[Relation of obesity to blood pressure behavior in patients with borderline hypertension--a ten-year follow-up study].
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Biomedical subjects
Publications and source records attributed to Y Furuta.
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The effects of high sodium intake on erythrocyte 22Na efflux rate constants were studied in 25 patients with essential hypertension and 9 normal subjects. With changes in sodium intake from 100 mEq to 300 mEq/day, both total and ouabain sensitive 22Na efflux rate constants decreased significantly (p less than 0.001) in "salt-sensitive" patients (-0.031 +/- 0.005 and -0.035 +/- 0.006 /hr, respectively), but these responses were variable in "nonsalt-sensitive" patients and in normal subjects. The "salt-sensitive" patients showed a significant increase in their body weight, while intraerythrocyte sodium contents remained unchanged in the both groups. These results suggest that the abnormal change in membrane Na-K-ATPase activity may, at least in part, be involved in the mechanism of sodium susceptibility in patients with essential hypertension.
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To evaluate the relevant factors of left ventricular peak filling velocity, M-mode echocardiograms showing the left ventricular cavity were recorded and digitized for 81 patients with hypertrophic hearts (HTH) due to hypertensive heart disease (HHD, n = 30), hypertrophic cardiomyopathy (HCM, n = 25), aortic valve stenosis (AS, n = 9), and HHD and HCM with congestive heart failure (HHD and HCM with CHF, n = 17). Peak rates of increase or decrease in dimension (Vf and Ve, respectively) and peak values of instantaneous circumferential fiber lengthening and shortening velocities (Vf/D and Ve/D, respectively) were determined by computer analysis of left ventricular internal dimensions. Systolic excursion (SE), percent fractional shortening (%FS), mean circumferential fiber shortening velocity (mVcf), thickness of the interventricular septum and posterior wall at end-diastole and the sum of them (WThivs, WThpw, and WThivs + pw, respectively) were also calculated. Their variables were compared with those of normal subjects (n = 24). The results obtained were as follows: Systolic functions in HTH without CHF were similar to those of the normal subjects, but Vf and Vf/D were significantly decreased. Differences in Vf and Vf/D between various HTH without CHF were not significant. In AS and HTH with CHF, Vf and Vf/D were significantly decreased together with systolic function. Vf correlated significantly with WThivs + pw, SE, Ve, and WThivs, and Vf/D with %FS, SE, Ve/D, and Ve.(ABSTRACT TRUNCATED AT 250 WORDS)
Echocardiography was performed for 246 patients with hypertension. Among the 246 patients, echocardiographic features simulating dilated cardiomyopathy (DCM) were observed in 12. These patients had past history of hypertension and prominent left ventricular dilatation with reduced left ventricular contractility, but no left ventricular wall thickening. To elucidate the mechanism producing DCM-like features in patients with hypertension, the clinical and echocardiographic findings of the 12 hypertensive patients (HT-DCM) were compared with those of 50 hypertensive patients without dilated left ventricles and of 31 patients with DCM. On admission, all patients with HT-DCM had congestive heart failure (CHF) without high blood pressure and their echocardiograms revealed the abnormal findings described above. There were no differences of the clinical and echocardiographic findings on admission between HT-DCM and DCM. Following medical treatment, relatively early improvement of CHF was noted in all patients with HT-DCM; the LV dimension decreased and diffuse wall motion abnormality improved steadily with gradual elevation of blood pressure during the follow-up periods. The LV function of most patients with HT-DCM improved markedly but never reached normal levels. There were no significant differences the right ventricular endomyocardial biopsy findings of between DCM and HT-DCM. It was suggested the DCM-like features in these cases are caused, not only by hypertension, but by other factors, as well.
