Sinus node function was analysed in 15 aged patients, including 8 with sick sinus syndrome and 7 without apparent sinus node dysfunction, by rapid atrial pacing and premature atrial stimulation during sinus rhythm and 5 beats of atrial pacing.
Three patterns of sinoatrial response were identified by premature atrial stimulation during atrial pacing. Type I response (3 cases) represented approximately constant return cycles and type II (2 cases) represented a markedly prolonged return cycles following premature stimulation. Type III response was characterized by a progressive shortening of return cycles as the prematurity of atrial extrastimuli was increased.
Underlying mechanisms responsible for these responses were discussed in relation to the sinus node automaticity and sinoatrial conduction.

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Serial study of 72-lead precordial ST-maps, SGOT, and SLDH was done in 30 cases of acute myocardial infarction. Infarct size was estimated by sum of ST elevation in all leads (Σ ST), number of sites showing ST elevation (NST), peak SGOT, and peak SLDH levels, and correlated with each other and with clinical features and hospital course.
Σ ST correlated well with NST (r=0.92), but the correlations of Σ ST with SGOT (r=0.99) and SLDH (r=0.84) were better than those of NST with SGOT (r=0.22) and SLDH (r=0.53).
There were close agreements between Σ ST and peak SGOT and peak SLDH except in the cases of non-transmural infarction, in whom smaller Σ ST suggesting small infarct occurred with higher enzyme peaks indicating moderate or large infarct.
Longer duration of chest pain, larger number of associated conditions (e.g. angina, hypertension, diabetes), complications (e.g. congestive heart failure, shock, arrhythmias) and mortality were associated with larger infarcts.

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Echocardiographic evaluation of left ventricular volume change during rapid and atrial filling periods was made in patients with mital stenosis.
The significant reduction of rapid filling volume was observed and the rate of rapid filling was approximately the half of normal in mitral stenosis. The rapid filling period showed a good correlation to the mitral valve area measured at operation. After surgical treatment, the rate of rapid filling was significantly increased but was still significantly smaller than normal. It was suggested that the remained structural abnormality of mitral apparatus depressed the inflow through the mitral valve in early diastole despite successful mitral valvotomy.
Left ventricular filling during atrial contraction (atrial filling) was augmented twice as much as normal in patients with milder mitral stenosis, compensating the decreased early diastolic filling. In contrast, the atrial filling did not increase in severe mitral stenosis, resulting in the decreased cardiac output. Following mitral commissurotomy, the atrial filling in milder mitral stenosis was reduced but remained significantly larger than normal. There was no change of atrial filling in severe mitral stenosis postoperatively. This fact suggested the existence of impaired contraction of left atrium in cases with severe mitral stenosis. Our results show that the altered left atrial transport function plays an important role in the left ventricular filling in mitral stenosis.

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The effect of amyl nitrite (AN) on the vectorcardiographic T loop was studied in 17 cases who had negative T waves in the left chest leads of ECG. Thirty sec after AN inhalation the maximum T vector was displaced to the left and anteriorly in 15 and to the left and posteriorly in 2 cases. The magnitude of maximum spatial T vector was decreased and the spatial T loop became more circular. Changes in the amplitude of T loop projected to the scalar lead X were closely related with changes in the heart rate which would represent the sympathetic tone.

