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Biomedical subjects

T Takatsu

Publications and source records attributed to T Takatsu.

At least 55 records · Page 3Linked to original sources
PubMed1984

Effects of captopril on arterial and venous pressure, renal function, and humoral factors in severe chronic congestive heart failure.

The effects of captopril in several humoral factors were studied to elucidate the role of the renin-angiotensin (RA) system in arterial and venous pressures and renal function in patients with severe chronic congestive heart failure. A single oral dose of captopril in 20 subjects reduced mean arterial blood pressure from 77 to 67 mm Hg; this decrease correlated with baseline plasma renin activity (PRA). The increase in PRA and the decrease in plasma aldosterone levels after captopril were much greater in subjects with higher PRA. Plasma norepinephrine (NE) levels decreased, while those of epinephrine did not change. Peripheral venous pressure declined from 107 to 77 mm H2O; this decrease correlated with the change in NE levels. During 7-day captopril therapy, urine volume and sodium excretion increased (1145 to 1136 ml/day and 76 to 94 mEq/day) in 11 subjects in whom renal function was followed. Renal plasma flow (RPF) rose from 237 to 364 ml/min, while glomerular filtration rate did not change; the filtration fraction decreased from 32% to 23%. Simultaneous infusion of aprotinin in six of the subjects did not affect the captopril-induced increase in RPF, despite the suppression of plasma bradykinin levels. These results suggest that captopril reduces arterial blood pressure in patients with high PRA through inhibition of the RA system and dilates veins by attenuation of sympathetic nervous activity. Increased RPF and urinary sodium excretion induced by captopril might result from inhibition of the RA system; the kallikrein-kinin system or bradykinin-mediated prostaglandins do not appear to play a major role.

Adult↗
PubMed1982

Hypertrophic nonobstructive cardiomyopathy: a precise assessment of hemodynamic characteristics and clinical implications.

A precise assessment of left ventricular function was performed in 20 patients with hypertrophic nonobstructive cardiomyopathy to elucidate the basic pathophysiology, and the data were compared with those in 22 normal subjects. Whereas end-diastolic pressure was high in those with cardiomyopathy, a more accurate index of preload, end-diastolic stress, did not differ from normal value. Afterload was about half the normal value. Both isovolumic indexes [peak positive dP/dt and (dP/dt)/DP40] and ejection phase indexes of contractility (ejection fraction) were in the normal range; however, the end-systolic stress volume ratio was significantly reduced (43% of the normal value). Although the left ventricular minute work index was in the normal range, the unit muscle performance (minute work/mass) was very low (49%). An abnormality of left ventricular relaxation was demonstrated by low peak negative dP/dt (56%) and prolonged time constant T (191%), and a stiff left ventricle was demonstrated by a high diastolic elastic stiffness constant (129%). These observations suggest that the contraction of a unit muscle is inappropriate to produce an adequate contraction of the whole ventricle, and that hypertrophy might be an adaptive process to maintain normal systolic function by increasing mass and reducing afterload.

Adult↗
PubMed1982

A clinical study on the role of the renin-angiotensin-aldosterone system and catecholamines in chronic congestive heart failure.

