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In view of the fact that stable echocardiograms are easily obtained during atrial pacing, pacing echocardiography was performed to evaluate the usefulness for detecting regional wall motion abnormalities during pacing-induced ischemia and to investigate the relationship between changes in the R wave and left ventricular dimension. The patients were 12 cases of angina pectoris (10 of coronary artery disease; CAD, and 2 of coronary patent aortic valvular disease; AVD) and 6 control cases. Simultaneous recording of two-dimensional and M-mode echocardiograms and electrocardiograms was done before, during and after the atrial pacing at increasing heart rate until angina appeared or the heart rate of at least 140/min was reached. In 12 angina cases, angina and ST depression were induced in 10 and 11, respectively. Excursion of the interventricular septum (IVS) decreased during pacing-induced ischemia in 6 of 7 CAD cases, in which the left anterior descending coronary artery was significantly stenosed (more than 75%). Excursion of the left ventricular posterior wall (LVPW) decreased during pacing-induced ischemia in 4 of 7 CAD cases, in which the vessels giving rise to posterior descending coronary artery were significantly stenosed (more than 75%). In 2 AVD cases, excursion of both IVS and LVPW decreased during ischemia. Left ventricular end-diastolic dimension (LVEDD) increased in only 2 angina cases, although R wave amplitude increased in 6 angina cases.

Effects of cardiac size on surface potential magnitude were investigated by induction of acute changes in ventricular dimensions by rapid atrial pacing in 17 cases with ischemic heart disease (IHD) and in 15 cases without IHD. Left ventricular end-diastolic dimensions (LVDd), estimated by echocardiography, decreased along with certain changes in surface potential magnitude during atrial pacing in each case. A positive correlation between LVDd and the amplitudes of RV5, RX, and the maximum spatial QRS magnitude was observed in most of the cases and might be explained by changes in distance between the heart and the chest electrode and/or the Brody effect. However, an inverse correlation was observed in 4 of 17 cases with IHD, and could not be explained by these factors. Other factors, such as changes in the ventricular activation sequence, should be considered as the mechanism.

Changes of the surface ECG and monophasic action potential induced by isoproterenol injection were investigated under normo- and hypercalcemic conditions in dogs. (1) Biphasic time course of T wave changes, initially inverted and subsequently uprightly tall, was observed after intravenous injection of isoproterenol in doses of more than 2 microgram. (2) Initial prolongation and subsequent shortening of the phase 2 of action potential were observed on the ventricular surface in accordance with the biphasic time course of the T wave changes on the surface ECG after isoproterenol injection. (3) Giant T wave inversion associated with QT prolongation was obtained by isoproterenol injection under hypercalcemia. (4) Marked prolongation of total duration as well as phase 2 of action potential was observed in accordance with the giant negative T wave on the surface ECG. Although the mechanism of this experimental model of giant negative T wave is not clear, this model could have important suggestions on the unknown mechanism of giant negative T wave observed in various clinical status.

In 30 patients with nocturnal angina, the night-time ECGs were continuously recorded, and the time and duration of attack, cyclic character of attacks, the relation of chest pain to ischemic ECG changes and arrhythmias during attack were compared between 18 cases with ST elevation and 12 cases with ST depression during attack. In cases with ST elevation, 1) attacks occurred between 2:00 and 8:00 a.m., being most frequent between 4:00 and 5:00 a.m. 2) the duration of attack measured from the duration of ischemic ECG changes was less than 5 min in 88% of the attacks, 3) the attack often recurred with intervals less than 30 min and ECG changes were often unaccompanied bt chest pain, 4) the attack was complicated with various kinds of arrhythmias. These features were in marked contrast to the cases with ST depression, in which attacks were evenly distributed over the night-time, of longer duration, sporadic in occurrence and far less complicated with arrhythmias. These data suggest that the difference of mechanisms causing attacks between both groups.