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Effects of nitroglycerin, phenylephrine, isoproterenol, and propranolol on the cardiovascular system were studied sequentially using echocardiography to evaluate a method for a more precise assessment of cardiac function.
Nitroglycerin reduced systolic blood pressere (sBP, 3.9%, p<0.01), enddiastolic (EDVI, 11.3%, p<0.001), end-systolic volume indices (ESVI, 10.0%, p<0.05), stroke index (SI, 13.1%, p<0.005), and cardiac index (CI, 7.1%, p<0.05) without changes in diastolic pressure (dBP), mean velocity of circumferential fiber shortening (mean Vcf), or ejection fraction (EF). Mid-systolic left ventricular (LV) endocardial stress (STRESS) as an index of afterload decreased by 13.6% (p<0.02).
Afterload augmentation by phenylephrine infusion resulted in bradycardia, reductions of CI (9.6%, p<0.05) and mean Vcf (11.2%, p<0.001) without changes in ER.
Tachycardia, reductions of EDVI (13.5%, p<0.05), ESVI (46.8%, p<0.00I), and STRESS (20.3%, p<0.005), and augmentations of CI (29.1%, p<0.001), mean Vcf (62.4%, p<0.001), and EF (16.2%, p<0.001) were induced by isoproterenol administration.
Whereas no significant changes were observed in mean Vcf, EF, or other parameters of cardiac performance, decrease in LV minute work index (12.9%, p<0.05) with equivalent EDVI suggested minimal depression of LV function with intravenous injection of propranolol.
These hemodynamic changes are in good agreement with the results obtained by animal experiments and invasive investigations. Indices of the 4 major determinants of cardiac performance, preload as enddiastolic dimension or EDVI, afterload as STRESS, contractility as EF or mean Vcf, and heart rate can all be assessed by this noninvasive method. The proposed method of sequential assessment of these parameters, changing preload, afterload, and contractility, i.e., dynamic echoventriculography should be a useful tool for the precise evaluation of cardiac function.

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This study was designed to evaluate the usefulness of non-invasive parameters in the follow-up of cardiopathic patients without valvular cardiac diseases.
In 49 patients suffering from heart disease we have studied the changes of radiologic cardiac measurements and systolic time intervals (STI) in the 4 functional classes of the NYHA classification, investigating also the existence of any relationship between these different parameters. Only the patients in the 3rd and the 4th functional classes showed significant changes in STI and radiologic measurements, as compared with the control group. Moreover, significant negative correlations have been observed between relative heart volume and LVET (r=0.69, P<0.001) and LVETc (r=0.82, P<0.001) and positive correlations between relative heart volume and PEP (r=0.59, P<0.01) and PEP/LVET ratio (r=0.75, P<0.001).
These results, while confirming the close correlation between STI and cardiac performance, seem to demonstrate that relative heart volumetry is a fairly accurate index of the cardiac conditions in non-valvular heart diseases.

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In an attempt to evaluate the role of renin-angiotensin system in the controls of blood pressure and aldosterone secretion in the patients with cirrhosis and ascctes, 7 patients were infused of an antagonist of angiotensin II, Sar-1 Ile-8 angiotensin II, intravenously to inhibit the action of renin-angiotensin system and to observe changes in arterial pressure and plasma aldosterone. In 1 patient with recent onset of severe ascites and high plasma renin activity, blood pressure and plasma aldosterone decreased during the infusion. In contrast, mild rise in blood pressure and various changes in plasma aldosterone were observed in the other 6 patients with normal plasma renin activity.
These results suggest variable angiotensin dependency in the controls of blood pressure and plasma aldosterone in the patients with cirrhosis and ascites according to the stage of the disease, the states of sodium and water balance and/or plasma renin activity.

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Agents responsible for the entry of cholesterol-bearing lipoproteins into the arterial wall represent local risk factors in atherogenesis. In an attempt to identify these agents, we inserted a catheter into the ascending aorta of rabbits and 5ml of arterial blood sample was withdrawn. The contraction of the aortic strip of rabbit against Piper and Vane's antagonists with application of this sample was observed. Samples ob-tained after feeding of 1Gm/Kg of cholesterol and after an intravenous administration of thromboxan A₂ (TXA₂) contracted the aortic strip. Samples from non-treated rabbits or those obtained after intravenous administration of 10μg of epinephrine or norepinephrine did not contract the strip. Previous administration of 20mg/Kg of indomethacin decreased the contraction developed after feeding of 1Gm/Kg of cholesterol. It was suggested that TXA₂ might be released into the arterial blood by the ingestion of cholesterol and might be one of the agents responsible for the entry of lipoproteins.

