenomena of the LV pressure during the pre-ejection phase was stressed.

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How an acute ischemic attack is induced in a patient with coronary atherosclerosis is unknown and we carried out studies using thromboxane A2 (TXA₂) to determine if acute myocardial ischemia and necrosis could be induced in rabbits. TXA₂ was perfused through the coronary artery for 5 seconds by means of a Swan-Ganz catheter through the right common carotid artery. Significant serial changes of ST-T on ECG and hypotension were observed from 1 minute to more than 1 day after the perfusion in all 22 rabbits. The TXA₂ that was composed of both aggregated platelets and prostaglandin H2 induced the same response, and such was dose dependent. The inactivated TXA₂ was without effect. Seventeen of the experimental rabbits were autopsied. Histological studies of the hearts showed focal myocardial ischemia and necrosis in all rabbits except one autopsied 10 minutes after the perfusion. TXA₂ is apparently capable of inducing acute myocardial ischemia and necrosis.

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In a patient with intermittent type A Wolff-Parkinson-White (WPW) syndrome, the echocardiogram revealed late "double peaked " anterior motions (the former in the late systole, the latter in the early diastole) of left ventricular posterior wall during WPW conduction. In the same condition, phonocardiographic and mechanocardiographic observations indicated a prolonged electromechanical interval, but the external isovolumic contraction time (EICT) and left ventricular ejection time/EICT ratio remained unaltered. In addition, definite but slight alteration in the spatial ventricular gradient was observed. These observations by non-invasive methods present additional informations supporting the concept that conduction abnormalities per se are not responsible for abnormalities of ventricular function unless there is severe underlying heart disease.

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A typical case of hypertrophy of the column of Bertin is first documented in Japan, which is characterized with the adolescence (13-year-old), intermittent gross hematuria, and the confirmation and recovery by the segmental resection. Emphasis is placed on the possibility of its concealment in so-called idiopathic hematuria, and the necessity of the recognition earlier among children with unknown hematuria. The term "hypertrophy of the column of Bertin" was proposed to be used unifyingly henceforce, because it most well describes the pathoanatomy.

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