The chronic effects of oral administration of an angiotensin converting enzyme inhibitor (captopril, 63-80 mg/Kg/day) on blood pressure and the renin-angiotensin-aldosterone system were-studied in normotensive male Wistar rats. Blood pressure (BP), plasma renin activity (PRA), plasma renin concentration (PRC), plasma renin substrate concentration (PRS), plasma aldosterone concentration (PAC) and renal renin content (RRC) were measured after 2, 9, 19, 29 and 58 days of captopril administration. BP was determined in awake rats and blood samples were obtained by decapitation. In addition, BP responses to bolus injections of angiotensin I (AI, 80 ng/Kg), angiotensin II (AII, 80 ng/Kg) and bradykinin (BK, 10 micrograms/Kg) were examined in conscious rats which had received captopril for 20 days. The BP of the rats which had been given captopril for 9 days or longer was significantly lower than that of the control rats. PRA and PRC were markedly increased, and both PRS and PAC were decreased in the captopril-treated rats. RRC, which was reduced after 2 days of captopril administration, was substantially increased thereafter. Although the pressor responses to AII were similar in the captopril treated and the control rats, the responses to AI were reduced to 50% of those to AII in the former. The depressor responses to BK in the captopril-treated rats were 2.3 times as large as those in the control rats. Our results show that long-term use of captopril lowers BP in normotensive rats on a normal sodium intake.(ABSTRACT TRUNCATED AT 250 WORDS)

This study compared responses of blood pressure, plasma concentrations of norepinephrine (PNE) and aldosterone (PA), plasma renin activity (PRA) and urinary excretion of aldosterone during a 5-day period of high salt intake in 11 untreated patients with essential hypertension and 11 age-matched normotensive control subjects. The hypertensive patients all had blood pressures that had been above 160 systolic and/or 90 mmHg diastolic before admission and had decreased to below 150/90 mmHg with only bed-rest and mild salt restriction (6 Gm per day). Sodium balance was also measured before and after high salt intake (16 Gm per day). The hypertensive patients showed both a significant reduction in blood pressure after hospitalization and a significant blood pressure elevation when salt intake was increased. In contrast, no obvious changes in blood pressure were observed in the normotensive subjects. Sodium retention and decreases in PNE and PRA during the high salt period were similar in both groups. However, the reduction in PA and urinary aldosterone excretion in response to excessive salt intake was less pronounced in the hypertensive patients than in the normotensive subjects. The ratio of percentage changes in PA to percentage changes in PRA after salt loading was significantly lower in the hypertensive patients than in the normotensive subjects. In addition, the changes in PA during salt loading were inversely proportional to changes in blood pressure (r = 0.66, p less than 0.01). Thus, it is suggested that the sensitivity of blood pressure to increased dietary salt intake in hypertensive patients may be related to altered aldosterone dynamics, and that the blunt responses of the PA and urinary excretion of aldosterone can be attributed to reduced sensitivity of the adrenal cortex to changes in circulating angiotensin.

In a case with the Wolff-Parkinson-White syndrome, the phenomenon "entrainment without interruption" was observed during spontaneous tachycardia. Electrophysiologic study revealed that the tachycardia was due to reentry with the antegrade limb being the AV node-His axis and the retrograde limb being the accessory pathway. This report is the second report showing "entrainment" phenomenon which is consistent with macro reentry as the mechanism of tachycardia as shown in atrial flutter.

The effect of electrical stimulation of the efferent cardiac sympathetic nerves on activity of afferent cardiac fibers in the sympathetic nerves and coronary hemodynamics of anesthetized dogs has been examined. During partial constriction of the coronary artery, a brief stimulation of the efferent cardiac sympathetic nerves resulted in sustained excitation of the afferent fibers and a sustained decrease in blood flow of the constricted artery which were associated with systolic bulge of the left ventricle and elevation of the ST segment of electrocardiogram. These changes were not produced without constriction. Pretreatment with phentolamine suppressed excitation of the afferent fibers, development of systolic bulge and elevation of the ST segment. Also, the decrease in coronary blood flow induced by stimulation was replaced by an increase after the administration of the agent. Propranolol suppressed excitation of the fibers, systolic bulge and elevation of the ST segment, but could not eliminate the decrease in blood flow. The results indicate that sympathetic stimulation caused a decrease in coronary blood flow through excitation of the alpha-adrenergic receptors while increasing cardiac work load and energy requirements through excitation of the beta-adrenergic receptors, leading to more severe myocardial ischemia and excitation of the afferent fibers.