In order to evaluate the roles of the renin-angiotensin-aldosterone system and of catecholamines in 117 normotensive patients with chronic congestive heart failure (CHF), a study was made of the relationships between plasma concentrations, hepatic extraction of these humoral factors and hemodynamic parameters. In 6 patients with moderate to severe CHF, the acute effect of oral; administration of angiotensin I converting enzyme inhibitor, SQ 14225 (captopril), on mean arterial pressure (MAP), peripheral venous pressure (VP) and these humoral factors was investigated. In patients with CHF of Class III-IV (according to NYHA classification), the urinary norepinephrine (U-NE) excretion increased. Plasma norepinephrine (P-NE) levels increased in proportion to the severity of CHF (p less than 0.001) and had a positive correlation with systemic vascular resistance (SVR) (p less than 0.01), VP (p less than 0.05), pulmonary artery wedge pressure (PWP) (p less than 0.01) and plasma renin activity (PRA) (p less than 0.01). P-NE correlated negatively with the cardiac index (p less than 0.02). Hepatic extraction of norepinephrine (EX-NE) was reduced in patients with elevated right atrial pressure (RAP) (p less than 0.05) and negatively correlated with VP (p less than 0.05). In patients with elevated P-NE, U-NE increased significantly (p less than 0.01), despite their decreased renal clearance of norepinephrine (CNE) (p less than 0.02). There was no significant difference in EX-NE between these patients and patients with normal P-NE. PRA was higher in Class III-IV patients than in Class I-II patients in the prediuretic period (p less than 0.01). PA showed a significant positive correlation with PRA (p less than 0.001). Hepatic extraction of aldosterone (EX-A) was reduced in patients with elevated RAP (p less than 0.05) and was negatively correlated with VP (p less than 0.05). Following captopril administration, PRA increased consistently and PA decreased. MAP fell, especially in 2 patients with mitral stenosis. The heart rate tended to decrease. VP also fell with symptomatic improvement. The decline in VP was correlated with the decrease in P-NE (p less than 0.01). These findings suggest that the sympathetic nervous system contributes to the elevation of SVR and PWP even before frank heart failure develops. The rise of P-NE seems to be due to increased norepinephrine release from sympathetic nerve beds, whereas a decrease in hepatic extraction and renal clearance probably has only a minor effect. The renin-angiotensin system also seems to contribute to elevation of SVR, to maintain effective arterial pressure by enhanced sympathetic activity, and the renin-angiotensin system seems to be a main determinant of PA in CHF.

Aldosterone↗
PubMed1981

Cardiovascular status in asymptomatic alcoholics, with reference to the level of ethanol consumption.

One hundred and forty-five alcoholics without known causes of heart disease, who were serially admitted to the alcohol detoxification centre, were studied to see the incidence of cardiac abnormalities and dose related effects of ethanol. All patients were divided into heavy (consumed more than the equivalent amount of 125 ml of pure ethanol daily for 10 years or more) and moderate drinkers (consumed 75 to 125 ml of ethanol daily). All of them were ambulatory and free from cardiac symptoms. There was no difference among heavy and moderate drinkers in the incidence of abnormalities detected by the electrocardiograms and chest x-ray films. In the alcoholics, the most frequent finding was a prolonged QTc interval of more than 0.44 s on the electrocardiogram (62 patients, 42.8%), unrelated to serum electrolytes imbalance. Cardiomegaly on chest x-ray film was observed in 25 patients (17.2%). M-mode echocardiogram was recorded in randomly selected patients and compared with age and sex matched controls. The interventricular septum and posterior wall were thicker in alcoholics, while left ventricular volume showed no difference. Left ventricular muscle mass was significantly increased only in heavy drinkers. Left ventricular function at rest was not depressed in these patients at an average of 31 days after the last drink of ethanol. Severe heart failure was not found even among the group of heavy drinkers, of whom more than 90% had liver dysfunction. Cardiac hypertrophy seems to occur in heavy drinkers, but is clinically well compensated in the majority of alcoholics.

Adult↗
PubMed1981

Studies on the mechanism of "exaggerated natriuresis" in essential hypertension.

Prompt and exaggerated natriuresis and diuresis were seen one to two hours after the starting of an infusion of 300 ml of 3% saline for one hour in patients with essential hypertension on a high sodium chloride intake. There were no significant differences in urinary volume and sodium excretion after the saline load in patients with normal and low plasma renin activity. The inhibition of angiotensin converting enzyme with SQ 14225 in patients with normal plasma renin activity did not produce additional natriuresis and diuresis after the saline load. Mean arterial blood pressure and/or changes in mean arterial blood pressure after the saline load showed a positive correlation with urinary volume and sodium excretion in each collection period in hypertensive subjects. Free water reabsorption in hypertensives was lower at high levels of osmolar clearance than that in control subjects. These results suggest that "exaggerated natriuresis" in essential hypertension is due to a decrease in tubular sodium reabsorption, which may be the result of intrarenal hemodynamic changes related to high blood pressure per se. The decreased medullary osmolar gradient is a possible contributing factor in the enhanced sodium and water excretion, while the renin-angiotensin-aldosterone system does not seem to play an important role.

Aldosterone↗
PubMed1981

Electrocardiographic and echocardiographic changes after one to two-years' treatment of hypertension. Analyses of voltages (Sv1+RV5), wall thickness, cavity, mass, and hemodynamics of the left ventricle.