7-Ethoxycarbonyl-4-hydroxymethyl-6,8-dimethyl-1(2H)-phthalazinone (EG 626) (0.3-3 mg/kg i.v.), a new cyclic AMP phosphodiesterase inhibitor, increased femoral, renal, coronary, carotid, vertebral and sagittal blood flows in anesthetized dogs. Systolic tension in left ventricular wall, heart rate and cardiac output also increased. These properties of EG 626 resembled those of papaverine (0.1-1 mg/kg i.v.). However, the heart rate increasing activity of EG 626 was less than that of papaverine at equipotent does on the vasodilator actions. In the isolated right atria of guinea pigs, EG 626 was more selective for increasing contractility than for increasing the sinus rate. The cardiovascular actions of EG 626 were also examined in perfused vascular beds and papillary muscle preparations of dogs. An i.v. infusion of EG 626 or papaverine (0.3 mg/kg/min) enhanced the increasing action of isoprenaline on left ventricular systolic pressure and coronary sinus outflow. The vasodilator effect of EG 626 was no suppressed by atropine, propranolol nor clemastine, and the inotropic action was not modified by pindolol. These results indicate that EG 626 may be a useful vasodilator with a cardiotonic activity but with less potency to cause tachycardia than papaverine.
A 64-year-old man was hospitalized in March 1983 for recurrent episodes of dyspnea and palpitation despite medical treatment. At 48 years of age (1967), hypertension was diagnosed, but well controlled by propranolol. At the age of 59 years (1979), his first episode of dyspnea and palpitation was noted, with electrocardiographic (ECG) evidence of left ventricular hypertrophy (LVH), and abnormal Q waves in leads III and a VF. The echocardiogram, however, showed mild LVH with neither asymmetric septal hypertrophy (ASH) nor systolic anterior movement (SAM). On admission (1983), his blood pressure was 130/70 mmHg, and a grade III systolic murmur was heard along the left sternal border and over the apex. On ECG, the left precordial voltage (Sv1 + Rv5) was diminished and the depth of the Q wave in lead III increased compared with that of 1978. On echocardiography, we observed prominent septal hypertrophy (IVST: 20 mm) with ASH (IVST/PWT = 2.0), SAM, an enlarged left atrium, and a diminished left ventricular (LV) cavity. Left ventricular catheterization showed a pressure gradient of 90 mmHg between the LV apex and outflow tract and histological examination of the bi-ventricular endomyocardial biopsy material showed markedly hypertrophied and mildly disarranged myocardial fibers with bizarre nuclei. We considered that this was an interesting case in which ASH and SAM developed in the progression of LVH during the follow-up period.
A Ni-45 wt% Ti (Ni-50 at % Ti) alloy was cast into molds of magnesia and silica investments by use of a dental argon-arc pressure casting machine with a copper crucible . The castings exhibited shape memory properties. The shape recovery process was sharper in the specimens cast in magnesia investment molds than in those cast in silica (phosphate-bonded) investment molds. The latter casting had a hard region of the periphery, suggesting that shape recovery process may be affected by reaction of molten metal with silica. Furthermore, the alloy possessed the adequate mechanical properties for consideration as crown-and-bridge prostheses.
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Changes of left ventricular (LV) pressure-diameter-velocity relations by alterations in heart rate (HR) were investigated in 6 conscious dogs, instrumented with a pair of ultrasonic crystal probe, a micromanometer in LV and pacing electrodes on the left atrium. By atrial pacing the following four stages of HR were produced: stage (S)-I 112, S-II 134, S-III 158 and S-IV 179 bpm (mean HR). These alterations in HR were repeated before and during acute pressure loadings by methoxamine infusion. LV pressure-diameter and pressure-velocity relations were evaluated by the slope value of LV peak systolic pressure (LVSP)-end-systolic diameter, E (D) max, and by the ratio of changes in mV cf (mean velocity circumferential fiber shortening) and LVSP before and during pressure loading, delta mVcf/delta LVSP, respectively. The average of E(D) max at each stage of HR was 9.45, 12.63, 12.59, 11.22 mmHg/mm, and delta mVcf/delta LVSP was -0.009, -0.006, -0.007, -0.009 circ./sec.mmHg, respectively. E(D) max increased more at S-II and S-III than at S-I, and reversely, E(D) max decreased more at S-IV than at S-II. Similarly, delta mVcf/delta LVSP increased more at S-II than at S-I and decreased more at S-IV than at S-II, while delta LVSP and delta EDD (end-diastolic diameter) were not different between stages. These changes in E(D) max and delta mVcf/delta LVSP presented the mountainous pattern effected by alterations in HR, whose changes were almost similar to that of LV peak positive dp/dt and mVcf before pressure loading. Thus, E(D) max is augmented by an increase in HR, which suggests the Bowditch-effect. Reversely, a decrease in E(D) max at a higher rate indicates a depressed inotropic state. E(D) max is dependent on HR and is a sensitive indicator of the contractility of LV.