Prognosis of 36 patients with congestive cardiomyopathy was studied in relation to various clinical factors. Half life of the survival curve after overt heart failure was about 7 years. Although left ventricular function was a major determinant of clinical course in congestive cardiomyopathy in general, its relation to prognosis was variable according to the type of cardiac involvement. In peripartal cardiomyopathy and in a type of cardiomyopathy named subacute cardiomyopathy with pulmonary thrombosis in this paper, factor(s) other than left ventricular function, possibly including pulmonary thrombosis, may be operative as more important determinant of extremely poor prognosis in these subtypes. Alcoholic cardiomyopathy was also unique in its favorable prognosis in association with reversible cardiomegaly following abstention from alcohol.

Long term clinical courses of a patient and her family with idiopathic cardiomyopathy and WPW syndrome were described. The mother and her brother (the first generation) had died of heart disease, and 1 sibling had also died suddenly of heart disease when the study began. Seven out of the 8 siblings (the second generation) were followed for 17 years from 1958 to 1976. The 4 siblings had both typical or atypical WPW syndrome and cardiomegaly in 1958, 2 of them died suddenly and unexpectedly, 1 of them died of congestive heart failure, and 1 of them did not have any complaint during the period. One was normal in 1958 but developed cardiomegaly and atypical WPW syndrome in 1976. The other 2 were normal in both 1958 and 1976. The 2 children of the second sibling (the third generation) were followed simultaneously for 15 years. Both had WPW syndrome without cardiomegaly. It was suggested that a late onset of the disease could occur in the family with young onset, that the clinical course might become different mainly by sudden cardiac death which occurred only in the members with abnormal findings, and that WPW syndrome and cardiomegaly could be inherited or occur together in the same generation but separately in the different generation.

The changes of monophasic action potential durations due to stellate stimulation for the period of 3 sec were studied in dogs with suction electrodes from the anterior surface of the right ventricle and the posterior surface of the left ventricle. Prolongation of monophasic action potential duration was observed from the period of 2 to 3 sec during stimulation to that of 10 to 20 sec after the termination of stimulation. Prolongation of monophasic action potential duration due to right stellate stimulation was predominant in the right ventricle and that due to left stellate stimulation was predominant in the left ventricle. The transient T wave change in the surface electrocardiogram occurring immediately after the beginning of stellate stimulation could be explained by this local difference in prolongation of ventricle repolarization. Since the onset of prolongation of monophasic action potential duration preceded increase in blood pressure following stellate stimulation, this prolongation of monophasic action potential duration did not result from the hemodynamic changes and could be a primary effect of the sympathetic nerve stimulation.

The effect of vagal stimulation on activity of afferent sympathetic nerve fibers from the dog's left ventricle has been examined. During partial constriction of the coronary artery, a brief electrical stimulation of the cervical vagus nerves resulted in a decrease in blood flow of the constricted artery, systolic bulge of the left ventricle, elevation of the ST segment of electrocardiogram and excitation of the afferent nerve fibers, which continued for up to 15 min. These changes were not produced without coronary artery constriction. Intravenous injection of phentolamine eliminated the decrease in blood flow, and suppressed systolic bulge, elevation of the ST segment and excitation of afferent fibers. Propranolol could not eliminate the decrease in blood flow while suppressed the other changes. Atropine eliminated all of these changes. The results indicate participation of adrenergic alpha-receptors in sustained decrease of coronary blood flow and excitation of afferent cardiac sympathetic nerve fibers which can be produced by a brief vagal excitation.

Whether apical hypertrophic cardiomyopathy is a variant of classic hypertrophic cardiomyopathy or a separate entity is controversial. This is a case report of an apical hypertrophic cardiomyopathy. The patient was a 67-year-old man associated with giant negative T waves in electrocardiogram and asymmetric apical hypertrophy on echocardiogram. He died of liver cirrhosis and liver cell carcinoma. At necropsy the heart showed apical hypertrophy grossly and extensive disarray of myocardial fibers near the apex of the left ventricle histologically. The necropsy findings were indistinguishable from those of classic hypertrophic cardiomyopathy. This suggests that apical hypertrophic cardiomyopathy is a variant of hypertrophic cardiomyopathy.