The changes of left ventricular anatomy and function following treatment with antihypertensive agents for 1 to 2 years were studied by echo-cardiography in 34 patients with hypertension whose blood pressures and electrocardiographic voltages (SV1+RV5) were significantly decreased (p less than 0.001 and 0.01, respectively). The drugs administered or used were trichlormethiazide, beta-blockers, alpha-methyldopa, clonidine hydrochloride, and guanethidine. Most patients received 2 or more of the above drugs. The interventricular septal thickness, the left ventricular posterior wall thickness, the calculated left ventricular mass, the atrial dimensions, all decreased following treatment of hypertension for 1 to 2 years (p less than 0.001-0.05), and the ejection fraction improved (p less than 0.001). It is concluded that cardiac hypertrophy is not irreversible in patients with hypertension if their blood pressure is adequately controlled.

Adult↗
PubMed1981

[Pathophysiology of hypertrophic and congestive cardiomyopathies: a guide of fundamental therapeutic approach (author's transl)].

A precise assessment of left ventricular (LV) function was performed in 20 patients with hypertrophic cardiomyopathy (HCM) and 14 patients with congestive cardiomyopathy (CCM) to elucidate the pathophysiology of these diseases, expecting to establish a fundamental therapeutic approach of them. Twenty-two patients who underwent cardiac catheterization and were found to have normal LV function served as normal control. LV preload, defined as LV end-diastolic stress, was normal in HCM, and it was elevated in patients with CCM and congestive heart failure (CHF). While an index of afterload, defined as mid-systolic stress, was markedly reduced in HCM, it was elevated in CCM and CHF. Although three indices of LV contractility including the rate of LV pressure rise divided by developed pressure of 40 mmHg ((dp/dt)/DP40), ejection fraction (EF) and LV minute work index, were all in a normal range in HCM, they were very low in CCM. This observation indicates that the systolic function of HCM is normal as a pump, and that it is markedly reduced in CCM. One index of LV relaxation, which was the peak rate of LV pressure fall (peak negative dp/dt) was reduced in both HCM and CCM, and the other index, which was the time constant of LV pressure fall (the time constant T) was prolonged in both of these diseases. An index of compliance, defined as diastolic elastic stiffness constant (K) was high in HCM and normal in CCM, and the other index, defined as end-diastolic elastic stiffness was normal in HCM and high in patients with CCM and CHF. This observation suggests that chamber compliance is low in HCM, and that muscle compliance begins to decline with the appearance of CHF in CCM. Although poor systolic function is evident in CCM, poor contractility or inadequate contraction of a unit muscle is also suspected in HCM since 1) normal EF was maintained with very low afterload, 2) LV end-systolic volume index was normal with very low end-systolic stress, and 3) LV unit muscle minute work about one half of normal value with normal preload. Several important therapeutic guidelines can be derived from this study: As CCM is a disease of reduced LV contractility, the main therapy for this disease is to enhance the contractility. Elevation of preload and afterload are associated with the appearance of CHF, and this coincides with New York Heart Association functional class III. Therefore, the indication of preload and/or afterload reducing agents, such as diuretics and vasodilators, is considered for such patients. Although preload and/or afterload reducing agents are well known to be contraindicated in obstructive type of HCM, since they increase the intracardiac pressure gradient, these agents must be used with great precaution in nonobstructive type, as they reduce preload suddenly, and life-threatening low cardiac output might take place. For the same reason, strenuous exercise must be prohibited in HCM...

Adolescent↗
PubMed1980

Comparison of three luting agents.

Three types of luting cements were compared for acidity, disintegration, and film thickness. The pH during setting of the two types of polycarboxylate cements exceeded 6 after 5 hours; that of the water-settable polycarboxylate cement was the highest, almost reaching neutral. The zinc phosphate cement reached pH 3.4 after 5 hours and 5.5 after 24 hours. All cements tested showed remarkably greater disintegration in the lactic acid solution than in the distilled water. The disintegration of the water-settable zinc polycarboxylate cement in distilled watter was about half that of the other cements. The disintegration in the lactic acid solution was approximately the same for all cements tested. The film thickness was smallest with the water-settable zinc polycarboxylate cement.

Acrylic Resins↗