Net sodium (Na) efflux and potassium (K) influx were determined in Na-loaded/K-depleted erythrocytes derived from 37 patients with essential hypertension and 25 age-matched normotensive subjects with no family history of hypertension, together with the measurement of basal red cell sodium and potassium contents. Intraerythrocyte sodium content was significantly higher in the essential hypertensives than in the normotensives (10.9 +/- 1.4 vs 10.0 +/- 1.2 mmol/L X cells, mean +/- SD, p less than 0.02), but potassium content was nearly equal between the two groups. Net Na efflux in the hypertensives was significantly reduced compared with that in the normotensives (4.57 +/- 0.70 vs 5.18 +/- 1.02 mmol/L X cells X hr, p less than 0.01), but both net K influx and net Na/K flux ratio were not significantly different between the two groups. Net Na efflux and K influx showed a significant inverse correlation with red cell sodium content (r = -0.64 and r = -0.56, respectively, p less than 0.001). These results suggest that the reduced net Na efflux with the increase of red cell sodium content may be related to the pathogenesis of essential hypertension. However, it is impossible to determine the genetic marker of essential hypertension by using the net Na/K flux ratio of Japanese subjects, although Garay et al. have reported that this index was abnormally low in the case of Europeans.
Different types of heart rate (HR)-cardiac output (COP) relationships were compared with their clinical features and hemodynamic findings in 56 patients with brady-arrhythmias (BA). HR was raised by increments of 10 beats per minute (bpm) at 3 min intervals, from spontaneous rates to 100 or 110 bpm by right ventricular pacing. Cardiac and left ventricular (LV) functions at BA were evaluated by intra-cardiac pressures, COP measured by the thermo-dilution method and echocardiographic data. HR-COP relationships were divided into the following 3 types: 24 patients of flat (F), 18 of peaked (P) and 14 of increased (I) type. There were more patients with complete atrio-ventricular block, particularly His-ventricular block, and cardiomyopathic patients with the "P" type than with the other types. Cardiac index, stroke index, stroke work index and systemic vascular resistance were greater in "I", but these differences were not significant. LV peak systolic pressure (LVSP) and end-diastolic pressure (EDP) in "I" increased more than in "F". EDP, LV end-diastolic and end-systolic dimension (ESD) in "P" increased more than in "F". Systolic excursion and LVSP/ESD ratio in "I" increased more than in the other types. Heart failure prior to implantation of pacemaker (PM) and post-PM occurred more frequently in "P". "F" and "I" patients showed comparatively good clinical courses after PM. Thus, cardiac and LV function during BA are maintained in "F" and are impaired in "P", as reported previously. On the other hand, cardiac functions are maintained in "I" as they are in "F", mainly due to contributions of the Frank-Starling mechanism and partly due to maintenance or slight augmentation of contractility.
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9, 11-Epithio-11, 12-methano-thromboxane A2 (STA2), a stable analogue of thromboxane A2, caused a rapid rise in cytoplasmic free Ca2+ concentration ([Ca2+]i) in human platelets as measured with the fluorescent Ca2+ indicator quin2. Concomitantly, this compound induced phosphorylation of myosin light chain which is catalyzed by Ca2+, calmodulin-dependent protein kinase. These reactions were fast enough to trigger serotonin release. 13-Azaprostanoic acid, a receptor level antagonist of thromboxane A2 inhibited STA2-induced elevation of [Ca2+]i, phosphorylation of myosin light chain and serotonin release. These results provide evidence that STA2 interacts with a thromboxane A2 receptor which leads to elevation of [Ca2+]i.
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