Three patients with mitral regurgitation (MR) associated with aortitis syndrome are presented. All had multiple lesions of the large sized arteries, calcification of the aorta, mild inflammatory findings, a chronic course, and congestive heart failure. MR was observed by ventriculography in all 3 patients. Case 1 had mitral valve prolapse and secondary systemic hypertension. Case 2 showed mildly thickened mitral valve leaflets and had moderate aortic regurgitation (AR). Case 3 had massive AR. The grade of MR was moderate in Cases 1 and 2, and massive in Case 3. The left ventricle was moderately dilated in Cases 1 and 2 but contracted sufficiently and symmetrically in all 3 patients. Other than the prolapse, no significant mitral valve deformity or left ventricular asynergy was evident by ventriculography. The incidence of MR was 3.1% of 128 patients with aortitis syndrome observed in our clinic. MR may be found in the late stage of aortitis syndrome. It may be caused by a mild valvular lesion related to aortitis syndrome and be exacerbated by increased hemodynamic loads such as those which occur in secondary hypertension and AR.

The effect of angiotensin-converting enzyme inhibition on regional blood flow was studied in a total of 21 normotensive Wistar rats fed on either low or high salt diet. A new potent angiotensin-converting enzyme inhibitor (CEI), SQ 14,225 was administered intravenously in a dose of 2 mg/Kg to the conscious animals, and changes in fractional distribution of cardiac output were determined with a microsphere method. Prior to administration of CEI, there was no significant difference in mean arterial pressure (MAP) or regional blood flow between salt-depleted and salt-loaded rats. With CEI, MAP did not change significantly in either group. Fractional distribution of cardiac output increased to the kidneys (p less than 0.002), and decreased to the stomach, spleen, and skeletal muscle (p less than 0.02, p less than 0.002, and p less than 0.01, respectively) in the salt-depleted group, while a pattern of blood flow distribution was not changed in the salt-loaded group. These results suggest that angiotensin II plays an important role in regulating regional blood flow in salt-depleted conscious animals, but not in salt-loaded ones.

Thirty-one patients with angina pectoris and 15 patients with myocardial infarction who performed exercise test by Master's double two-step test have been longitudinally followed up for 4-10 years. Exercise electrocardiogram was taken by Frank's lead and T loop was constructed in frontal and horizontal planes from 3 scalar tracings recorded at a paper speed of 100 mm/sec. ST vector was determined at 100 msec from the beginning of Q wave and the line connecting 2 ST vectors before exercise and at the point of the maximal ST change after exercise was determined as ST exercise vector. To indicate width of the T loop, the length to width ratio (L/W) was used and the change of width of the T loop induced by exercise was expressed by a ratio of L/W between before exercise and at the maximal change in frontal and horizontal planes. In cases having ST exercise vector of 0.1 mV or more the magnitude or the direction of the ST exercise vector alone has little prognostic value and widening of the T loop in addition to the ST exercise vector of 0.1 mV or more occurring after exercise was a predictive sign of poor prognosis and no widening of the T loop was a predictive sign of good prognosis.

Long-term clinical effects of beta-blockers (propranolol in most cases) and calcium inhibitors (nifedipine in most cases) were studied in 16 patients with hypertrophic cardiomyopathy. On overall subjective symptoms, beta-blockers were effective in 50% of symptomatic patients, while calcium inhibitors were effective in only 33%. On angina pectoris, however, calcium inhibitors were superior to beta-blockers in our patients. Blood pressure decreased with each drug, and the decrease was significant with nifedipine. Otherwise there was no change in physical findings with either drug. Long-term (more than 6 months) use of beta-blockers resulted in an increase in cardiothoracic ratio on chest X-ray, a decrease in left ventricular ejection fraction on echocardiogram and more pronounced ST-T change on electrocardiogram. Prolonged use of nifedipine resulted in a slight decrease in cardiothoracic ratio, but no systematic change on echocardiogram and on electrocardiogram.