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The effect of thyroxine on membrane bound (Na⁺, K⁺)-ATPase isolated as a microsomal fraction from rabbit heart and kidney was investigated. In the heart, thyroxine administration produced an increased Ki value (a concentration of ouabain required for half maximal inhibition of (Na⁺, K⁺)-ATPase activity) without alteration of the specific activity of cardiac (Na⁺, K⁺)-ATPase, indicating that the digitalis sensitivity of cardiac (Na⁺, K⁺)-ATPase was decreased. On the contrary, a significant increase of the specific activity of renal (Na⁺, K⁺)-ATPase was observed without change in its digitalis sensitivity. These results suggest that (1) a decreased sensitivity of cardiac (Na⁺, K⁺)-ATPase to digitalis glycosides in thyrotoxic animals may contribute to the decrease in the inotropic and toxic effects of the digitalis glycosides in the hyperthyroid state, and that (2) there may be an organ difference in (Na⁺, K⁺)ATPase.

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A new antihypertensive agent, labetalol, has potent hypotensive effects in the anesthetized rat and dog when given intravenously and also in the unanesthetized beagle when given orally. Labetalol slightly increased renal blood flow of the anesthetized dog while decreasing blood pressure. Labetalol slightly increased blood flow of canine femoral artery under constant pressure perfusion. However as compared with hydralazine, labetalol seems to have no marked vasodilatatory effect which accounts for its hypotensive effect.
Pharmacologically, labetalol possessed both α- and β-blocking activities, though weaker than phentolamine and propranolol respectively. Another specific action of labetalol was that it has stronger β-blocking action on β₁ receptor (heart rate response) than on β₂ receptor (blood pressure response). Like several other β-blockers, Labetalol seems to block neuronal uptake of noradrenaline.

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The dog heart-lung preparations were prepared. The "equilibrium point", which could be defined as the point at which the cardiac output (CO)-curve and the venous return (VR)-curve crossed, when the CO and VR were plotted against the right atrial pressure, was recorded directly by utilizing an X-Y recorder. The CO-curve was obtained, as a locus of the equilibrium point, by raising and lowering the level of blood in the venous reservoir (competence test). The meaning of the procedure was shown to increase or decrease the mean systemic pressure, and to cause the corresponding parallel shift in the VR-curve. The VR-curve was obtained by changing myocardial contractility. When heart failure was induced by pentobarbital or by chloroform, the equilibrium point shifted downwards to the right, depicting the VR-curve. During development of the failure, the slopes of CO-curves decreased gradually. Effects of cinobufagin and norepinephrine were also analyzed. Utilization of the X-Y recorder enabled us to settle the uniform experimental conditions more easily, and to follow the effects of drugs continuously on a diagram equating the CO- and VR-curves (Guyton's scheme).

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A prospective survey on the comparative studies of the renin-angiotensin system (RAS) was made at the final session of the Japan-U.S. Cooperative Seminar, held on November 14-19, 1977, at Jichi Medical School, Tochigi-ken, Japan. Strategies and tactics of the research have been clarified. In morphological studies, the strategy is to clarify structure of the juxtaglomerular apparatus in representative species of vertebrate classes. In chemical studies, each component of the RAS must be established in each vertebrate class. Since we now know the existence of severel new angiotensins in vertebrates, their amino-acid sequences must be determined. They must be synthesized in sufficient purity. It is necessary to establish the international purity and assay criteria for synthetic angiotensins. In comparative studies on physiological aspects, the strategy is to establish the physiological roles of the RAS in vertebrate classes. Controls of blood pressure, of aldostrone secretion, of glomerular filtration rate and tubular transport, and of drinking and intestinal absorption are the candidates. Physiological roles of extrarenal renin as well as renal one are interesting. A renin-like substance in the corpuscles of Stannius in the teleosts has been identified preliminarily as hypocalcin. Many frontiers exist in these fields, and one can expect fruitful contributions to research of the cardiovascular disease in humans through comparative studies of the RAS.