Exercise tests were performed in 14 patients with untreated variant angina with frequent spontaneous attacks and in 15 patients after treatment abolished the attacks. (1) Anginal attacks associated with ST elevation were induced by exercise in 79% of untreated patients. By contrast, ST elevation was not observed in treated patients and ST depression was induced in 53% of the cases. (2) Exercise-induced ST elevation in untreated patients was shown in the same leads as the spontaneous attacks. (3) Exercise-induced ST elevation appeared initially during the recovery phase after exercise in 36% of untreated patients. Exercise-induced ST depression appeared during or immediately after exercise. (4) The reproducibility of exercise-induced ST elevation was low with repeated tests at different stages, but exercise-induced ST depression was consistently observed. (5) The exercise-induced ST depression and lack of ST changes in treated patients were highly suggestive of the presence and absence of organic coronary artery disease, respectively. However, the exercise-induced ST elevation in untreated patients did not differentiate between the presence or absence of organic stenosis of the coronary arteries. The results of exercise tests vary with the stage of variant angina. It is suggested that a coronary arterial spasm is a trigger mechanism for exercise-induced angina in cases of variant angina with frequent spontaneous attacks.

The hemodynamic and metabolic changes, during coronary occlusion and during coronary perfusion with non-oxygenated solution, were studied in anesthetized dogs. Coronary perfusion with non-oxygenated Tyrode's solution was performed through a cannula inserted into the left circumflex coronary artery. Left ventricular peak systolic and end-diastolic pressure (LVSP and LVEDP) were measured, and peak LV-dp/dt/IIP calculated. Stroke volume was measured, and the changed of the local myocardial segment length were recorded by a strain gauge arch sutured on that portion of the myocardium perfused through the left circumflex coronary artery. The efflux of lactic acid into the venous blood from the myocardium perfused through the left circumflex coronary artery was calculated. After 10 sec of coronary occlusion, LVSP, SV, and peak LV-dp/dt/IIP declined; LVEDP elevated and a systolic bulge appeared on the local myocardial segment length curve. There was almost no change in these parameters during 3 min of perfusion with non-oxygenated solution. The efflux of lactic acid was more marked during the perfusion with non-oxygenated solution than during coronary occlusion. The delay of the depression of cardiac function during perfusion with the non-oxygenated solution could be related partly to the "wash-out" of metabolites, such as lactic acid, accumulated in the anoxic myocardium.

Etiology of QT prolongation and T wave high voltage was studied in 90 chronic alcoholics in relation to history of alcoholism, blood chemical values, heart rate and QRS voltage with a technic of multiple regression analysis. Incidences of QT prolongation (22%), T wave high voltage in lead V2 (9%), hypopotassemia (23%), hypocalcemia (26%) and hypomagnesemia (28%) were high, despite these examinations were done after relatively long abstention period (35 days on average). Sinus tachycardia (19%) and QRS high voltage (SV1 + RV5 exceeding 4 mV, 41%) were also frequent. Unexpectedly, QT interval did not correlate to serum electrolytes, including calcium. Major factors associated with QT prolongation were sinus tachycardia, longer abstention period and larger amount of daily alcohol consumption. Although the reason of each association was not quite clear, alcoholic myocardial damage may be a cause of QT prolongation. Voltage of T wave in lead V2 was sensitive to serum potassium level, but the observed tendency of hypopotassemia acted to the direction against high voltage of T wave. The sole factor positively associated with high voltage of TV2 was high QRS voltage, which may be a manifestation of left ventricular hypertrophy.

The effect of a new chemical agent, SG 75, on coronary blood flow of anesthetized dogs has been examined. Intravenous administrations of this agent in a dose of 10 microgram/Kg or over caused a significant increase in blood flow of non-constricted coronary artery. Percent increases in flow were 40 (10 microgram/Kg), 95 (50 microgram/Kg), 145 (100 microgram/Kg), and 195 (250 microgram/Kg). The increases were significantly larger than those caused by the same doses of diltiazem, verapamil, nitroglycerin, isosolbide dinitrate, and papaverine. The durations of the increase in flow were 12 (10 microgram/Kg), 23 (50 microgram/Kg), 28 (100 microgram/Kg), and 46 min (250 microgram/Kg), and they were longer than those caused by diltiazem and verapamil. A slight reduction in left ventricular tension and an increase in aortic blood flow were also observed following the administrations of SG 75 in a dose of over 50 microgram/Kg. A decrease in heart rate was produced with a dose of over 500 microgram/Kg. However, PQ interval of electrocardiogram became shorter. Intravenous administrations of SG 75 in doses of 50 and 150 microgram/Kg caused an increase in blood flow of the constricted coronary artery, while nitroglycerin (10 and 30 microgram/Kg) and nifedipine (1 and 3 microgram/Kg) reduced it. The results indicate that SG 75 is a potent and long-acting coronary vasodilating agent and it causes an increase in blood flow of constricted as well as non-constricted coronary artery.

The effects of the agents that inhibited synthesis of prostaglandins (PGs) and thromboxanes (TXs) on cyclical reduction of blood flow in partially constricted coronary artery of anesthetized dog were examined. The cyclical reduction of coronary blood flow was eliminated by intravenous injections of aspirin that inhibited synthesis of endoperoxides, of benzydamine that inhibited synthesis of endoperoxides and TX A2, and of phenylbutazone that inhibited synthesis of PG E2, but was not of reduced glutathione that inhibited synthesis of TX A2 and accelerated synthesis of PG E2. In the preparations in which cyclical reduction of blood flow did not occur spontaneously, intracoronary injection of PG E2, but not of PG F2a, induced the cyclical reduction. The cyclical reduction was also induced by intravenous injections of epinephrine and reduced glutathione that accelerated synthesis of PG E2. The results indicate participation of PG E2 in the cyclical reduction of coronary blood flow.

The effects of coronary vasodilating agents and alpha- and beta-adrenergic blocking agents on cyclical reductions of blood flow in the partially constricted coronary artery of anesthetized dogs were examined. Intravenous injections of nitroglycerin (50 microgram/Kg), SG 75 (150 microgram/Kg), papaverine (1 mg/Kg), and nicotinic acid (10 mg/Kg) eliminated both cyclical reductions of flow and ST elevation (group 1). Nifedipine (10 microgram/Kg), verapamil (500 microgram/Kg), diltiazem (500 microgram/Kg), and propranolol (500 microgram/Kg) suppressed ST elevation, but they could not eliminate cyclical reductions of flow (group 2). Dipyridamole (1 mg/Kg) and phenotolamine (500 microgram/Kg) augmented both ST elevation and cyclical reductions of flow (group 3). The results indicate that ST elevation due to cyclical reductions of coronary blood flow was eliminated by spasmolytic actions of group 1 on coronary artery, was suppressed by negative chronotropic and/or inotropic actions of group 2, and was augmented by peripheral actions of group 3.

Slow cyclic fluctuations were frequently observed in blood pressure of the distal portion of the partially constricted coronary artery of anesthetized dogs. Lowering the mean peripheral coronary blood pressure below 50% of the control value was required for initiation of fluctuations. Each fluctuation in pressure was composed of 2 phases; the phase of rise and phase of fall. Almost invariably, the phase of rise and phase of fall were accompanied by increase and decrease in coronary blood flow, respectively. When the mean peripheral coronary blood pressure fell below 20% of the control value during the phase of fall, systolic bulge and elevation of the ST segment of surface ventriculra electrocardiogram occurred. Period duration of each fluctuation ranged from 30 sec to 14 min. The cyclic fluctuations in pressure, flow, electrocardiogram and left ventricular wall motion were eliminated by nitroglycerin, but were not affected by phentolamine, propranolol, atropine, cervical vagotomy, and stellectomy.