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The presence and absence of renin activity and juxtaglomerular cells (JGC) in the kidney have been extensively studied among the vertebrates. Renin and JGC have been found in the kidneys of tetrapods and teleostean fishes. Therefore the renin-angiotensin system probably appeared first during early evolution of teleosts. However, the findings of various investigators need to be analyzed precisely to summarize and the subjects remained for further research need to be pointed out. There still remains a possibility that a similar hormone is present in the cyclostomes and elasmobranchs. There are some discrepancies between the renal renin activity determined biochemically and the histological visualization of the granules in some primitive bony fishes. There are contradictory reports regarding the presence of macula densa in nonmammalian kidney. The fact that JGC are present extrarenally in sea-horses may suggest some function of this system. Renin-like activity has been reported extra-renally in various mammalian tissues and in the corpuscles of Stannius (CS) in teleosts. Physiological roles of these extrarenal renin have not been clarified. It has been demonstrated that CS contain 'hypocalcin' which lowers plasma Ca level. It is of interest in determining the possible relationship between the renin-angiotensin substances in CS and hypocalcin.

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Comparative biochemistry of renins and angiotensins was discussed. Renin extracted from hog kidney was different from that from mouse submaxillary glands in immunoreactivity and carbohydrate content. Rat kidney renin was also different from hog kidney renin in the amino acid composition. The presence of big and big-big renins was pointed out immunochemically. These big renins were considered to be precursors of kidney renin.
Angiotensins in mammalian and nonmammalian species produced by renal or extrarenal renin have been differentiated by some biochemical and pharmacological criteria. Some of these angiotensins were analyzed sequentially. The replacements of amino acid residues at positions 1, 5, and/or 9 of angiotensin I have been demonstrated in nonmammalian species.
Specific pressor activities have been determined using synthetic angiotensins by a 4 point assay in rat. Specific pressor activities of various angiotensins were obtained from the dose-blood pressure-response curves using a single angiotensin sample per assay rat.

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The renin-angiotensin system (RAS) in mammals may participate in the controls of blood pressure and aldosterone secretion, and possibly in the regulation of renal function. It has been shown that renin release is controlled by: 1) two intrarenal receptors, the renal arteriolar receptor and the macula densa; 2) the sympathetic nervous system; and 3) several humoral agents. Recent studies indicate interrelations between the RAS and renal prostaglandins and the kallikrein-kinin system.
Comparative studies have revealed that renal renin and the juxtaglomerular (JG) cells emerged during the early evolution of bony fishes, whereas the macula densa evolved later in the vertebrate phylogeny. Exogenously administered angiotensins and renin produce vasopressor actions in representative species of all vertebrate classes from elasmobranchs to mammals, and increase secretions of mineralocorticoids from the adrenal cortex (interrenal) in amphibians, reptiles, and possibly in teleosts. Angiotensin causes glomerular diuresis in teleosts and lungfishes, which may be ascribed to increased dorsal aortic pressure, while angiotensin may have both glomerular and tubular actions in some amphibians. Intracranial injection of angiotensin stimulates drinking in teleosts, reptiles, and birds, but not in amphibians.
Hemorrhage and acute hypotension are potent stimuli for causing renin release in an aglomerular teleost and a bird. When we consider this fact together with the anatomical evidence that the evolution of the JG cells precedes that of the macula densa, it appears that the RAS has evolved with a close relationship to blood pressure homeostasis. On the other hand, there is no clear evidence that the RAS is activated in depleted teleosts and amphibians.
Although the RAS appears to exert several functions in man and other mammals, some of them may be more important in primitive animals, while a similar function remains in mammals as a relic of the primitive system. Comparative approaches provide a perspective of biological history and unique experimental model that will eventually aid in understanding of the underlying mechanisms operating in mammals.

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A case of aortic regurgitation observed in a thalidomide deformed child is presented. Possibility of thalidomide as an etiologic factor was discussed.

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