The effects of a stable prostaglandin I2 analogue, ZA 36374, on recurring reduction of blood flow in the partially constricted canine coronary artery were compared with those of prostaglandin I2. Intravenous bolus injections of 0.3 micrograms/Kg ZK 36374 and 0.15 micrograms/Kg prostaglandin I2 eliminated the recurring reductions. Intravenous infusion of 0.1 micrograms/Kg/min ZK 36374 and 0.01 micrograms/Kg/min prostaglandin I2 also eliminated the recurring reductions. The results indicate that although weaker than prostaglandin I2, ZK 36374 is effective in eliminating recurring reduction in coronary flow related to coronary vasospasm and/or thrombosis.

Electrographic changes associated with cyclical reduction of blood flow in partially constricted one or two coronary arteries of anesthetized dogs were examined. In the preparations with single vessel constriction, cyclical ST elevation occurred along with cyclical reduction of coronary blood flow below 25% of the control value. The ST elevation was associated with reciprocal ST depression in the contralateral ventricular surface. In the preparations with double vessel constriction, cyclical reduction of flow frequently occurred in both vessels. The reduction of flow in one vessel occurred not synchronously with that in another vessel in the majority of preparations. The reduction of flow in both vessels was associated with ST elevation in the corresponding areas of the left ventricle. Premature ventricular contractions frequently occurred at the beginning of or immediately after disappearance of ST elevation, or when ST elevation persisted for more than 10 min. Ventricular fibrillation frequently occurred in the preparations with double vessel constriction.

This study examined the immunohistochemical findings in renal arterioles from biopsy specimens, and related the findings to those of light and electron microscopy. The renal biopsy specimens were obtained from 57 normotensive patients with primary glomerular diseases or idiopathic hematuria, 14 hypertensive patients with associated primary glomerular diseases, 4 patients with essential hypertension and 1 with primary aldosteronism. The tissue slices for the immunohistochemical study were processed with FITC-labelled rabbit antihuman immunoglobulin antisera. Deposits of IgM were detected on the renal arterioles in 16 of the hypertensive patients (84%), but in only 7 of the normotensive patients (12%). The difference in incidence was significant (p less than 0.005). C3 was almost always deposited in the renal arterioles regardless of whether the patient was hypertensive or normotensive. IgG, IgA or fibrinogen were demonstrated only in a few cases, and albumin in no cases. When sections stained with horseradish peroxidase-conjugated anti-IgM antibody were compared under a light microscope with the adjacent PAS-stained sections, it was demonstrated that IgM was deposited only in the portions of the arteriolar walls which showed hyalinotic changes. Electron microscopic examination demonstrated that electron-dense deposits in the subendothelial or intercellular spaces of arteriolar walls were more frequent in the hypertensive patients (11 of 14 cases, 79%) than in the normotensive patients (5 of 18 cases, 28%, p less than 0.05). The deposits appeared to be similar to those which are often found in the glomeruli of patients with glomerulonephritis and which are considered to be immune complexes. These findings suggest that some immunologic mechanism mediated by IgM antibody might be a factor in the development of hypertensive vascular lesions.

The dilatation of the aortic valve portion was evaluated by angiography in 70 patients with aortitis syndrome (Takayasu's arteritis). The diameter at aortic valve commissure was 20 +/- 2.8 min/M2 (NS, vs control) in 46 patients without aortic insufficiency (AI), 23 +/- 2.0 (p less than 0.02, vs without AI) in 11 patients with AI (I or II in grade), 27 +/- 2.0 (p less than 0.01, vs I or II in grade) in 13 patients with AI (III or IV in grade). The diameter was 20 +/- 2.0 in 13 normal control cases and 20 +/- 4.0 in 6 patients with rheumatic AI. The diameters at the levels of aortic valve annulus, sinus of Valsalva and ascending aorta increased also significantly in the patients with AI secondary to aortitis syndrome. The diameter at aortic valve commissure in 24 patients with AI was correlated (r = -0.48, p less than 0.05) to the diastolic blood pressure. Any diameter at the aortic valve portion was not different significantly by the complication of systolic hypertension (greater than or equal to 180 mmHg) in both groups of cases with and without AI. These results indicated that the dilatation of the aortic valve portion was observed in the patient with AI secondary to aortitis syndrome and might be the primary and common cause of AI in all grades, and that the dilatation might not be accelerated by the associated hypertension.

Blood glucose, free fatty acid and insulin responses to oral glucose and the fasting serum lipids were measured in 3 groups: 32 non-obese (mean age: 47.5 years) and 9 obese (mean age: 84.5 years), male patients with coronary heart disease and 12 non-obese male controls (mean age: 46.5 years). The oral glucose tolerance tests were repeated after 3 years in 16 of the non-obese patients with coronary heart disease. The results were as follows: 1) Glucose tolerance was impaired in 19 of 32 non-obese patients (59.4%). There was a significant correlation between impaired glucose tolerance and hyperlipidemia (hypercholesterolemia and/or hypertriglyceridemia). 2) In obese patients FFA levels at 30, 60, and 120 min after oral glucose administration were significantly elevated and FFA decrease was delayed with a drop to minimum levels at 180 min. 3) The insulin response after oral glucose administration in the group of non-obese patients with normal glucose tolerance was similar to that of non-obese controls. In the group of non-obese patients with impaired glucose tolerance, serum insulin levels went up to normal levels, but the peak was delayed. The serum insulin levels in obese patients were significantly higher than those of controls of 0, 60, 120, and 180 min. After 3 years the change in insulin response to oral glucose was not related to anginal symptoms or ECG findings, but was related to body weight change in patients with minor changes in glucose tolerance. 4) The metabolic pattern in the non-obese group with impaired glucose tolerance resembled that of "mild diabetes" in delayed response of insulin and FFA, and mild hyperlipidemia. These findings suggest that obesity may contribute to hyperinsulinemia in patients with coronary heart disease and that impaired glucose tolerance observed in patients with coronary heart disease is in part due to "latent diabetes".

The inhibition of renin release by angiotensin II (AII) is well documented. However, the interaction of this short loop feedback mechanism of AII with the sympathetic nervous system is still unclear. This study was designed to investigate the possible functional relationship between AII and the beta-adrenergic receptors with respect to renin release in vivo. First, the effect of propranolol on captopril-induced renin release was examined in conscious rats. Secondly, the effect of AII on isoproterenol-induced renin release was determined. Captopril (1 mg/Kg) increased plasma renin activity (PRA) from 1.6 +/- 0.3 ng/ml/hr to 4.5 +/- 0.6 ng/ml/hr (p less than 0.01). In contrast, there was no significant change in PRA in rats which received both captopril and propranolol (before 0.9 +/- 0.2 ng/ml/hr, after 1.3 +/- 0.3 ng/ml/hr). Thus, propranolol attenuated the increase in PRA caused by captopril. Isoproterenol infusion (0.1 micrograms/Kg/min) provoked a significant increase in PRA (before 1.3 +/- 0.4 ng/ml/hr, after 6.6 +/- 1.7 ng/ml/hr, p less than 0.01). AII infusion in combination with isoproterenol also increased PRA from 1.6 +/- 0.4 ng/ml/hr to 5.2 +/- 0.3 ng/ml/hr (p less than 0.01). AII in this dose did not suppress isoproterenol-induced renin release. These results suggest that the beta-adrenergic receptor mediating renin release is functionally located distal to the AII receptor in the short loop mechanism controlling renin release.

Effects of new inhibitors of thromboxane synthetase, (E)-3-([1-imidazolmethyl) phenyl]-2-propenoic acid and (E)-3-[4-(pyridylmethyl) phenyl]-2-methyl-2-propenoic acid on cyclical reduction of flow in the partially constricted coronary artery were examined in anesthetized beagle dogs. Intravenous injections of both agents with a dose of 20 mg/Kg eliminated the cyclical reduction induced by constriction in the majority of experiments. However, they failed to eliminate the cyclical reduction induced by indomethacin. Indomethacin-induced reduction was eliminated by prostaglandin I2 in all experiments. It is suggested that thromboxane A2 acted as an accelerator in the cyclical reduction of coronary flow induced by coronary constriction, but did not in the reduction induced by indomethacin.